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Molecular underpinnings of prefrontal cortex development in rodents provide insights into the etiology of neurodevelopmental disorders

D Schubert, G J M Martens, S M Kolk

Molecular Psychiatry · 2014 · Review

doi:10.1038/mp.2014.147

Abstract

The prefrontal cortex (PFC), seat of the highest-order cognitive functions, constitutes a conglomerate of highly specialized brain areas and has been implicated to have a role in the onset and installation of various neurodevelopmental disorders. The development of a properly functioning PFC is directed by transcription factors, guidance cues and other regulatory molecules and requires the intricate and temporal orchestration of a number of developmental processes. Disturbance or failure of any of these processes causing neurodevelopmental abnormalities within the PFC may contribute to several of the cognitive deficits seen in patients with neurodevelopmental disorders. In this review, we elaborate on the specific processes underlying prefrontal development, such as induction and patterning of the prefrontal area, proliferation, migration and axonal guidance of medial prefrontal progenitors, and their eventual efferent and afferent connections. We furthermore integrate for the first time the available knowledge from genome-wide studies that have revealed genes linked to neurodevelopmental disorders with experimental molecular evidence in rodents. The integrated data suggest that the pathogenic variants in the neurodevelopmental disorder-associated genes induce prefrontal cytoarchitectonical impairments. This enhances our understanding of the molecular mechanisms of prefrontal (mis)development underlying the four major neurodevelopmental disorders in humans, that is, intellectual disability, autism spectrum disorders, attention deficit hyperactivity disorder and schizophrenia, and may thus provide clues for the development of novel therapies.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 23, 2026. Paragraph numbers are ours, so an answer can point at one.

The prefrontal cortex in neurodevelopmental disorders

Neurodevelopmental disorders affect a large percentage of the population worldwide. Although the available drugs can alleviate some of the symptoms associated with these disorders, they are not curative and adverse drug reactions are often observed. In addition, many neurodevelopmental disorder-associated symptoms, especially cognitive symptoms, still cannot be treated effectively. To improve the prognosis of a given neurodevelopmental disorder, the effectiveness of existing therapies and the potential for finding new treatment strategies, detailed knowledge of the development and pathophysiology of the disorders is mandatory., Neurodevelopmental disorders such as intellectual disability (ID), autism spectrum disorders (ASDs), attention deficit (hyperactivity) disorder (AD(H)D) and schizophrenia share particular cytoarchitectonical, connectional and functional features suggesting a similar neurodevelopmental origin. Unfortunately, for the most part, detailed molecular studies of developmental events within brain areas that are involved in the etiology of these neurodevelopmental disorders are still lacking.

A wealth of data indicates that the prefrontal cortex (PFC) contributes to the cognitive deficits or endophenotypes of many, if not all, neurodevelopmental disorders.,,,,,,,,, As a conglomerate of individually unique subareas, the PFC has a key role in the execution of higher-order cognitive functions, for example, language comprehension and cognitive functions involved in decision making such as planning and reasoning.,,, In this respect, the different subareas within the PFC mediate various processes including response inhibition, working memory, attention or autonomic control.,,, Furthermore, the medial regions of the PFC, the mPFC, such as the infralimbic, prelimbic and cingulated areas, have a role in the cognitive deficits of many neurodevelopmental disorders.,

The main neurodevelopmental disorders—ID, ASDs, AD(H)D and schizophrenia—have a complex etiology involving a large number of genes and environmental factors that also affect prefrontal brain regions, including those of the mPFC. Although multiple genes have been found to be associated with each of these disorders, the actual function and involvement of individual genes in the developmental aspects of mPFC formation in particular are largely unknown. Abnormalities in the expression of these genes often lead to impaired or deviant functioning of several brain structures, including the mPFC, affecting behavior as previously shown in animal studies.,

In the following, we will give an overview of the main neurodevelopmental disorders with a particular focus on the defects in the development of the mPFC, bearing in mind that areas other than the mPFC may also contribute to the etiology of the disorders.

ID

The diagnostic category mental retardation groups a number of syndromes with severe ID that are associated with chromosomal abnormalities such as Down Syndrome (trisomy of chromosome 21), Prader–Willi and Angelman Syndromes, Williams–Beuren Syndrome, Smith–Magenis Syndrome, DiGeorge Syndrome and monosomy of chromosome 1p36.1.,,, Other ID syndromes show mild-to-moderate phenotypes and are associated with mutations, small insertions/deletions or copy number variations affecting a single gene, for example, fragile X syndrome, caused by a mutation in the FMR1 gene, and Kleefstra syndrome, caused by a functional loss of the EHMT1 gene. Most ID syndromes are associated with developmental deficits in general, including distorted development of the mPFC.,,, In this respect, during the development of the mPFC of ID patients, molecular/cellular defects have been shown to occur in (a) the proliferation of neuronal progenitor cells,, (b) migration of cortical neurons,,,, and (c) synaptogenesis.,,

ASDs

The ASDs include autism, Asperger's syndrome and ‘pervasive developmental disorder not otherwise specified' Diagnostic and Statistical Manual of Mental Disorders-5th edition (DSM-V). They constitute a group of wide-ranging neurodevelopmental disorders that are characterized by variable impairments in three core symptom domains, that is, reciprocal social interaction, (verbal and nonverbal) communication, and restricted, repetitive and stereotyped patterns of behavior, interests and activities.,,, Although many of these behavioral impairments are driven by deficits in basal ganglia and amygdala functioning, cognitive dysfunctions such as memory deficits and deficits in social interaction and perception are integrated by the mPFC. The neurodevelopmental basis underlying the defects in language and speech, which are often part of the diagnosis in ASDs relates to abnormalities in fronto-striatal functioning.,,,, Regarding the development of the mPFC of ASD patients, molecular/cellular defects have been reported to occur in (a) the proliferation of neuronal progenitor cells, resulting in macrocephalic and minicolumn pathology in several brain areas including the PFC,,,,,, (b) migration and differentiation of GABA ergic parvalbumin+ (PV+) interneurons toward the PFC,,, (c) axon guidance, as there seems to be a disconnection of long-distance axonal pathways, and (d) synaptogenesis, particularly of GABAergic synapses.,, Deficits in integration and early information processing can be explained by hyperconnectivity combined with slower synapses. Furthermore, there is evidence for amplified activation and density of microglia within the PFC of ASD patients.,,

AD(H)D

Inattention, hyperactivity/impulsivity and motivational/emotional dysregulation are the core symptom domains in AD(H)D. In AD(H)D patients, the mPFC-directed cognitive functions are affected and frequently of early onset.,, A delay in cortical maturation specifically in the most prefrontal areas and its connections to other brain areas has often been observed and there is increasing evidence that glutamate signaling is affected. During development, the PFC of patients with AD(H)D shows molecular/cellular defects in (a) the white matter, suggesting axon guidance deficits,, (b) dopaminergic and noradrenergic connectivity with the cerebellum and striatum,,,,, and (c) synaptogenesis influencing the electrophysiological properties and functioning of PFC neurons.,,

Schizophrenia

Schizophrenia is thought to affect mainly (social) cognition, but it usually is also associated with chronic problems of behavioral and emotional regulation. Schizophrenia is characterized by a breakdown of thought processes manifested as delusions and hallucinations (positive symptoms) and by poor emotional responsiveness, and disorganized thinking and speech (negative symptoms). People with schizophrenia are likely to have co-morbidities such as major depression and anxiety disorders. Furthermore, working and long-term memory, attention, executive functioning and speed of processing are often affected. All of these symptoms can at least to some extent be linked to (impaired) PFC functioning.,,,,, During development of the mPFC in schizophrenia patients, molecular/cellular defects may occur in the (a) proliferation of neuronal progenitor cells, as reflected by the observed severely decreased gray-matter volume, as well as of GABAergic PV+ interneurons,, (b) postnatal pruning of dendritic trees and synapse loss,,,, (c) general connectivity of various neurotransmitter systems such as the glutamate, GABA and dopamine systems together with a reduced connectivity with other cortical areas.,,,,,,,

Rodent models of neurodevelopmental disorders

Before one can start to develop better and more target-specific therapies for patients with neurodevelopmental disorders, it is necessary to first unravel elementary processes of brain development in adequate animal models and to understand subsequent developmental processes in those areas associated with the endophenotypes of neurodevelopmental disorders. In this way, fundamental hypotheses can be created and tested in relation to the etiology of these disorders. Such parallel approaches are crucial to eventually design optimal treatment strategies.

