Abstract
Synaptic plasticity alters the strength of information flow between presynaptic and postsynaptic neurons and thus modifies the likelihood that action potentials in a presynaptic neuron will lead to an action potential in a postsynaptic neuron. As such, synaptic plasticity and pathological changes in synaptic plasticity impact the synaptic computation which controls the information flow through the neural microcircuits responsible for the complex information processing necessary to drive adaptive behaviors. As current theories of neuropsychiatric disease suggest that distinct dysfunctions in neural circuit performance may critically underlie the unique symptoms of these diseases, pathological alterations in synaptic plasticity mechanisms may be fundamental to the disease process. Here we consider mechanisms of both short-term and long-term plasticity of synaptic transmission and their possible roles in information processing by neural microcircuits in both health and disease. As paradigms of neuropsychiatric diseases with strongly implicated risk genes, we discuss the findings in schizophrenia and autism and consider the alterations in synaptic plasticity and network function observed in both human studies and genetic mouse models of these diseases. Together these studies have begun to point toward a likely dominant role of short-term synaptic plasticity alterations in schizophrenia while dysfunction in autism spectrum disorders (ASDs) may be due to a combination of both short-term and long-term synaptic plasticity alterations.
Highlights
SYNAPTIC NEUROSCIENCENeural circuits, and the emerging role of altered short-term information processing in schizophrenia
NEUROPSYCHIATRIC DISEASE MANIFESTATIONS AND HYPOTHESES OF NEURAL CIRCUIT DYSFUNCTION The recent advances over the past several decades in molecular biology, human genomics, and bioinformatics has helped to enable the identification of numerous candidate genes and distinct genetic mutations in a variety of human neuropsychiatric illnesses that may be the responsible agents for causing their symptomology
The identification of highly penetrant risk genes for schizophrenia and autism has led the creation of etiologically valid mouse models for these diseases that have enabled detailed investigations directed at identifying synaptic, neuronal, and neural circuit dysfunction
Summary
Neural circuits, and the emerging role of altered short-term information processing in schizophrenia. While short-term synaptic plasticity leads to shortterm changes in synaptic function (lasting from milliseconds to minutes) that regulate the moment-to-moment information flow through a neural circuit, long-term synaptic plasticity leads to persistent changes in synaptic function (lasting from hours to the lifetime of the synapse) that fundamentally and adaptively alters microcircuit function in response to activity indicating changing computational demands (Zucker and Regehr, 2002; Collingridge et al, 2010; Granger and Nicoll, 2013) Due to this critical role in controlling microcircuit computation, here we consider dysfunction in both long-term and short-term synaptic plasticity mechanisms as promising candidates underlying the neural
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
