Pat Levitt

Children's Hospital Los Angeles, Los Ángeles, California, United States

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Publications (171)1183.92 Total impact

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    ABSTRACT: Children with autism spectrum disorder (ASD) may present with multiple medical conditions in addition to ASD symptoms. This study investigated whether there are predictive patterns of medical conditions that co-occur with ASD, which could inform medical evaluation and treatment in ASD, as well as potentially identify etiologically meaningful subgroups. Medical history data were queried in the multiplex family Autism Genetic Resource Exchange (AGRE). Fourteen medical conditions were analyzed. Replication in the Simons Simplex Collection (SSC) was attempted using available medical condition data on gastrointestinal disturbances (GID), sleep problems, allergy and epilepsy. In the AGRE cohort, no discrete clusters emerged among 14 medical conditions. GID and seizures were enriched in unaffected family members, and together with sleep problems, were represented in both AGRE and SSC. Further analysis of these medical conditions identified predictive co-occurring patterns in both samples. For a child with ASD, the presence of GID predicts sleep problems and vice versa, with an approximately 2-fold odds ratio in each direction. These risk patterns were replicated in the SSC sample, and in addition, there was increased risk for seizures and sleep problems to co-occur with GID. In these cohorts, seizure alone was not predictive of the other conditions co-occurring, but behavioral impairments were more severe as the number of co-occurring medical symptoms increased. These findings indicate that interdisciplinary clinical care for children with ASD will benefit from evaluation for specific patterns of medical conditions in the affected child and their family members. Autism Res 2015. © 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research. © 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research.
    Autism Research 05/2015; DOI:10.1002/aur.1492 · 4.53 Impact Factor
  • Shenfeng Qiu, Zhongming Lu, Pat Levitt
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    ABSTRACT: The MET receptor tyrosine kinase (RTK), implicated in risk for autism spectrum disorder (ASD) and in functional and structural circuit integrity in humans, is a temporally and spatially regulated receptor enriched in dorsal pallial-derived structures during mouse forebrain development. Here we report that loss or gain of function of MET in vitro or in vivo leads to changes, opposite in nature, in dendritic complexity, spine morphogenesis, and the timing of glutamatergic synapse maturation onto hippocampus CA1 neurons. Consistent with the morphological and biochemical changes, deletion of Met in mutant mice results in precocious maturation of excitatory synapse, as indicated by a reduction of the proportion of silent synapses, a faster GluN2A subunit switch, and an enhanced acquisition of AMPA receptors at synaptic sites. Thus, MET-mediated signaling appears to serve as a mechanism for controlling the timing of neuronal growth and functional maturation. These studies suggest that mistimed maturation of glutamatergic synapses leads to the aberrant neural circuits that may be associated with ASD risk. Copyright © 2014 the authors 0270-6474/14/3416166-14$15.00/0.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 12/2014; 34(49):16166-79. DOI:10.1523/JNEUROSCI.2580-14.2014 · 6.75 Impact Factor
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    NIH Workshop - Presentation by Dr. Cameron (U of Pittsburgh), Washington, DC; 05/2014
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    ABSTRACT: The anatomical and functional architecture of the human brain is mainly determined by prenatal transcriptional processes. We describe an anatomically comprehensive atlas of the mid-gestational human brain, including de novo reference atlases, in situ hybridization, ultra-high resolution magnetic resonance imaging (MRI) and microarray analysis on highly discrete laser-microdissected brain regions. In developing cerebral cortex, transcriptional differences are found between different proliferative and post-mitotic layers, wherein laminar signatures reflect cellular composition and developmental processes. Cytoarchitectural differences between human and mouse have molecular correlates, including species differences in gene expression in subplate, although surprisingly we find minimal differences between the inner and outer subventricular zones even though the outer zone is expanded in humans. Both germinal and post-mitotic cortical layers exhibit fronto-temporal gradients, with particular enrichment in the frontal lobe. Finally, many neurodevelopmental disorder and human-evolution-related genes show patterned expression, potentially underlying unique features of human cortical formation. These data provide a rich, freely-accessible resource for understanding human brain development.
    Nature 04/2014; DOI:10.1038/nature13185 · 42.35 Impact Factor
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    ABSTRACT: PURPOSE To examine relationships between prosodic speech cues and autism spectrum disorder (ASD) severity, hypothesizing a mutually interactive relationship between the psychologists' and the children's speech characteristics. We objectively quantified acoustic-prosodic cues of psychologists and children with ASD during spontaneous interaction, establishing a methodology for future large-sample analysis. METHODS Speech acoustic-prosodic features were semi-automatically derived from segments of semi-structured interviews (Autism Diagnostic Observation Schedule; ADOS) with 28 children previously diagnosed with ASD. Prosody was quantified in terms of intonation, volume, rate, and voice quality. Research hypotheses were tested via correlation and hierarchical and predictive regression between ADOS severity and prosodic cues. RESULTS Automatically extracted speech features demonstrated prosodic characteristics of dyadic interactions. As rated ASD severity increased, both participants demonstrated effects for turn-end pitch slope, and both spoke with atypical voice quality. The psychologist's acoustic cues predicted the child's symptom severity better than the child's acoustic cues. CONCLUSION The psychologist, acting as evaluator and interlocutor, was shown to adjust behavior in predictable ways based on the child's social-communicative impairments. The results support future study of speech prosody of both interaction partners during spontaneous conversation, while making use of automatic computational methods that allow for scalable analysis on much larger corpora.
    Journal of Speech Language and Hearing Research 02/2014; 57(4). DOI:10.1044/2014_JSLHR-S-13-0062 · 1.93 Impact Factor
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    Elizabeth A D Hammock, Pat Levitt
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    ABSTRACT: Oxytocin (OXT) has drawn increasing attention as a developmentally relevant neuropeptide given its role in the brain regulation of social behavior. It has been suggested that OXT plays an important role in the infant brain during caregiver attachment in nurturing familial contexts, but there is incomplete experimental evidence. Mouse models of OXT system genes have been particularly informative for the role of the OXT system in social behavior, however, the developing brain areas that could respond to ligand activation of the OXT receptor (OXTR) have yet to be identified in this species. Here we report new data revealing dynamic ligand-binding distribution of OXTR in the developing mouse brain. Using male and female C57BL/6J mice at postnatal days (P) 0, 7, 14, 21, 35, and 60 we quantified OXTR ligand binding in several brain areas which changed across development. Further, we describe OXTR ligand binding in select tissues of the near-term whole embryo at E18.5. Together, these data aid in the interpretation of findings in mouse models of the OXT system and generate new testable hypotheses for developmental roles for OXT in mammalian systems. We discuss our findings in the context of developmental disorders (including autism), attachment biology, and infant physiological regulation. Summary: Quantitative mapping of selective OXTR ligand binding during postnatal development in the mouse reveals an unexpected, transient expression in layers II/III throughout the mouse neocortex. OXTR are also identified in several tissues in the whole late embryo, including the adrenal glands, brown adipose tissue, and the oronasal cavity.
    Frontiers in Behavioral Neuroscience 12/2013; 7:195. DOI:10.3389/fnbeh.2013.00195 · 4.16 Impact Factor
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    ABSTRACT: Based on clinical experience, we hypothesized that rigid-compulsive behaviors are associated with severe constipation and co-occurring diarrhea or underwear staining in children with autism spectrum disorder. Using data from the Autism Treatment Network, we evaluated the association between these gastrointestinal symptoms and measures of rigid compulsive behavior in children ages 2-17. Following statistical correction, four of five primary measures were significantly associated with constipation and diarrhea or underwear staining, including parental report of repetitive behavior, parental report of compulsive behavior, clinician diagnosis of obsessive-compulsive disorder, and report of rituals observed on the autism diagnostic observation schedule. This association could point to a causal connection between these symptoms or to a common biological pathway that impacts both gut and brain.
    Journal of Autism and Developmental Disorders 11/2013; 44(6). DOI:10.1007/s10803-013-2009-2 · 3.06 Impact Factor
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    ABSTRACT: MET, a replicated autism risk gene, encodes a pleiotropic receptor tyrosine kinase implicated in multiple cellular processes during development and following injury. Previous studies suggest that Met modulates excitatory synapse development in the neocortex and hippocampus, although the underlying mechanism is unknown. The peak of Met expression corresponds to the period of process outgrowth and synaptogenesis, with robust expression in hippocampal and neocortical neuropil. Resolving whether neuropil expression represents presynaptic, postsynaptic or glial localization provides insight into potential mechanisms of Met action. The subcellular distribution of Met was characterized using complementary ultrastructural, in situ proximity ligation assay (PLA) and biochemical approaches. At postnatal day (P) 7, immuno-electron microscopy revealed near-equivalent proportions of Met-immunoreactive pre- (axons and terminals) and post- (dendritic shafts and spines) synaptic profiles in the stratum radiatum in the hippocampal CA1 region. Staining was typically in elements in which the corresponding pre- or postsynaptic apposition was unlabeled. By P21, Met-immunoreactive presynaptic profiles predominated and approximately 20% of Met-expressing profiles were glial. A different distribution of Met-immunoreactive profiles was observed in layer V of somatosensory cortex: Met-labeled spines were rare and a smaller proportion of glial profiles expressed Met. Strikingly, Met-immunoreactive presynaptic profiles predominated over postsynaptic profiles as early as P7. PLA analysis of neurons in vitro and biochemical analysis of tissue subsynaptic fractions confirmed the localization of Met in specific synaptic subcompartments. The study demonstrates that Met is enriched at synapses during development and its activation may modulate synapse formation and stability through both pre- and post-synaptic mechanisms. J. Comp. Neurol. , 2013. © 2013 Wiley Periodicals, Inc.
    The Journal of Comparative Neurology 10/2013; 521(14). DOI:10.1002/cne.23343 · 3.51 Impact Factor
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    ABSTRACT: Attachment to an abusive caregiver has wide phylogenetic representation, suggesting that animal models are useful in understanding the neural basis underlying this phenomenon and subsequent behavioral outcomes. We previously developed a rat model, in which we use classical conditioning to parallel learning processes evoked during secure attachment (odor-stroke, with stroke mimicking tactile stimulation from the caregiver) or attachment despite adversity (odor-shock, with shock mimicking maltreatment). Here we extend this model to mice. We conditioned infant mice (postnatal day (PN) 7-9 or 13-14) with presentations of peppermint odor and either stroking or shock. We used (14) C 2-deoxyglucose (2-DG) to assess olfactory bulb and amygdala metabolic changes following learning. PN7-9 mice learned to prefer an odor following either odor-stroke or shock conditioning, whereas odor-shock conditioning at PN13-14 resulted in aversion/fear learning. 2-DG data indicated enhanced bulbar activity in PN7-9 preference learning, whereas significant amygdala activity was present following aversion learning at PN13-14. Overall, the mouse results parallel behavioral and neural results in the rat model of attachment, and provide the foundation for the use of transgenic and knockout models to assess the impact of both genetic (biological vulnerabilities) and environmental factors (abusive) on attachment-related behaviors and behavioral development.
    Genes Brain and Behavior 08/2013; 12(7). DOI:10.1111/gbb.12067 · 3.51 Impact Factor
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    ABSTRACT: Etiology is unknown in the majority of individuals with autism spectrum disorder (ASD). One strategy to investigate pathogenesis is to stratify this heterogeneous disorder based on a prominent phenotypic feature that enriches for homogeneity within population strata. Co-occurring gastrointestinal dysfunction (GID) characterizes a subset of children with ASD. Our current objective was to investigate a potential pathophysiological measure to test the hypothesis that children with both ASD and GID have a more severe metabolic dysfunction than children with ASD-only, given that the highly metabolically active brain and gastrointestinal system may additively contribute measurable impairment. Plasma levels of F2t-Isoprostanes (F2-IsoPs), a gold standard biomarker of oxidative stress, were measured in 87 children in four groups: ASD-GID, ASD-only, GID-only and Unaffected. F2-IsoP levels were elevated in all 3 clinical groups compared to the Unaffected group, with the ASD-GID group significantly elevated above the ASD-only group (mean, SD in pg/mg: ASD-GID 53.6, 24.4; ASD-only 36.5, 13.3; p = 0.007). Adjusting for age, sex, and triglyceride levels, F2-IsoP levels remained significantly different between study groups, with a moderate effect size of ηp (2) = 0.187 (p = 0.001). Elevation in peripheral oxidative stress is consistent with, and may contribute to, the more severe functional impairments in the ASD-GID group. With unique medical, metabolic, and behavioral features in children with ASD-GID, the present findings serve as a compelling rationale for both individualized approaches to clinical care and integrated studies of biomarker enrichment in ASD subgroups that may better address the complex etiology of ASD.