As mentioned before, although the PFC is often referred to as a single brain region, many subdivisions into distinct areas can be made, each of which possesses its own specific cytoarchitecture, cytochemistry, connectivity and functional properties. Defining these areas across species suffers from the fact that large interspecies differences exist in the layering per area, fueling the debate on whether or not rodents possess a region equivalent to the human PFC as they lack a granular zone in this area., However, it should be noted that the formation of the general laminar pattern in the PFC shows a relation with phylogenesis: in ‘higher' mammalian species, such as primates and humans, PFC regions can be granular, that is, they possess a granular layer IV, as well as an agranular layer. The ‘lower' the species, the smaller the proportion of granular PFC regions (for reviews, see refs, ). Thus the concept of homologous structures with similar functions may apply.

In this review, we will focus on the rodent mPFC and its structure–function relationships with connected brain areas in the context of neurodevelopmental disorders., One example of a well-defined rodent model for neurodevelopmental disorders is the apomorphine-susceptible and apomorphine-unsusceptible Wistar rat. The behavioral impairments seen in the apomorphine-susceptible rats resemble features of schizophrenia.,, At least part of this phenotype can be attributed to the differences in the mesocorticolimbic projections.

Furthermore, mouse models are ideally suited to study targeted molecular alterations.,,,,,,, In this way, genetic variants identified through association studies can be tested for their biological function and correlated with cognitive endophenotypes of human neurodevelopmental disorders. However, the traditional techniques of targeted mutation used in these kinds of model systems are systemic in nature and often result in inducing compensation mechanisms. Cre-Lox and knock-in systems still affect a large part of the brain, but can offer cell-type selective and temporally controlled strategies to achieve targeted mutations at different pre- and postnatal ages. Although in utero electroporation-mediated gene transfer spatially restrict gene repression or genetic rescues to early developmental time-points (app. E10-E17), virally mediated gene transfer can be performed pre- as well as postnatally. Furthermore, intersectional genetics (Flpe/Cre) to selectively mutate genes of interest in overlapping areas between a Cre and a Flpe allele (for example, Dlx5 Flpe and a region-specific Cre to selectively target GABAergic interneurons in a region of interest) increases the spatial selectivity of such approaches. Using these techniques, it is possible to knock down or rescue a particular gene in a specific part of the brain (for example, PFC) and at a specific time during brain development.

By employing various behavioral tasks, it is now possible to specifically test endophenotypes associated with mPFC function in rodent models, such as working memory, conditioned associative learning, attentional set shifting and reversal learning.,,,,, Consequently, by combining the targeted mutation with specific behavioral tests and instead of having to study a particular disease as a whole, one can now molecularly unravel the individual cognitive endophenotypes., A further advantage of such an approach is that a causal inference can be made between the expression of a particular gene in a specific brain locus and one or more cognitive (endo)phenotypes, which is not yet possible in humans.

Developmental aspects of PFC formation

The PFC represents the functionally most advanced brain area with the longest period of maturation. This maturation includes proliferation and migration of neurons, growth of dendrites, the formation of neural micro- and macro-circuits through efferent/afferent axonal projections, and the fine-tuning of synaptic contacts and neuronal density steered by experience. This maturation process starts with an initial phase of cell division within an intrinsically specified PFC region, in which specific transcription factors (TFs) have a timing-critical role (Figure 1). Developmental events such as induction, migration and axon guidance are under the control of extrinsic cues and sculpt the identity of frontal areas. Appropriate cognitive behavior is fine-tuned over time by activity-dependent processes including sensory stimuli and social interactions, which in turn leads to pruning and cell death of unused connections. As a result, intricate convergence of connections with various other brain areas occurs, eventually creating the unique identity of the PFC and the subareas it encompasses (Figure 1). Here, the initial focus will be on the early developmental events of the (fore)brain as a whole and the molecules that are relevant during this phase. Although little is known about the early developmental characteristics of the PFC, many early principles and main mechanisms of forebrain compartmentalization and maturation are also applicable to PFC development. Important to keep in mind is the influence of external stimuli (for example, stress, drugs and hormones) that, if excessive, can lead to an altered development of the PFC and its connected areas. Thus, the knowledge about the genes that are involved in the structural and functional development of the (fore)brain and in particular the PFC is important for a better understanding of the molecular mechanisms underlying (disturbed) cognitive functions. Eventually, this knowledge may enable us to therapeutically intervene when this ‘developmental balance' is shifted toward neuropsychiatric disorder.

Induction of (pre)frontal boundaries

The developmental progression of the forebrain starts with regional expansion through division of neuronal progenitor cells in proliferative zones lining the embryonic ventricles of the brain. The most anterior part of the neural tube develops into three primary vesicles even before the posterior section of the tube has formed: the prosencephalon (forebrain), mesencephalon (midbrain) and rhombencephalon (hindbrain). After closure, the neural tube is characterized by a sequence of swellings and constrictions along the anteroposterior axis, some of which subsequently develop into strict boundaries.

Except for the specific boundary compartment, the zona limitans intrathalamica (ZLI), no unique set of boundary markers has been identified for regions of the forebrain and most of the telencephalon develops in an unsegmented way. Anterior of the midbrain–hindbrain border (MHB) or isthmus, the diencephalon consists of three neuromeres (p1–p3) according to the so-called prosomeric model.,, The more anterior prosomeres (p4–p6) subdivide the secondary prosencephalon (hypothalamus and telencephalon). The boundaries that are created function to arrange and stabilize local signaling centers or ‘organizers' important for the early patterning of the embryonic brain (Figures 2a and b). Gradually, gradients of soluble morphogens and growth factors (Fgfs, BMPs, SHH and Wnts), are secreted from signaling centers and regulate the graded expression of certain intrinsic TFs, a process that is called induction (Figures 2a and b).

Fgfs, especially Fgf8, Fgf17 and Fgf18 from the rostral patterning center (also called anterior neural ridge) provide, apart from their role in other areas, positional information on the presumptive prefrontal region along the rostro-caudal axis of the forebrain., The dorsal patterning center or cortical hem secretes Bmp4/Wnt3A, which has a role in medial and dorsal pallium patterning,,, but in combination with SHH also steers prefrontal formation (Figures 2a and b). SHH is expressed by the ventral signaling center and regulates Fgf8 expression through the transcriptional repressor Gli3.,,, Absence of Fgf17 leads to a reduced PFC size and abnormal social behavior., Thus, Bmp, Wnt and Fgf proteins all work coordinately to pattern the most rostral telencephalon., Interference with each of the three Fgf receptor subtypes results in reduced numbers of either excitatory or inhibitory neurons, specifically in the prefrontal area and often resulting in altered behavior.,,,,,

Regional identity of the PFC through intrinsic patterning

The gradients of morphogens and signaling molecules from the early patterning centers impart positional information influencing the expression of intrinsic TFs (Figure 2b). These have a crucial role in the regionalization of the forebrain and correlate with morphologic boundaries, the so-called regional specification underlying the spatio-temporal control of postnatal arealization.,,, The regional identity that is created by the expression of TFs includes the final cell-type specification. The inductive signals provided by morphogens and signaling molecules regulate the combinatorial expression of TFs and other regulatory factors, resulting in the generation of specific neuronal subtypes, (Figure 2a and b).

The interaction between extrinsic growth factors and intrinsic TFs during the early developmental events evolves through rostral patterning by the factors Fgf8 and Fgf17 through the Fgf receptors. This Fgf-signaling promotes the expression of the TFs Foxg1, Six3, Sp8, Pax6, Erm (etv5), Er81 (etv1), Nkx2.1 and Pea3, and represses the expression of Coup-tf1 and Emx2 more caudally.,, Although it is most likely the expression of a combination of multiple TFs that underlies the identity of an area, there are a few individual TFs that are specifically linked to the development of the most rostral part of the cortex. The expression of the TFs Pax6 and Emx2, for example, is known to have a role in cortical identity in general.,, Yet, very few TFs are specifically expressed in and linked to early PFC development.

During the course of development, distinct neuronal cell types will express a variety of proteins that are involved in migration, targeting (for example, axon guidance) and specific neurotransmitter release. This set of proteins is unique for each cell type, thereby regulating the formation of functional areas. The expression of the respective genes (extrinsic genes) is under the control of a distinct combinatorial code of TFs generating neuronal diversity(Figure 1 and Figure 2). Other TFs such as Rest4 and Nurr1 display increased expression in the PFC and are involved in various aspects of cognitive behavior., Although an abundance of genome-wide expression data shows that specific TFs are expressed in later stages of PFC development, their downstream targets and functional relevance are largely unknown.,,, In fact, the existing data are now congruent with a model in which each neuronal cell type within the PFC (but also other areas) most likely uses an exclusive code of intrinsic genes to control the expression of extrinsic genes. This code is unique to each particular cell type essential for the sequential steps in development. The next level of complexity starts off when extrinsic mechanisms such as migration and afferent input begin to have a role in the development of the prefrontal areas.

Proliferation and migration of PFC neurons

The PFC, like other cortical areas, expands by generating new neurons through (a)symmetric divisions of radial glia cells in the (sub)ventricular zone lining the ventricles., During this process, reduction of the extrinsic morphogen Fgf8 results in less proliferation and more apoptosis, which ultimately changes the identity of the cortex.,, In particular Fgf has a determining role in the production of excitatory glutamatergic pyramidal neurons in the most anterior part of the cortex with deletion of the gene resulting in a reduced number of excitatory cortical neurons. Many TFs controlling the cell cycle, including cyclinD1, drive prefrontal expansion. Some newborn progenitors or intermediate progenitor cells expressing Tbr2 migrate to the subventricular zone to generate neurons. Lack of Tbr2 expression results in reduced cortical surface and thickness.,,, It is furthermore widely accepted that classical neurotransmitters such as dopamine and serotonin have an early role in controlling the neuron numbers within the PFC.,,

The differential expression of TFs but also of adhesion and axon guidance molecules reflects a signage map for migrating neurons. The expression patterns are graded along the anterior–posterior and medial–lateral axes of the embryonic brain instructing neurons to establish functionally distinct lamina. During embryogenesis, most brain areas deploy radial migration in multiple waves as their major route to establish lamination within the structure.,, Radial glia cells, with their cell body within the ventricular zone, send out their glial processes toward the pial surface where they attach to the basal membrane. Newborn neurons that become (excitatory) projection neurons use the glial scaffold to migrate to their final place in the brain by using either somal translocation or locomotion.,, The ventricular zone generates the deeper layer neurons, including the subplate, layer VI and subsequently layer V projection neurons. Additionally, Cajal–Retzius neurons are generated within the cortical hem and to a lesser extent at other sites in the subpallium and septum. These layer I neurons express Reelin, a large secreted glycoprotein intricately involved in the inside-out laminar patterning of cortical neurons., At later stages, the subventricular zone gives birth to neurons which migrate radially into the cortical plate past the deep layer neurons and form layers IV, III and II of the PFC, creating an inside-out pattern. Most of the projection neurons (80%) use glutamate as their neurotransmitter projecting to distant cortical and subcortical targets. The basic molecular developmental mechanisms that have been elucidated in rodent studies are in principle similar to those in humans, even though the human brain has gone through a series of additional evolutionary steps, including size, shape and gyrification modifications.,,

Migration of GABAergic interneurons towards the PFC

A small proportion of neurons, which includes the majority of GABAergic (GAD65/67+) interneurons originating from the ganglionic eminences, migrate tangentially to the cortical plate, then radially to reach their target lamina. The subpallial interneurons migrate via a lengthy route towards the PFC using directional cues to eventually position themselves between pyramidal projection neurons on which they synapse., Medial ganglionic eminence-derived interneurons will generate PV and somatostatin interneurons that populate all cortical structures (as well as hippocampus, striatum, amygdala, etc). These interneurons are specified in the medial ganglionic eminence by the expression of Nkx2.1 and Lhx6 followed by Sox6 expression as they start migrating. In contrast, caudal ganglionic eminence-derived interneurons encompass all 5-HT3A-expressing interneurons of various morphology and physiology. The homeobox TFs Dlx1 and Dlx2 mainly regulate the maturation of GABAergic (inter)neurons within the ganglionic eminences, having the TF Arx as a downstream target. However, the combinatorial expression of TFs such as Olig2, Dlx5, Arx, Lhx6, Cux2, NPAS1 and MafB define the various subpopulations of interneurons within the subpallium that end up in the (prefrontal) cortex., As development progresses, interneurons within the (prefrontal) cortex start to express transporters (GAT-1 and -3), VGAT and components of GABAergic synapses making them highly adaptive to the maturing PFC.

Axon guidance, target selection and synapse formation of PFC neurons

The assembly of neuronal circuits during embryonic development relies upon the guidance of growing axons to their synaptic targets. To help them find their synaptic partners, developing axons are tipped with a highly motile sensory structure, the growth cone. Growth cones are instructed to follow predetermined trajectories by heterogeneously distributed guidance molecules in the extracellular environment. Binding of axon guidance molecules to receptor complexes on the growth cone surface initiates intracellular signaling events, which modulate growth cone morphology and directionality through local modifications of the cytoskeleton. Axon guidance molecules can act as attractants or repellents, that is, either directing growth cones toward a specific structure or preventing them from entering inappropriate regions. Furthermore, these cues exist as membrane-associated molecules acting at short ranges or as soluble agents with long-distance effects.,,, The responses of growing axons to particular cues, however, may change as they grow toward their final targets. For example, Semaphorin 3F is such a bidirectional guidance cue that, through binding with Neuropilin-2, initially repels dopaminergic axons from the rostral ventral tegmental area on their way to the mPFC, and later attracts and orients them within the mPFC. When the axonal growth cone has been guided to the proper target, synaptic contacts can be formed that are mediated by adhesion molecules such as the cadherins., Newly formed synaptic contacts change their functional properties as development progresses and contribute to the maturation and functioning of an area., Furthermore, the immature afferent projections are refined via the same guidance molecules in topography (pruning of branches), convergence (less efferent projections onto one cell) as well as postsynaptic compartment (less afferent dendritic innervation) in specific brain areas.,, Changes occurring in pyramidal morphology in terms of expansion of dendritic complexity are specifically apparent in layer III. Furthermore, during the first four postnatal weeks the local inhibitory interneuron networks in the mPFC undergo an extensive process of maturation, both at the level of intrinsic functional as well as network properties., Given that inhibitory network activity is thought to contribute to the proper construction of cortical networks, the refinement of synaptic connectivity in inhibitory and excitatory networks leads to developmental plasticity and fine-tuning of complex behavior.

Topographic map formation in PFC connectivity: parcellation versus lamination

As mentioned above, in rodents and other phylogenetically ‘higher' species, the PFC is not one homogeneous cortical region but is compartmentalized into a number of structurally and functionally distinct prefrontal areas, each of which is thought to possess characteristic input–output profiles. In general, the rodent PFC can be subdivided into medial, lateral and ventral sections. Within the medial portion, the anterior cingulate (Cg), prelimbic (PL) and infralimbic (IL) cortices (Figure 3) and dorsal peduncular cortex can be distinguished from dorsal to ventral. The lateral and ventral PFC consists of the orbitofrontal cortex and the agranular insular cortices. The different areas of the PFC are connected to various other brain regions through highly organized projections controlling decision-directed behavior.,,

Input connectivity of the mPFC

In terms of the afferent connectivity of the mPFC, a comprehensive and detailed comparison of area-specific input connectivity is still lacking. The mPFC is known to receive long ascending projections from the ventral hippocampus,, from cholinergic neurons of the basal forebrain,, from dopaminergic neurons of the rostral part of the medial ventral tegmental area,, and from serotonergic/cholinergic neurons of the brainstem along a highly defined trajectory., Functionally, the connection with the ventral hippocampus is thought to be of particular importance for the functioning of the mPFC during cognitive tasks., The cholinergic and dopaminergic systems are considered to modulate mPFC activity and attentional performance., Interestingly, the dopaminergic projections from the ventral tegmental area show strong laminar and cell-type specificity. They form dense contacts exclusively with interneurons in layers V and VI,,,, while for example projections from limbic and thalamic regions innervate both PV+ interneurons and pyramidal cells throughout layers II–VI.,, Furthermore, connections of the mPFC with both the basolateral amygdala, and the striatum are implicated in motivated behavior., Interestingly, the long-range connections originating from the basolateral amygdala have been shown to not only be layer- but also cell-type specific. Neurons in the basolateral amygdala preferentially target layer II pyramidal neurons in the mPFC, such as PL, and amygdala, with which they can form reciprocal connections.,

Output connectivity of the mPFC

As in other cortical areas, the long-range efferent connections of the PFC are mediated by excitatory projection neurons, that is, glutamatergic pyramidal cells. Depending on the PFC area, the pyramidal cells project to many structures such as the basal forebrain, olfactory and cortical structures, amygdala, striatum, (hypo)thalamus and the brainstem.,,,, In addition, prefrontal pyramidal neurons project to various subcortical areas thereby modulating dopaminergic, adrenergic, cholinergic and serotonergic projection systems., The targets of the projection neurons show distinct layer specificity. Layer III pyramidal neurons connect the mPFC mainly to other cortical areas, whereas layers V and VI pyramidal cells project primarily to subcortical targets., Furthermore, there is evidence for layer specificity of projections onto individual subcompartments of single brain structures. In terms of the nucleus accumbens, mPFC layer II pyramidal neurons preferentially innervate the core region, whereas neurons of deep layers V and VI innervate the core as well as the shell region.

In contrast to the input connectivity, there is ample data demonstrating that the output connectivity properties of the mPFC are area dependent, which supports the notion that prefrontal areas are involved in modulating various aspects of cognitive behavior,,, not only in rodents but also in a number of other species.,, The dorsomedial areas of the PFC establish connections with the sensorimotor and association cortex, which are lacking in the ventral parts of the PFC. The ventral parts, however, establish relatively strong connections with the amygdaloid complex and limbic association cortices. Furthermore, the IL has been shown to mainly project to autonomic/visceral related sites, supporting its role in visceromotor activity, whereas the PL primarily innervates limbic sites that are thought to affect cognition.

Future translational avenues of research

In summary, substantial progress has been made in the past decades toward understanding the etiology of neurodevelopmental disorders at the molecular, cellular and systems levels. Nevertheless, we have only just begun to thoroughly study the development of a conglomerate of specific brain areas that as a group define the PFC and that are involved in the etiology of these disorders. In this context, it is remarkable that the exact molecular orchestration of the development of the PFC is still largely unknown. What are the molecular mechanisms that create a correctly parcellated and layered PFC? How are the extensive and highly specific interactions between various signaling pathways that are connecting the individual areas fine-tuned and how can we manipulate these? We are also only beginning to shed light on the large variety of neuronal cells and their integration in prefrontal local and global networks, let alone that we would know all the molecules that guide their differentiation and projections.

To test targeted molecular variations, rodents have emerged as an excellent model. Animal models and functional assays are invaluable as it comes to decipher the exact functions of the large number of genes that are involved in the various aspects of PFC development, that is, induction of prefrontal boundaries, intrinsic patterning of the PFC, proliferation and migration of (pyramidal) PFC neurons, migration of GABAergic interneurons toward the PFC, axon guidance, target selection and synapse formation of PFC neurons, and PFC connectivity formation. Slowly, the view is emerging that some of these genes are identical to the susceptibility genes of neurodevelopmental disorders (Table 1). However, up to now only a few of the genes could be directly linked to one or more of the developmental events within the PFC as well as one or more of the four major neurodevelopmental disorders, that is, ID, ASDs, AD(H)D and/or schizophrenia.

Especially the availability of in utero electroporation-mediated gene transfer and other genetic approaches and hence the possibility to locally knock down or rescue particular genes will hopefully enable us to unravel the exact orchestration of brain areas such as those within the PFC in the near future. Such knowledge will assist in developing early intervention approaches by altering the susceptibility genes at a particular time and place, such that we deviate from the predetermined developmental path, even before the onset of the neurodevelopmental disorder(s) in question. Considering that individual susceptibility genes of neurodevelopmental disorders have often been found to be associated with multiple disorders, we can assume that several disorders share a common neurodevelopmental origin. It will be a challenge to dissect the individual genetic (and possibly even epigenetic) contributions to a disorder by using functional studies combined with behavioral tasks. For example, gene-environment interactions are crucial to distinguish between risk and vulnerability.

It is to be expected that in the coming years many more genes regulating developmental processes in the PFC and other brain structures will be linked to neurodevelopmental disorders and vice versa. Animal models, in which we can specifically alter gene expression in the PFC, can be instrumental for the understanding of the aetiopathological aspects of the disorder(s), as we can monitor the early disturbances that will eventually lead to defects in brain maturation and behavior. In order to move toward better and more preventive treatment of the neurodevelopmental disorders, bridges need to be built between disciplines such as combining genetic analyses of patients suffering from neurodevelopmental disorders with structural and functional brain imaging and in-depth molecular in vitro and in vivo approaches with cell and animal models. Exploring the molecular and cellular aspects during the progression of the disease process in animal models will clarify the pathological mechanisms, which in turn may provide clues to develop novel treatments for these disorders. The earlier during life and the more personalized the treatment strategies are applied, the better, alleviating symptoms at an early stage and reducing medical costs dramatically.

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    Hebert JM Hayhurst M Marks ME Kulessa H Hogan BL McConnell SK BMP ligands act redundantly to pattern the dorsal telencephalic midlineGenesis2003 35214219

    Not in our library10.1002/gene.10183

  135. 135.

    Fernandes M Gutin G Alcorn H McConnell SK Hebert JM Mutations in the BMP pathway in mice support the existence of two molecular classes of holoprosencephalyDevelopment (Cambridge, England)2007 13437893794

    Not in our library10.1242/dev.004325

  136. 136.

    Hebert JM Mishina Y McConnell SK BMP signaling is required locally to pattern the dorsal telencephalic midlineNeuron2002 3510291041

    Not in our library10.1016/s0896-6273(02)00900-5

  137. 137.

    Rash BG Grove EA Patterning the dorsal telencephalon: a role for sonic hedgehogJ Neurosci2007 271159511603

    Not in our library10.1523/jneurosci.3204-07.2007

  138. 138.

    Kuschel S Ruther U Theil T A disrupted balance between Bmp/Wnt and Fgf signaling underlies the ventralization of the Gli3 mutant telencephalonDev Biol2003 260484495

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  139. 139.

    Ohkubo Y Chiang C Rubenstein JL Coordifnate regulation and synergistic actions of BMP4, SHH and FGF8 in the rostral prosencephalon regulate morphogenesis of the telencephalic and optic vesiclesNeuroscience2002 111117

    Not in our library10.1016/s0306-4522(01)00616-9

  140. 140.

    Blaess S Stephen D Joyner AL Gli3 coordinates three-dimensional patterning and growth of the tectum and cerebellum by integrating Shh and Fgf8 signalingDevelopment (Cambridge, England)2008 13520932103

    Not in our library10.1242/dev.015990

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    Cholfin JA Rubenstein JL Frontal cortex subdivision patterning is coordinately regulated by Fgf8, Fgf17, and Emx2J Comp Neurol2008 509144155

    Not in our library10.1002/cne.21709

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    Scearce-Levie K Roberson ED Gerstein H Cholfin JA Mandiyan VS Shah NM Abnormal social behaviors in mice lacking Fgf17Genes Brain Behav2008 7344354

    Not in our library10.1111/j.1601-183x.2007.00357.x

  143. 143.

    Shimogori T Banuchi V Ng HY Strauss JB Grove EA Embryonic signaling centers expressing BMP, WNT and FGF proteins interact to pattern the cerebral cortexDevelopment (Cambridge, England)2004 13156395647

    Not in our library10.1242/dev.01428

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    Shin DM Korada S Raballo R Shashikant CS Simeone A Taylor JR Loss of glutamatergic pyramidal neurons in frontal and temporal cortex resulting from attenuation of FGFR1 signaling is associated with spontaneous hyperactivity in miceJ Neurosci.2004 2422472258

    Not in our library10.1523/jneurosci.5285-03.2004

  145. 145.

    Thomson RE Kind PC Graham NA Etherson ML Kennedy J Fernandes AC Fgf receptor 3 activation promotes selective growth and expansion of occipitotemporal cortexNeural Dev2009 44

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  146. 146.

    Thomson RE Pellicano F Iwata T Fibroblast growth factor receptor 3 kinase domain mutation increases cortical progenitor proliferation via mitogen-activated protein kinase activationJ Neurochem2007 10015651578

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  147. 147.

