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It is also required for the maturation of the\n                    <jats:styled-content style=\"fixed-case\">GABAergic<\/jats:styled-content>\n                    system during adolescence, a phase that is critical for the development of several neuropsychiatric diseases. Mice bearing a null mutation of the\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    gene develop hyperexcitability of the amygdala and hippocampus, and a phenotype of increased anxiety and pathological fear memory reminiscent of posttraumatic stress disorder. Although genetic association of\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    in human has not yet been reported, these findings are in line with observations of reduced\n                    <jats:styled-content style=\"fixed-case\">GABAergic<\/jats:styled-content>\n                    function in these brain regions of anxiety disorder patients. The particular value of\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    (\u2212\/\u2212) mice thus lies in modeling the effects of reduced\n                    <jats:styled-content style=\"fixed-case\">GABAergic<\/jats:styled-content>\n                    function in the mature nervous system. The expression of\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    and a second\n                    <jats:styled-content style=\"fixed-case\">GAD<\/jats:styled-content>\n                    isozyme,\n                    <jats:styled-content style=\"fixed-case\">GAD67<\/jats:styled-content>\n                    , are differentially regulated in response to stress in limbic brain areas suggesting that by controlling\n                    <jats:styled-content style=\"fixed-case\">GABAergic<\/jats:styled-content>\n                    inhibition these enzymes determine the vulnerability for the development of pathological anxiety and other stress\u2010induced phenotypes. In fact, we could recently show that\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    haplodeficiency, which results in delayed postnatal increase of\n                    <jats:styled-content style=\"fixed-case\">GABA<\/jats:styled-content>\n                    levels, provides resilience to juvenile\u2010stress\u2010induced anxiety to\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    (+\/\u2212) mice thus foiling the increased fear and anxiety in homozygous\n                    <jats:styled-content style=\"fixed-case\">GAD65<\/jats:styled-content>\n                    (\u2212\/\u2212) mice.\n                  <\/jats:p>","DOI":"10.1111\/gbb.12188","type":"journal-article","created":{"date-parts":[[2014,12,2]],"date-time":"2014-12-02T19:25:54Z","timestamp":1417548354000},"page":"37-45","source":"Crossref","is-referenced-by-count":65,"title":["The\n              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