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• W2109107029 abstract "Autism and autism spectrum disorders such as Angelman syndrome, affect the ability to successfully integrate and participate in social interactions or to understand social exchanges between others. Ongoing interdisciplinary research aims to identify genetic, molecular, and neurophysiologic causes of autistic phenotypes. Multiple lines of evidence from different disciplines are intersecting at the synapse, the site of chemical communication between neurons and also believed to be the key site of learning in the brain. The human brain contains an estimated 1011 neurons, each of which communicates with thousands of other neurons via synaptic connections ( 1 Braitenberg V. Schüz A. Anatomy of the Cortex Statistics and Geometry. 2nd ed. Springer Verlag, Berlin, Heidelberg, New York1998 Google Scholar , 2 Williams R.W. Herrup K. The control of neuron number. Annu Rev Neurosci. 1988; 11: 423-453 Crossref PubMed Scopus (450) Google Scholar ). The estimated number of synapses in the entire human brain is astronomical 1014 ( 1 Braitenberg V. Schüz A. Anatomy of the Cortex Statistics and Geometry. 2nd ed. Springer Verlag, Berlin, Heidelberg, New York1998 Google Scholar ). The neuronal networks formed by this large number of massively interconnected neurons generate complex spatiotemporal patterns of neuronal activity that require coordinated activity across large populations of neurons using both short- and long-range synaptic connections. On an even larger scale, the mammalian brain is composed of many structurally diverse networks, including the neocortex, thalamus, basal ganglia, etc. Healthy brains are characterized by the continuous generation of behavior-related spatiotemporal activity patterns that propagate across multiple brain areas. These patterns, which include synchronous events as well as oscillatory activity at frequencies between approximately .1 and 200 Hz, are believed to be causally linked to higher cognition, including memory formation and retrieval ( 3 Ward L.M. Synchronous neural oscillations and cognitive processes. Trends Cogn Sci. 2003; 7: 553-559 Abstract Full Text Full Text PDF PubMed Scopus (718) Google Scholar ). Consistent with this view are findings of abnormalities in large-scale brain activity patterns in patients with cognitive disorders including autism ( 4 Uhlhaas P.J. Singer W. What do disturbances in neural synchrony tell us about autism?. Biol Psychiatry. 2007; 62: 190-191 Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar ). It seems likely that even comparatively minor deficits in the development or maintenance of millions of synaptic connections may have cumulatively large effects on the coordination of spatiotemporal activity patterns associated with cognitive processes. With hundreds of genes involved in the formation of the postsynaptic density in humans, synaptic abnormalities may be a common denominator for many heritable cognitive disorders including autism and schizophrenia ( 5 Grant S.G. Synaptopathies: diseases of the synaptome [published online ahead of print March 10]. Curr Opin Neurobiol. 2012; Crossref PubMed Scopus (177) Google Scholar ). In addition to network dynamics, deficient synaptic transmission may also be responsible for deficits in the release of neuromodulatory transmitters such as dopamine, which have been associated with autism and schizophrenia ( 6 Rogers T.D. Dickson P.E. Heck D.H. Goldowitz D. Mittleman G. Blaha C.D. Connecting the dots of the cerebro-cerebellar role in cognitive function: neuronal pathways for cerebellar modulation of dopamine release in the prefrontal cortex. Synapse. 2011; 65: 1204-1212 Crossref PubMed Scopus (86) Google Scholar ). Reversal of Impaired Hippocampal Long-Term Potentiation and Contextual Fear Memory Deficits in Angelman Syndrome Model Mice by ErbB InhibitorsBiological PsychiatryVol. 72Issue 3PreviewAngelman syndrome (AS) is a human neuropsychiatric disorder associated with autism, mental retardation, motor abnormalities, and epilepsy. In most cases, AS is caused by the deletion of the maternal copy of UBE3A gene, which encodes the enzyme ubiquitin ligase E3A, also termed E6-AP. A mouse model of AS has been generated and these mice exhibit many of the observed neurological alterations in humans. Because of clinical and neuroanatomical similarities between AS and schizophrenia, we examined AS model mice for alterations in the neuregulin-ErbB4 pathway, which has been implicated in the pathophysiology of schizophrenia. Full-Text PDF" @default.
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• W2109107029 title "The Social Life of Neurons: Synaptic Communication Deficits as a Common Denominator of Autism, Schizophrenia, and Other Cognitive Disorders" @default.
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• W2109107029 doi "https://doi.org/10.1016/j.biopsych.2012.05.013" @default.
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