Developmental oxidative stress leads to T-type Ca²⁺ channel hypofunction in thalamic reticular nucleus of mouse models pertinent to schizophrenia.

ABSTRACT: Impairment of parvalbumin interneurons induced by oxidative stress (OxS) is a "hub" on which converge several genetic and environmental risk factors associated with schizophrenia. In patients, this could be a mechanism leading to anomalies of the thalamic reticular nucleus (TRN) whose major neuronal population expresses parvalbumin. The TRN shapes the information flow within thalamo-cortical circuits. The low-threshold voltage-gated T-type Ca²⁺ (T-Ca²⁺) channels (CaV3.2, CaV3.3) contribute to the excitability and rhythmic bursting of TRN neurons which mediates cortical sleep spindles, known to be affected in schizophrenia. Here, we investigated the impact of OxS during postnatal development and adulthood on firing properties and T-Ca²⁺ channels of TRN neuro

SUBMITTER: El Khoueiry C 

PROVIDER: S-EPMC9126813 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature