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      Synaptic Wiring of Corticostriatal Circuits in Basal Ganglia: Insights into the Pathogenesis of Neuropsychiatric Disorders


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          The striatum is a key hub in the basal ganglia for processing neural information from the sensory, motor, and limbic cortices. The massive and diverse cortical inputs entering the striatum allow the basal ganglia to perform a repertoire of neurological functions ranging from basic level of motor control to high level of cognition. The heterogeneity of the corticostriatal circuits, however, also renders the system susceptible to a repertoire of neurological diseases. Clinical and animal model studies have indicated that defective development of the corticostriatal circuits is linked to various neuropsychiatric disorders, including attention-deficit hyperactivity disorder (ADHD), Tourette syndrome, obsessive-compulsive disorder (OCD), autism spectrum disorder (ASD), and schizophrenia. Importantly, many neuropsychiatric disease-risk genes have been found to form the molecular building blocks of the circuit wiring at the synaptic level. It is therefore imperative to understand how corticostriatal connectivity is established during development. Here, we review the construction during development of these corticostriatal circuits at the synaptic level, which should provide important insights into the pathogenesis of neuropsychiatric disorders related to the basal ganglia and help the development of appropriate therapies for these diseases.

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          Most cited references142

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          Parallel organization of functionally segregated circuits linking basal ganglia and cortex.

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            Shank3 mutant mice display autistic-like behaviours and striatal dysfunction

            Autism spectrum disorders (ASDs) comprise a range of disorders that share a core of neurobehavioural deficits characterized by widespread abnormalities in social interactions, deficits in communication as well as restricted interests and repetitive behaviours. The neurological basis and circuitry mechanisms underlying these abnormal behaviours are poorly understood. Shank3 is a postsynaptic protein, whose disruption at the genetic level is thought to be responsible for development of 22q13 deletion syndrome (Phelan-McDermid Syndrome) and other non-syndromic ASDs. Here we show that mice with Shank3 gene deletions exhibit self-injurious repetitive grooming and deficits in social interaction. Cellular, electrophysiological and biochemical analyses uncovered defects at striatal synapses and cortico-striatal circuits in Shank3 mutant mice. Our findings demonstrate a critical role for Shank3 in the normal development of neuronal connectivity and establish causality between a disruption in the Shank3 gene and the genesis of autistic like-behaviours in mice.
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              Modulation of striatal projection systems by dopamine.

              The basal ganglia are a chain of subcortical nuclei that facilitate action selection. Two striatal projection systems--so-called direct and indirect pathways--form the functional backbone of the basal ganglia circuit. Twenty years ago, investigators proposed that the striatum's ability to use dopamine (DA) rise and fall to control action selection was due to the segregation of D(1) and D(2) DA receptors in direct- and indirect-pathway spiny projection neurons. Although this hypothesis sparked a debate, the evidence that has accumulated since then clearly supports this model. Recent advances in the means of marking neural circuits with optical or molecular reporters have revealed a clear-cut dichotomy between these two cell types at the molecular, anatomical, and physiological levels. The contrast provided by these studies has provided new insights into how the striatum responds to fluctuations in DA signaling and how diseases that alter this signaling change striatal function.

                Author and article information

                Society for Neuroscience
                16 May 2019
                4 June 2019
                May-Jun 2019
                : 6
                : 3
                : ENEURO.0076-19.2019
                [1 ]Institute of Neuroscience, National Yang-Ming University , Taipei 11221, Taiwan
                [2 ]Brain Research Center, National Yang-Ming University , Taipei 11221, Taiwan
                Author notes

                The authors declare no competing financial interests.

                Author contributions: H.-Y.K. and F.-C.L. wrote the paper.

                This work was supported by Ministry of Science and Technology-Taiwan Grants MOST107-2321-B-010-002 and MOST107-2320-B-010-041-MY3, the Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education in Taiwan (F.-C.L.), and Postdoctoral Fellowship Grants MOST107-2811-B-010-011 and MOST107-2321-B-010-010-MY3 (to H.-Y.K.).

                Correspondence should be addressed to Fu-Chin Liu at fuchin@ 123456ym.edu.tw
                Copyright © 2019 Kuo and Liu

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

                : 28 February 2019
                : 26 April 2019
                : 7 May 2019
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 171, Pages: 14, Words: 12446
                Funded by: http://doi.org/10.13039/501100004663Ministry of Science and Technology, Taiwan (MOST)
                Award ID: MOST107-2321-B-010-002
                Award ID: MOST107-2320-B-010-041-MY3
                Award ID: MOST107-2811-B-010-011
                Award ID: MOST107-2321-B-010-010-MY3
                Funded by: http://doi.org/10.13039/100010002Ministry of Education (MOE)
                Custom metadata
                May/June 2019

                basal ganglia,corticostriatal circuits,neurodevelopmental diseases,striatum,synapse


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