Cortical inhibitory neuron disturbances in schizophrenia: role of the ontogenetic transcription factor Lhx6.
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ABSTRACT: Disturbances in parvalbumin- and somatostatin-containing neurons, including deficits in the gamma-aminobutyric acid (GABA)-synthesizing enzyme GAD67 in the prefrontal cortex (PFC) in schizophrenia, may be related to disrupted pre- and/or postnatal development. Deficits in the transcription factor Lhx6, which regulates parvalbumin and somatostatin neuron development, are associated with GAD67 deficits in schizophrenia. Therefore, we investigated the potential pre- and postnatal roles of Lhx6 in GABA-related disturbances using qPCR and/or in situ hybridization to quantify PFC levels of (1) Lhx6 mRNA in a new cohort of schizophrenia subjects; (2) Lhx6 mRNA in monkeys across postnatal development; (3) GABA-related mRNAs in Lhx6 heterozygous (Lhx6+/−) mice, which model Lhx6 deficits in schizoph
SUBMITTER: Volk DW
PROVIDER: S-EPMC4133682 | biostudies-literature | 2014 Sep
REPOSITORIES: biostudies-literature
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