    Stevens HE Smith KM Maragnoli ME Fagel D Borok E Shanabrough M Fgfr2 is required for the development of the miedial prefrontal cortex and its connections with limbic circuitsJ Neurosci.2010 3055905602

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  148. 148.

    Muller Smith K Fagel DM Stevens HE Rabenstein RL Maragnoli ME Ohkubo Y Deficiency in inhibitory cortical interneurons associates with hyperactivity in fibroblast growth factor receptor 1 mutant miceBiol Psychiatry2008 63953962

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  149. 149.

    Inglis-Broadgate SL Thomson RE Pellicano F Tartaglia MA Pontikis CC Cooper JD FGFR3 regulates brain size by controlling progenitor cell proliferation and apoptosis during embryonic developmentDev Biol2005 2797385

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  150. 150.

    Hoch RV Rubenstein JL Pleasure S Genes and signaling events that establish regional patterning of the mammalian forebrainSemin Cell Dev Biol2009 20378386

    Not in our library10.1016/j.semcdb.2009.02.005

  151. 151.

    Sur M Rubenstein JL Patterning and plasticity of the cerebral cortexScience (New York, NY2005 310805810

    Not in our library10.1126/science.1112070

  152. 152.

    Mason I Initiation to end point: the multiple roles of fibroblast growth factors in neural developmentNat Rev2007 8583596

    Not in our library10.1038/nrn2189

  153. 153.

    Schuurmans C Guillemot F Molecular mechanisms underlying cell fate specification in the developing telencephalonCurr Opin Neurobiol2002 122634

    Not in our library10.1016/s0959-4388(02)00286-6

  154. 154.

    Jessell TM Neuronal specification in the spinal cord: inductive signals and transcriptional codesNat Rev Genet2000 12029

    Not in our library10.1038/35049541

  155. 155.

    Goridis C Rohrer H Specification of catecholaminergic and serotonergic neuronsNat Rev2002 3531541

    Not in our library10.1038/nrn871

  156. 156.

    Hasegawa H Ashigaki S Takamatsu M Suzuki-Migishima R Ohbayashi N Itoh N Laminar patterning in the developing neocortex by temporally coordinated fibroblast growth factor signalingJ Neurosci2004 2487118719

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  157. 157.

    Chou SJ Perez-Garcia CG Kroll TT O'Leary DD Lhx2 specifies regional fate in Emx1 lineage of telencephalic progenitors generating cerebral cortexNat Neurosci2009 1213811389

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    Mangale VS Hirokawa KE Satyaki PR Gokulchandran N Chikbire S Subramanian L Lhx2 selector activity specifies cortical identity and suppresses hippocampal organizer fateScience (New York, NY2008 319304309

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  159. 159.

    Polleux F Ince-Dunn G Ghosh A Transcriptional regulation of vertebrate axon guidance and synapse formationNat Rev2007 8331340

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  160. 160.

    Flames N Pla R Gelman DM Rubenstein JL Puelles L Marin O Delineation of multiple subpallial progenitor domains by the combinatorial expression of transcriptional codesJ Neurosci2007 2796829695

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  161. 161.

    Uchida S Hara K Kobayashi A Funato H Hobara T Otsuki K Early life stress enhances behavioral vulnerability to stress through the activation of REST4-mediated gene transcription in the medial prefrontal cortex of rodentsJ Neurosci2010 301500715018

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  162. 162.

    Rojas P Joodmardi E Hong Y Perlmann T Ogren SO Adult mice with reduced Nurr1 expression: an animal model for schizophreniaMol Psychiatry2007 12756766

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  163. 163.

    Johnson MB Kawasawa YI Mason CE Krsnik Z Coppola G Bogdanovic D Functional and evolutionary insights into human brain development through global transcriptome analysisNeuron2009 62494509

    Not in our library10.1016/j.neuron.2009.03.027

  164. 164.

    Yang S Wang K Valladares O Hannenhalli S Bucan M Genome-wide expression profiling and bioinformatics analysis of diurnally regulated genes in the mouse prefrontal cortexGenome Biol2007 8R247

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  165. 165.

    Erraji-Benchekroun L Underwood MD Arango V Galfalvy H Pavlidis P Smyrniotopoulos P Molecular aging in human prefrontal cortex is selective and continuous throughout adult lifeBiol Psychiatry2005 57549558

    Not in our library10.1016/j.biopsych.2004.10.034

  166. 166.
    Accelerated Recruitment of New Brain Development Genes into the Human Genome · 2011
    No notice
  167. 167.

    Kriegstein AR Noctor SC Patterns of neuronal migration in the embryonic cortexTrends Neurosci2004 27392399

    Not in our library10.1016/j.tins.2004.05.001

  168. 168.

    Noctor SC Flint AC Weissman TA Dammerman RS Kriegstein AR Neurons derived from radial glial cells establish radial units in neocortexNature2001 409714720

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  169. 169.

    Storm EE Garel S Borello U Hebert JM Martinez S McConnell SK Dose-dependent functions of Fgf8 in regulating telencephalic patterning centersDevelopment (Cambridge, England)2006 13318311844

    Not in our library10.1242/dev.02324

  170. 170.

    Garel S Huffman KJ Rubenstein JL Molecular regionalization of the neocortex is disrupted in Fgf8 hypomorphic mutantsDevelopment (Cambridge, England)2003 13019031914

    Not in our library10.1242/dev.00416

  171. 171.

    Raballo R Rhee J Lyn-Cook R Leckman JF Schwartz ML Vaccarino FM Basic fibroblast growth factor (Fgf2) is necessary for cell proliferation and neurogenesis in the developing cerebral cortexJ Neurosci2000 2050125023

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  172. 172.

    Sessa A Mao CA Hadjantonakis AK Klein WH Broccoli V Tbr2 directs conversion of radial glia into basal precursors and guides neuronal amplification by indirect neurogenesis in the developing neocortexNeuron2008 605669

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  173. 173.

    Sessa A Mao CA Colasante G Nini A Klein WH Broccoli V Tbr2-positive intermediate (basal) neuronal progenitors safeguard cerebral cortex expansion by controlling amplification of pallial glutamatergic neurons and attraction of subpallial GABAergic interneuronsGenes Dev2010 2418161826

    Not in our library10.1101/gad.575410

  174. 174.

    Arnold SJ Huang GJ Cheung AF Era T Nishikawa S Bikoff EK The T-box transcription factor Eomes/Tbr2 regulates neurogenesis in the cortical subventricular zoneGenes Dev2008 2224792484

    Not in our library10.1101/gad.475408

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    Sweeney NT Tierney H Feldheim DA Tbr2 is required to generate a neural circuit mediating the pupillary light reflexJ Neurosci2014 3454475453

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  176. 176.

    Kolk SM Gunput RA Tran TS van den Heuvel DM Prasad AA Hellemons AJ Semaphorin 3F is a bifunctional guidance cue for dopaminergic axons and controls their fasciculation, channeling, rostral growth, and intracortical targetingJ Neurosci2009 291254212557

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  177. 177.
    Genetic and pharmacological manipulations of the serotonergic system in early life: Neurodevelopmental underpinnings of autism-related behaviour · 2013
    Not checked
  178. 178.

    Popolo M McCarthy DM Bhide PG Influence of dopamine on precursor cell proliferation and differentiation in the embryonic mouse telencephalonDev Neurosci2004 26229244

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  179. 179.

    Kriegstein A Noctor S Martinez-Cerdeno V Patterns of neural stem and progenitor cell division may underlie evolutionary cortical expansionNat Rev2006 7883890

    Not in our library10.1038/nrn2008

  180. 180.

    Ayala R Shu T Tsai LH Trekking across the brain: the journey of neuronal migrationCell2007 1282943

    Not in our library10.1016/j.cell.2006.12.021

  181. 181.

    Rakic P The radial edifice of cortical architecture: from neuronal silhouettes to genetic engineeringBrain Res Rev2007 55204219

    Not in our library10.1016/j.brainresrev.2007.02.010

  182. 182.

    Knuesel I Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseasesProg Neurobiol2010 91257274

    Not in our library10.1016/j.pneurobio.2010.04.002

  183. 183.

    Gaiano N Strange bedfellows: Reelin and Notch signaling interact to regulate cell migration in the developing neocortexNeuron2008 60189191

    Not in our library10.1016/j.neuron.2008.10.009

  184. 184.

    Lui JH Hansen DV Kriegstein AR Development and evolution of the human neocortexCell2011 1461836

    Not in our library10.1016/j.cell.2011.06.030

  185. 185.

    LaMonica BE Lui JH Wang X Kriegstein AR OSVZ progenitors in the human cortex: an updated perspective on neurodevelopmental diseaseCurr Opin Neurobiol2012 22747753

    Not in our library10.1016/j.conb.2012.03.006

  186. 186.

    Gertz CC Lui JH LaMonica BE Wang X Kriegstein AR Diverse behaviors of outer radial glia in developing ferret and human cortexJ Neurosci2014 3425592570

    Not in our library10.1523/jneurosci.2645-13.2014

  187. 187.

    Miyoshi G Butt SJ Takebayashi H Fishell G Physiologically distinct temporal cohorts of cortical interneurons arise from telencephalic Olig2-expressing precursorsJ Neurosci2007 2777867798

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  188. 188.

    Southwell DG Nicholas CR Basbaum AI Stryker MP Kriegstein AR Rubenstein JL Interneurons from embryonic development to cell-based therapyScience (New York, NY2014 3441240622

    Not in our library10.1126/science.1240622

  189. 189.

    Cobos I Long JE Thwin MT Rubenstein JL Cellular patterns of transcription factor expression in developing cortical interneuronsCereb Cortex2006 16i82i88

    Not in our library10.1093/cercor/bhk003

  190. 190.

    Le Magueresse C Monyer H GABAergic interneurons shape the functional maturation of the cortexNeuron2013 77388405

    Not in our library10.1016/j.neuron.2013.01.011

  191. 191.

    Tessier-Lavigne M Goodman CS The molecular biology of axon guidanceScience (New York, NY1996 27411231133

    Not in our library10.1126/science.274.5290.1123

  192. 192.

    Dickson BJ Molecular mechanisms of axon guidanceScience (New York, NY2002 29819591964

    Not in our library10.1126/science.1072165

  193. 193.

    O'Donnell M Chance RK Bashaw GJ Axon growth and guidance: receptor regulation and signal transductionAnnu Rev Neurosci2009 32383412

    Not in our library10.1146/annurev.neuro.051508.135614

  194. 194.

    Dudanova I Klein R Integration of guidance cues: parallel signaling and crosstalkTrends Neurosci2013 36295304

    Not in our library10.1016/j.tins.2013.01.007

  195. 195.

    Kiryushko D Berezin V Bock E Regulators of neurite outgrowth: role of cell adhesion moleculesAnn NY Acad Sci2004 1014140154

    Not in our library10.1196/annals.1294.015

  196. 196.

    Stoya G Redies C Schmid-Hertel N Inversion of layer-specific cadherin expression profiles and maintenance of cytoarchitectonic areas in the allocortex of the reeler mutant mouseJ Comp Neurol2014

    Not in our library10.1002/cne.23572

  197. 197.

    Lai KO Ip NY Synapse development and plasticity: roles of ephrin/Eph receptor signalingCurr Opin Neurobiol2009 19275283

    Not in our library10.1016/j.conb.2009.04.009

  198. 198.

    Tessier CR Broadie K Activity-dependent modulation of neural circuit synaptic connectivityFront Mol Neurosci2009 28

    Not in our library10.3389/neuro.02.008.2009

  199. 199.

    Vanderhaeghen P Cheng HJ Guidance molecules in axon pruning and cell deathCold Spring Harbor Perspect Biol2010 2a001859

    Not in our library10.1101/cshperspect.a001859

  200. 200.

    Petanjek Z Judas M Kostovic I Uylings HB Lifespan alterations of basal dendritic trees of pyramidal neurons in the human prefrontal cortex: a layer-specific patternCereb Cortex2008 18915929

    Not in our library10.1093/cercor/bhm124

  201. 201.

    de Almeida J Jourdan I Murer MG Belforte JE Refinement of neuronal synchronization with gamma oscillations in the medial prefrontal cortex after adolescencePloS One2013 8e62978

    Not in our library10.1371/journal.pone.0062978

  202. 202.

    Yang JM Zhang J Yu YQ Duan S Li XM Postnatal development of 2 microcircuits involving fast-spiking interneurons in the mouse prefrontal cortexCereb Cortex2014 2498109

    Not in our library10.1093/cercor/bhs291

  203. 203.

    Hoover WB Vertes RP Anatomical analysis of afferent projections to the medial prefrontal cortex in the ratBrain Struct Funct2007 212149179

    Not in our library10.1007/s00429-007-0150-4

  204. 204.

    George O Koob GF Individual differences in prefrontal cortex function and the transition from drug use to drug dependenceNeurosci Biobehav Rev2010 35232247

    Not in our library10.1016/j.neubiorev.2010.05.002

  205. 205.

    Lisboa SF Stecchini MF Correa FM Guimaraes FS Resstel LB Different role of the ventral medial prefrontal cortex on modulation of innate and associative learned fearNeuroscience2010 171760768

    Not in our library10.1016/j.neuroscience.2010.09.048

  206. 206.

    Diamond A Biological and social influences on cognitive control processes dependent on prefrontal cortexProg Brain Res2011 189319339

    Not in our library10.1016/b978-0-444-53884-0.00032-4

  207. 207.

    Thompson BM Baratta MV Biedenkapp JC Rudy JW Watkins LR Maier SF Activation of the infralimbic cortex in a fear context enhances extinction learningLearn Mem2010 17591599

    Not in our library10.1101/lm.1920810

  208. 208.

    Laroche S Davis S Jay TM Plasticity at hippocampal to prefrontal cortex synapses: dual roles in working memory and consolidationHippocampus2000 10438446

    Not in our library10.1002/1098-1063(2000)10:4<438::aid-hipo10>3.0.co;2-3

  209. 209.

    Little JP Carter AG Subcellular synaptic connectivity of layer 2 pyramidal neurons in the medial prefrontal cortexJ Neurosci2012 321280812819

    Not in our library10.1523/jneurosci.1616-12.2012

  210. 210.

    Golmayo L Nunez A Zaborszky L Electrophysiological evidence for the existence of a posterior cortical-prefrontal-basal forebrain circuitry in modulating sensory responses in visual and somatosensory rat cortical areasNeuroscience2003 119597609

    Not in our library10.1016/s0306-4522(03)00031-9

  211. 211.

    Henny P Jones BE Projections from basal forebrain to prefrontal cortex comprise cholinergic, GABAergic and glutamatergic inputs to pyramidal cells or interneuronsEur J Neurosci2008 27654670

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  212. 212.

    Hauber W Dopamine release in the prefrontal cortex and striatum: temporal and behavioural aspectsPharmacopsychiatry43S32S41

    Not in our library10.1055/s-0030-1248300

  213. 213.

    van Schouwenburg M Aarts E Cools R Dopaminergic modulation of cognitive control:distinct roles for the prefrontal cortex and the basal gangliaCurr Pharm Des2010 1620262032

    Not in our library10.2174/138161210791293097

  214. 214.

    Fitzgerald PJ A neurochemical yin and yang: does serotonin activate and norepinephrine deactivate the prefrontal cortexPsychopharmacology2011 213171182

    Not in our library10.1007/s00213-010-1856-1

  215. 215.

    Witteveen JS Middelman A van Hulten JA Martens GJ Homberg JR Kolk SM Lack of serotonin reuptake during brain development alters rostral raphe-prefrontal network formationFront Cell Neurosci2013 7143

    Not in our library10.3389/fncel.2013.00143

  216. 216.

    Goto Y O'Donnell P Altered prefrontal cortex-nucleus accumbens information processing in a developmental animal model of schizophreniaAnn NY Acad Sci2003 1003398401

    Not in our library10.1196/annals.1300.035

  217. 217.

    Goto Y Grace AA Limbic and cortical information processing in the nucleus accumbensTrends Neurosci2008 31552558

    Not in our library10.1016/j.tins.2008.08.002

  218. 218.

    Sarter M Hasselmo ME Bruno JP Givens B Unraveling the attentional functions of cortical cholinergic inputs: interactions between signal-driven and cognitive modulation of signal detectionBrain Res2005 4898111

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  219. 219.

    Del Arco A Mora F Neurotransmitters and prefrontal cortex-limbic system interactions: implications for plasticity and psychiatric disordersJ Neural Transm2009 116941952

    Not in our library10.1007/s00702-009-0243-8

  220. 220.

    Zhang ZW Burke MW Calakos N Beaulieu JM Vaucher E Confocal analysis of cholinergic and dopaminergic inputs onto pyramidal cells in the prefrontal cortex of rodentsFront Neuroanat2010 421

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  221. 221.

    Otani S Daniel H Roisin MP Crepel F Dopaminergic modulation of long-term synaptic plasticity in rat prefrontal neuronsCereb Cortex2003 1312511256

    Not in our library10.1093/cercor/bhg092

  222. 222.

    Gabbott P Headlam A Busby S Morphological evidence that CA1 hippocampal afferents monosynaptically innervate PV-containing neurons and NADPH-diaphorase reactive cells in the medial prefrontal cortex (Areas 25/32) of the ratBrain Res2002 946314322

    Not in our library10.1016/s0006-8993(02)02487-3

  223. 223.

    Gabbott PL Warner TA Busby SJ Amygdala input monosynaptically innervates parvalbumin immunoreactive local circuit neurons in rat medial prefrontal cortexNeuroscience2006 13910391048

    Not in our library10.1016/j.neuroscience.2006.01.026

  224. 224.

    Rotaru DC Barrionuevo G Sesack SR Mediodorsal thalamic afferents to layer III of the rat prefrontal cortex: synaptic relationships to subclasses of interneuronsJ Comp Neurol2005 490220238

    Not in our library10.1002/cne.20661

  225. 225.

    Little JP Carter AG Synaptic mechanisms underlying strong reciprocal connectivity between the medial prefrontal cortex and basolateral amygdalaJ Neurosci2013 331533315342

    Not in our library10.1523/jneurosci.2385-13.2013

  226. 226.

    Ernst M Fudge JL A developmental neurobiological model of motivated behavior: anatomy, connectivity and ontogeny of the triadic nodesNeurosci Biobehav Reviews2009 33367382

    Not in our library10.1016/j.neubiorev.2008.10.009

  227. 227.

    Ernst M Pine DS Hardin M Triadic model of the neurobiology of motivated behavior in adolescencePsychol Med2006 36299312

    Not in our library10.1017/s0033291705005891

  228. 228.

    Senn V Wolff SB Herry C Grenier F Ehrlich I Grundemann J Long-range connectivity defines behavioral specificity of amygdala neuronsNeuron2014 81428437

    Not in our library10.1016/j.neuron.2013.11.006

  229. 229.

    Heidbreder CA Groenewegen HJ The medial prefrontal cortex in the rat: evidence for a dorso-ventral distinction based upon functional and anatomical characteristicsNeurosci Biobehav Rev2003 27555579

    Not in our library10.1016/j.neubiorev.2003.09.003

  230. 230.

    Gabbott PL Warner TA Jays PR Salway P Busby SJ Prefrontal cortex in the rat: projections to subcortical autonomic, motor, and limbic centersJ Comp Neurol2005 492145177

    Not in our library10.1002/cne.20738

  231. 231.

    Dembrow NC Chitwood RA Johnston D Projection-specific neuromodulation of medial prefrontal cortex neuronsJ Neurosci2010 301692216937

    Not in our library10.1523/jneurosci.3644-10.2010

  232. 232.

    Ding DC Gabbott PL Totterdell S Differences in the laminar origin of projections from the medial prefrontal cortex to the nucleus accumbens shell and core regions in the ratBrain Res2001 9178189

    Not in our library10.1016/s0006-8993(01)02912-2

  233. 233.

    Cholfin JA Rubenstein JL Genetic regulation of prefrontal cortex development and functionNovartis Found Symp.2007 288165173discussion 73–7, 276–81.

    Not in our library

  234. 234.

    Schell-Apacik C Rivero M Knepper JL Roessler E Muenke M Ming JE SONIC HEDGEHOG mutations causing human holoprosencephaly impair neural patterning activityHum Genet.2003 113170177

    Not in our library10.1007/s00439-003-0950-4

  235. 235.

    Al-Ayadhi LY Relationship between Sonic hedgehog protein, brain-derived neurotrophic factor and oxidative stress in autism spectrum disordersNeurochem Res.2012 37394400

    Not in our library10.1007/s11064-011-0624-x

  236. 236.

    Heussler HS Suri M Young ID Muenke M Extreme variability of expression of a Sonic Hedgehog mutation: attention difficulties and holoprosencephalyArch Dis Child.2002 86293296

    Not in our library10.1136/adc.86.4.293

  237. 237.

    Raballo R Rhee J Lyn-Cook R Leckman JF Schwartz ML Vaccarino FM Basic fibroblast growth factor (Fgf2) is necessary for cell proliferation and neurogenesis in the developing cerebral cortexJ Neurosci.2000 2050125023

    Not in our library10.1523/jneurosci.20-13-05012.2000

  238. 238.

    Terwisscha van Scheltinga AF Bakker SC Kahn RS Kas MJ Fibroblast growth factors in neurodevelopment and psychopathologyNeuroscientist2013 19479494

    Not in our library10.1177/1073858412472399

  239. 239.

    Hashimoto K Shimizu E Komatsu N Nakazato M Okamura N Watanabe H Increased levels of serum basic fibroblast growth factor in schizophreniaPsychiatry Res.2003 120211218

    Not in our library10.1016/s0165-1781(03)00186-0

  240. 240.

    Simonis N Migeotte I Lambert N Perazzolo C de Silva DC Dimitrov B FGFR1 mutations cause Hartsfield syndrome, the unique association of holoprosencephaly and ectrodactylyJ Med Genet2013 50585592

    Not in our library10.1136/jmedgenet-2013-101603

  241. 241.

    Gaughran F Payne J Sedgwick PM Cotter D Berry M Hippocampal FGF-2 and FGFR1 mRNA expression in major depression, schizophrenia and bipolar disorderBrain Res Bull2006 70221227

    Not in our library10.1016/j.brainresbull.2006.04.008

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    Stachowiak MK Kucinski A Curl R Syposs C Yang Y Narla S Schizophrenia: a neurodevelopmental disorder – integrative genomic hypothesis and therapeutic implications from a transgenic mouse modelSchizophr Res2013 143367376

    Not in our library10.1016/j.schres.2012.11.004

  243. 243.

    Mahieu-Caputo D Sonigo P Amiel J Simon I Aubry MC Lemerrer M Prenatal diagnosis of sporadic Apert syndrome: a sequential diagnostic approach combining three-dimensional computed tomography and molecular biologyFetal Diagn Ther.2001 161012

    Not in our library10.1159/000053872

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    Crouzon′s syndrome: A review of literature and case report · 2011
    Not checked
  245. 245.

    Wentz E Vujic M Karrstedt EL Erlandsson A Gillberg C A case report of two male siblings with autism and duplication of Xq13-q21, a region including three genes predisposing for autismEuropean Child Adolesc Psychiatry2014 23329336

    Not in our library10.1007/s00787-013-0455-1

  246. 246.

    Kaga Y Shoemaker WJ Furusho M Bryant M Rosenbluth J Pfeiffer SE Mice with conditional inactivation of fibroblast growth factor receptor-2 signaling in oligodendrocytes have normal myelin but display dramatic hyperactivity when combined with Cnp1 inactivationJ Neurosci.2006 261233912350

    Not in our library10.1523/jneurosci.3573-06.2006

  247. 247.

    O'Donovan MC Norton N Williams H Peirce T Moskvina V Nikolov I Analysis of 10 independent samples provides evidence for association between schizophrenia and a SNP flanking fibroblast growth factor receptor 2Mol Psychiatry2009 143036

    Not in our library10.1038/mp.2008.108

  248. 248.

    Stevens HE Su T Yanagawa Y Vaccarino FM Prenatal stress delays inhibitory neuron progenitor migration in the developing neocortexPsychoneuroendocrinology2013 38509521

    Not in our library10.1016/j.psyneuen.2012.07.011

  249. 249.

    Theisen A Rosenfeld JA Shane K McBride KL Atkin JF Gaba C Refinement of the region for split hand/foot malformation 5 on 2q31.1Mol Syndromol2010 1262271

    Not in our library10.1159/000328405

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    Liu X Novosedlik N Wang A Hudson ML Cohen IL Chudley AE The DLX1and DLX2 genes and susceptibility to autism spectrum disordersEur J Hum Genet2009 17228235

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    Chang SC Pauls DL Lange C Sasanfar R Santangelo SL Common genetic variation in the GAD1 gene and the entire family of DLX homeobox genes and autism spectrum disordersAm J Med Genet B Neuropsychiatr Genet2011 156233239

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    Hou XJ Ni KM Yang JM Li XM Neuregulin 1/ErbB4 enhances synchronized oscillations of prefrontal cortex neurons via inhibitory synapsesNeuroscience2014 261107117

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    De Rubeis S Fernandez E Buzzi A Di Marino D Bagni C Molecular and cellular aspects of mental retardation in the Fragile X syndrome: from gene mutation/s to spine dysmorphogenesisAdv Exp Med Biol2012 970517551

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    Maurin T Zongaro S Bardoni B Fragile X Syndrome: from molecular pathology to therapyNeurosci Biobehav Rev2014 (in press).

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    Tranfaglia MR The psychiatric presentation of fragile x: evolution of the diagnosis and treatment of the psychiatric comorbidities of fragile X syndromeDev Neurosci2011 33337348

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    Hunter JE Epstein MP Tinker SW Abramowitz A Sherman SL The FMR1 premutation and attention-deficit hyperactivity disorder (ADHD): evidence for a complex inheritanceBehav Genet2012 42415422

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    Kovacs T Kelemen O Keri S Decreased fragile X mental retardation protein (FMRP) is associated with lower IQ and earlier illness onset in patients with schizophreniaPsychiatry Res.2013 210690693

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    Yadav R Gupta SC Hillman BG Bhatt JM Stairs DJ Dravid SM Deletion of glutamate delta-1 receptor in mouse leads to aberrant emotional and social behaviorsPloS One2012 7e32969

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    Griswold AJ Ma D Cukier HN Nations LD Schmidt MA Chung RH Evaluation of copy number variations reveals novel candidate genes in autism spectrum disorder-associated pathwaysHum Mol Genet2012 2135133523

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    Kolk SM Gunput RA Tran TS van den Heuvel DM Prasad AA Hellemons AJ Semaphorin 3F is a bifunctional guidance cue for dopaminergic axons and controls their fasciculation, channeling, rostral growth, and intracortical targetingJ Neurosci.2009 291254212557

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    Iafrati J Orejarena MJ Lassalle O Bouamrane L Gonzalez-Campo C Chavis P Reelin, an extracellular matrix protein linked to early onset psychiatric diseases, drives postnatal development of the prefrontal cortex via GluN2B-NMDARs and the mTOR pathwayMol Psychiatry2014 19417426

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    Zaki M Shehab M El-Aleem AA Abdel-Salam G Koeller HB Ilkin Y Identification of a novel recessive RELN mutation using a homozygous balanced reciprocal translocationAm J Med Genet2007 143A939944

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    Bartlett CW Gharani N Millonig JH Brzustowicz LM Three autism candidate genes: a synthesis of human genetic analysis with other disciplinesInt J Dev Neurosci.2005 23221234

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    Fatemi SH The role of Reelin in pathology of autismMol Psychiatry2002 7919920

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    Fatemi SH Reelin glycoprotein in autism and schizophreniaInt Rev Neurobiol.2005 71179187

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    Lakatosova S Ostatnikova D Reelin and its complex involvement in brain development and functionInt J Biochem Cell Biol.2012 4415011504

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    Frotscher M Role for Reelin in stabilizing cortical architectureTrends Neurosci2010 33407414

    Not in our library10.1016/j.tins.2010.06.001

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    Zhang W Peterson M Beyer B Frankel WN Zhang ZW Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizuresJ Neurosci.2014 3427542763

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    Samaco RC Neul JL Complexities of Rett syndrome and MeCP2J Neurosci.2011 3179517959

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    Lanz TA Guilmette E Gosink MM Fischer JE Fitzgerald LW Stephenson DT Transcriptomic analysis of genetically defined autism candidate genes reveals common mechanisms of actionMol Autism2013 445

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    Suter B Treadwell-Deering D Zoghbi HY Glaze DG Neul JL Brief report: MECP2 mutations in people without Rett syndromeJ Autism Dev Disord2014 44703711

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    Neul JL The relationship of Rett syndrome and MECP2 disorders to autismDialogues Clin Neurosci2012 14253262

    Not in our library10.31887/dcns.2012.14.3/jneul

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    McCarthy SE Gillis J Kramer M Lihm J Yoon S Berstein Y De novo mutations in schizophrenia implicate chromatin remodeling and support a genetic overlap with autism and intellectual disabilityMol Psychiatry2014 19652658

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    Piton A Gauthier J Hamdan FF Lafreniere RG Yang Y Henrion E Systematic resequencing of X-chromosome synaptic genes in autism spectrum disorder and schizophreniaMol Psychiatry2011 16867880

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    Xu B Goldman JS Rymar VV Forget C Lo PS Bull SJ Critical roles for the netrin receptor deleted in colorectal cancer in dopaminergic neuronal precursor migration, axon guidance, and axon arborizationNeuroscience2010 169932949

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    Manitt C Eng C Pokinko M Ryan RT Torres-Berrio A Lopez JP Dcc orchestrates the development of the prefrontal cortex during adolescence and is altered in psychiatric patientsTransl Psychiatry2013 3e338

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    Grant A Fathalli F Rouleau G Joober R Flores C Association between schizophrenia and genetic variation in DCC: a case-control studySchizophr Res.2012 1372631

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    El-Hassar L Simen AA Duque A Patel KD Kaczmarek LK Arnsten AF Disrupted in schizophrenia 1 modulates medial prefrontal cortex pyramidal neuron activity through cAMP regulation of transient receptor potential C and small-conductance K channelsBiol Psychiatry2014 76476485

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    Kilpinen H Ylisaukko-Oja T Hennah W Palo OM Varilo T Vanhala R Association of DISC1 with autism and Asperger syndromeMol Psychiatry2008 13187196

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    Zheng F Wang L Jia M Yue W Ruan Y Lu T Evidence for association between disrupted-in-Schizophrenia 1 (DISC1) gene polymorphisms and autism in Chinese Han population: a family-based association studyBehav Brain Funct.2011 714

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    Kenny EM Cormican P Furlong S Heron E Kenny G Fahey C Excess of rare novel loss-of-function variants in synaptic genes in schizophrenia and autism spectrum disordersMol Psychiatry2013 19872879

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    A review of the evidence for the canonical Wnt pathway in autism spectrum disorders · 2012
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    Jacobsen KK Halmoy A Sanchez-Mora C Ramos-Quiroga JA Cormand B Haavik J DISC1 in adult ADHD patients: an association study in two European samplesAm J Med Genet B Neuropsychiatr Genet2013 162B227234

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    Narayan S Nakajima K Sawa A DISC1: a key lead in studying cortical development and associated brain disordersNeuroscientist2013 19451464

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    Hikida T Gamo NJ Sawa A DISC1 as a therapeutic target for mental illnessesExpert Opin Ther Targets.2012 1611511160

    Not in our library10.1517/14728222.2012.719879

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    Duff BJ Macritchie KA Moorhead TW Lawrie SM Blackwood DH Human brain imaging studies of DISC1 in schizophrenia, bipolar disorder and depression: a systematic reviewSchizophr Res2013 147113

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    Drerup JM Hayashi K Cui H Mettlach GL Long MA Marvin M Attention-deficit/hyperactivity phenotype in mice lacking the cyclin- dependent kinase 5 cofactor p35Biol Psychiatry.2010 6811631171

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    Ramos-Miguel A Meana JJ Garcia-Sevilla JA Cyclin-dependent kinase-5 and p35/p25 activators in schizophrenia and major depression prefrontal cortex: basal contents and effects of psychotropic medicationsInt J Neuropsychopharmacol.2013 16683689

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    Engmann O Hortobagyi T Pidsley R Troakes C Bernstein HG Kreutz MR Schizophrenia is associated with dysregulation of a Cdk5 activator that regulates synaptic protein expression and cognitionBrain2011 13424082421

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    Rovelet-Lecrux A Campion D Copy number variations involving the microtubule-associated protein tau in human diseasesBiochem Soc Trans.2012 40672676

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    Not in our library10.1016/j.neulet.2009.02.023

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