    PLoS ONE 07/2013; 8(7):e68444. DOI:10.1371/journal.pone.0068444 · 3.53 Impact Factor
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    ABSTRACT: BACKGROUND: Several proteins involved in epigenetic regulation cause syndromic neurodevelopmental disorders when human genes are mutated. More general involvement of epigenetic mechanisms in neurodevelopmental phenotypes is unclear. METHODS: In an attempt to determine whether DNA methylation differentiates clinical subgroups, profiling was performed on bisulfite converted DNA from lymphoblastoid cell lines (LCLs) in discovery (n = 20) and replication (n = 40) cohorts of females with Rett syndrome (RTT; n = 18), autism (AUT; n = 17), seizure disorder (SEZ; n = 6), and controls (CTL; n = 19) using Illumina HumanMethylation27 arrays. TAC1 CpGs were validated using a Sequenom EpiTYPER assay and expression was measured in LCLs and postmortem brain. Chromatin immunoprecipitation was performed in HEK cells. Cells were treated with valproic acid and MeCP2 binding was assessed. RESULTS: Two female-only cohorts were analyzed. DNA methylation profiling in a discovery cohort identified 40 CpGs that exhibited statistically significant differential methylation (>=15%) between clinical groups (P <0.01). Hierarchical clustering and principal components analysis suggested neurodevelopmental groups were distinct from CTL, but not from each other. In a larger and more heterogeneous replication cohort, these 40 CpG sites suggested no clear difference between clinical groups. Pooled analysis of DNA methylation across all 60 samples suggested only four differentially methylated CpG sites (P <0.0005), including TAC1. TAC1 promoter CpG hypermethylation was validated in AUT and SEZ (P <0.005). Analyzed for the first time in postmortem brain, TAC1 expression was reduced in cingulate cortex in RTT and AUT+SEZ (P = 0.003). However, no significant difference in TAC1 promoter CpG methylation was detected in RTT and AUT+SEZ brains. Additional molecular analyses revealed that MeCP2 binds directly to the TAC1 promoter and is sensitive to antiepileptic drug treatment. CONCLUSION: These data suggest that DNA methylation is not widely altered in RTT, consistent with subtle changes in gene expression previously observed. However, TAC1 may be an important target for further functional analyses in RTT. Studies of larger sample cohorts using primary cells that also consider shared clinical features and drug treatments may be required to address apparent subtle disruptions of DNA methylation in neurodevelopmental disorders.
    Journal of Neurodevelopmental Disorders 06/2013; 5(1):15. DOI:10.1186/1866-1955-5-15 · 3.71 Impact Factor
  • Pat Levitt, A. Bonnin
    Neurotoxicology and Teratology 05/2013; 37. DOI:10.1016/j.ntt.2013.03.009 · 3.22 Impact Factor
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    Hsiao-Huei Wu, Pat Levitt
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    ABSTRACT: Signaling via MET receptor tyrosine kinase (MET) has been implicated in a number of neurodevelopmental events, including cell migration, dendritic and axonal development and synaptogenesis. Related to its role in the development of forebrain circuitry, we recently identified a functional promoter variant of the MET gene that is associated with autism spectrum disorder (ASD). The association of the MET promoter variant rs1858830 C allele is significantly enriched in families with a child who has ASD and co-occurring gastrointestinal conditions. The expression of MET in the forebrain had been mapped in detail in the developing mouse and rhesus macaque. However, in mammals, its expression in the developing brainstem has not been studied extensively throughout developmental stages. Brainstem and autonomic circuitry are implicated in ASD pathophysiology and in gastroin-testinal dysfunction. To advance our understanding of the neurodevelopmental influences of MET signaling in brainstem circuitry development, we employed in situ hybridization and immunohistochemistry to map the expression of Met and its ligand, Hgf, through prenatal development of the mouse midbrain and hindbrain. Our results reveal a highly selective expression pattern of Met in the brainstem, including a subpopulation of neurons in cranial motor nuclei (nVII, nA and nXII), B6 subgroup of the dorsal raphe, Barrington's nucleus, and a small subset of neurons in the nucleus of solitary tract. In contrast to Met, neither full-length nor known splice variants of Hgf were localized in the prenatal brainstem. RT-PCR revealed Hgf expression in target tissues of Met-expressing brainstem neurons, suggesting that MET in these neurons may be activated by HGF from peripheral sources. Together, these data suggest that MET signaling may influence the development of neurons that are involved in central regulation of gastrointestinal function, tongue movement, swallowing, speech, stress and mood.
