Abstract
Dysfunction of parvalbumin-expressing cortical interneurons (PV-CINs) is strongly implicated in neurodevelopmental disorders including schizophrenia (SZ). Normal cortical function is maintained, in part, by the proper development of CINs. CINs originate from the ventral ganglionic eminence and migrate tangentially to the neocortex where they form connections with excitatory pyramidal neurons. Evidence suggests that glutamate plays a critical role in modulating radial migration of excitatory neurons via functional ionotropic N-methyl-D-aspartate receptors (NMDARs).
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