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      Behavioral training reverses global cortical network dysfunction induced by perinatal antidepressant exposure.

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          Abstract

          Abnormal cortical circuitry and function as well as distortions in the modulatory neurological processes controlling cortical plasticity have been argued to underlie the origin of autism. Here, we chemically distorted those processes using an antidepressant drug-exposure model to generate developmental neurological distortions like those characteristics expressed in autism, and then intensively trained altered young rodents to evaluate the potential for neuroplasticity-driven renormalization. We found that young rats that were injected s.c. with the antidepressant citalopram from postnatal d 1-10 displayed impaired neuronal repetition-rate following capacity in the primary auditory cortex (A1). With a focus on recovering grossly degraded auditory system processing in this model, we showed that targeted temporal processing deficits induced by early-life antidepressant exposure within the A1 were almost completely reversed through implementation of a simple behavioral training strategy (i.e., a modified go/no-go repetition-rate discrimination task). Degraded parvalbumin inhibitory GABAergic neurons and the fast inhibitory actions that they control were also renormalized by training. Importantly, antidepressant-induced degradation of serotonergic and dopaminergic neuromodulatory systems regulating cortical neuroplasticity was sharply reversed. These findings bear important implications for neuroplasticity-based therapeutics in autistic patients.

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          Author and article information

          Journal
          Proc. Natl. Acad. Sci. U.S.A.
          Proceedings of the National Academy of Sciences of the United States of America
          Proceedings of the National Academy of Sciences
          1091-6490
          0027-8424
          Feb 17 2015
          : 112
          : 7
          Affiliations
          [1 ] Key Laboratory of Brain Functional Genomics of Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Sciences, East China Normal University, Shanghai 200062, China; NYU-ECNU Institute of Brain and Cognitive Science, NYU Shanghai, Shanghai 200062, China; xmzhou@bio.ecnu.edu.cn michael.merzenich@positscience.com.
          [2 ] Departments of Neurobiology and Anatomical Sciences.
          [3 ] Departments of Neurobiology and Anatomical Sciences, Psychiatry and Human Behavior, and.
          [4 ] Key Laboratory of Brain Functional Genomics of Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Sciences, East China Normal University, Shanghai 200062, China;
          [5 ] Keck Center for Integrative Neuroscience, University of California, San Francisco, CA 94143 xmzhou@bio.ecnu.edu.cn michael.merzenich@positscience.com.
          [6 ] Departments of Neurobiology and Anatomical Sciences, Psychiatry and Human Behavior, and Pediatrics, University of Mississippi Medical Center, Jackson, MS 39216; and.
          Article
          1416582111
          10.1073/pnas.1416582111
          4343129
          25646455
          ded7e1b7-cfcc-4618-a1a1-2285e2d3dcbd
          History

          antidepressant exposure,autism,behavioral training,cortical network,recovery of function

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