    Developmental Neuroscience 03/2013; 35(1). DOI:10.1159/000346367 · 2.45 Impact Factor
  • Masaaki Torii, Pasko Rakic, Pat Levitt
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    ABSTRACT: Corticothalamic (CT) feedback outnumbers thalamocortical projections, and regulates sensory information processing at the level of the thalamus. It is well established that EphA7, a member of EphA receptor family, is involved in the topographic mapping of CT projections. The aim of the present study is to dissect the precise impact of EphA7 on each step of CT growth. We used in utero electroporation-mediated EphA7 overexpression in developing somatosensory CT axons to dissect EphA7/ephrin-A-dependent mechanisms involved in regulating both initial targeting and postnatal growth of the CT projections. Our data revealed that topographic maps of cortical afferents in the ventrobasal complex and medial part of the posterior complex in the thalamus become discernible shortly after birth and are fully established by the second postnatal week. This process starts with the direct ingrowth of the CT axons to the designated areas within target thalamic nuclei and by progressive increase of axonal processes in the terminal zones. Large-scale overproduction and elimination of exuberant widespread axonal branches outside the target zone was not observed. Each developmental event was coordinated by spatially and temporally different responsiveness of CT axons to the ephrin-A gradient in thalamic nuclei, as well as by the matching levels of EphA7 in CT axons and ephrin-As in thalamic nuclei. These results support the concept that the topographic connections between the maps in the cerebral cortex and corresponding thalamic nuclei are genetically pre-specified to a large extent, and established by precise spatio-temporal molecular mechanisms that involve the Eph family of genes. J. Comp. Neurol., 2012. © 2012 Wiley Periodicals, Inc.
    The Journal of Comparative Neurology 02/2013; 521(3). DOI:10.1002/cne.23195 · 3.51 Impact Factor
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    ABSTRACT: [This corrects the article on p. 124 in vol. 3, PMID: 22934102.].
    Frontiers in Genetics 01/2013; 4:23. DOI:10.3389/fgene.2013.00023
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    ABSTRACT: Arginine-vasopressin (AVP) and the vasopressin V1a receptor (V1aR) acting within the forebrain are involved in social behavior in adult animals. Much less is known about the function of V1aR in neurobehavioral development. In the present study, at post-natal day 8 (P8) in neonatal C57BL/6J mice, we map V1aR and use an olfactory exposure paradigm to assess a role for V1aR on olfactory preferences. In addition to V1aR in the lateral septum and ventral tegmental area, we observe V1aR in the neocortex and hippocampus, not typically observed in adult mice, implicating a developmental sensitive period for V1aR to modulate these brain areas in an experience-dependent manner. Males and females were tested on P8 for orienting preferences after exposure to a non-social odor, presented either when the mother was in the home cage (contingent) or when the mother had been removed from the home cage (not contingent). Wild-type female mice show a selective orienting bias toward the exposed odor, but only in the contingent condition. Males did not show orienting bias after either training condition. Female Avpr1a(-/-) mice showed strong familiar odor bias, regardless of the training condition. This finding led us to test the ability of AVP to diminish odor bias in females. Central application of AVP eliminated odor bias in Avpr1a(+/+), but not Avpr1a(-/-) female mice. Together, these data indicate that AVP acting at V1aR eliminates the expression of familiar odor bias in neonatal mice. This suggests a developmental role for AVP on familiarity bias, which has implications for species-typical life history trajectories of social learning and natal dispersal.
    Hormones and Behavior 12/2012; 63(2). DOI:10.1016/j.yhbeh.2012.12.006 · 4.51 Impact Factor
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    ABSTRACT: As genes that confer increased risk for autism spectrum disorder (ASD) are identified, a crucial next step is to determine how these risk factors impact brain structure and function and contribute to disorder heterogeneity. With three converging lines of evidence, we show that a common, functional ASD risk variant in the Met Receptor Tyrosine Kinase (MET) gene is a potent modulator of key social brain circuitry in children and adolescents with and without ASD. MET risk genotype predicted atypical fMRI activation and deactivation patterns to social stimuli (i.e., emotional faces), as well as reduced functional and structural connectivity in temporo-parietal regions known to have high MET expression, particularly within the default mode network. Notably, these effects were more pronounced in individuals with ASD. These findings highlight how genetic stratification may reduce heterogeneity and help elucidate the biological basis of complex neuropsychiatric disorders such as ASD.
    Neuron 09/2012; 75(5):904-15. DOI:10.1016/j.neuron.2012.07.010 · 15.98 Impact Factor
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    Proceedings of InterSpeech; 09/2012
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    ABSTRACT: Understanding brain function involves improved knowledge about how the genome specifies such a large diversity of neuronal types. Transcriptome analysis of single neurons has been previously described using gene expression microarrays. Using high-throughput transcriptome sequencing (RNA-Seq), we have developed a method to perform single-neuron RNA-Seq. Following electrophysiology recording from an individual neuron, total RNA was extracted by aspirating the cellular contents into a fine glass electrode tip. The mRNAs were reverse transcribed and amplified to construct a single-neuron cDNA library, and subsequently subjected to high-throughput sequencing. This approach was applied to both individual neurons cultured from embryonic mouse hippocampus, as well as neocortical neurons from live brain slices. We found that the average pairwise Spearman's rank correlation coefficient of gene expression level expressed as RPKM (reads per kilobase of transcript per million mapped reads) was 0.51 between five cultured neuronal cells, whereas the same measure between three cortical layer 5 neurons in situ was 0.25. The data suggest that there may be greater heterogeneity of the cortical neurons, as compared to neurons in vitro. The results demonstrate the technical feasibility and reproducibility of RNA-Seq in capturing a part of the transcriptome landscape of single neurons, and confirmed that morphologically identical neurons, even from the same region, have distinct gene expression patterns.
    Frontiers in Genetics 07/2012; 3:124. DOI:10.3389/fgene.2012.00124
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    ABSTRACT: Autism spectrum disorders (ASD) are heterogeneous neurodevelopmental disorders that are characterized by deficits in social interaction, verbal and nonverbal communication, and restrictive interests and repetitive behaviors. While human genetic studies have revealed marked heritability in ASD, it has been challenging to translate this genetic risk into a biological mechanism that influences brain development relevant to the disorder phenotypes. This is partly due to the complex genetic architecture of ASD, which involves de novo gene mutations, genomic abnormalities, and common genetic variants. Rather than trying to reconstitute the clinical disorder, using genetic model animals to examine specific features of core ASD pathophysiology offers unique opportunities for refining our understanding of neurodevelopmental mechanisms in ASD. A variety of ASD-relevant phenotypes can now be investigated in rodents, including stereotyped and repetitive behaviors, and deficits in social interaction and communication. In this review, we focus on several prevailing mouse models and discuss how studies have advanced our understanding of synaptic mechanisms that may underlie ASD pathophysiology. Although synaptic perturbations are not the only alterations relevant for ASD, we reason that understanding the synaptic underpinnings of ASD using mouse models may provide mechanistic insights into its etiology and lead to novel therapeutic and interventional strategies.
    Developmental Neuroscience 05/2012; 34(2-3):88-100. DOI:10.1159/000336644 · 2.45 Impact Factor

Publication Stats

10k Citations
1,183.92 Total Impact Points

Institutions

  • 2013–2014
    • Children's Hospital Los Angeles
      Los Ángeles, California, United States
  • 2011–2013
    • Keck School of Medicine USC
      Los Angeles, California, United States
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • University of North Carolina at Chapel Hill
      • Department of Cell Biology and Physiology
      North Carolina, United States
  • 2010–2013
    • University of Southern California
      • • Department of Cell and Neurobiology
      • • Keck School of Medicine
      Los Angeles, California, United States
  • 2010–2012
    • University of California, Los Angeles
      Los Ángeles, California, United States
  • 2003–2011
    • Vanderbilt University
      • • Department of Pediatrics
      • • Department of Pharmacology
      • • Vanderbilt Kennedy Center (VKC)
      Nashville, MI, United States
  • 1997–2008
    • University of Pittsburgh
      • • Department of Psychiatry
      • • Department of Human Genetics
      • • Department of Neurobiology
      • • Department of Pathology
      Pittsburgh, PA, United States
    • Brown University
      • Department of Pediatrics
      Providence, Rhode Island, United States
  • 2000
    • University of Washington Seattle
      • Department of Radiology
      Seattle, WA, United States
  • 1996
    • York College of PA
      Philadelphia, Pennsylvania, United States
    • Philadelphia University
      Philadelphia, Pennsylvania, United States
  • 1995–1996
    • Robert Wood Johnson University Hospital
      New Brunswick, New Jersey, United States
  • 1992–1993
    • Philadelphia ZOO
      Filadelfia, Pennsylvania, United States