The NKCC1 antagonist bumetanide mitigates interneuronopathy associated with ethanol exposure in utero.

ABSTRACT: Prenatal exposure to ethanol induces aberrant tangential migration of corticopetal GABAergic interneurons, and long-term alterations in the form and function of the prefrontal cortex. We have hypothesized that interneuronopathy contributes significantly to the pathoetiology of fetal alcohol spectrum disorders (FASD). Activity-dependent tangential migration of GABAergic cortical neurons is driven by depolarizing responses to ambient GABA present in the cortical enclave. We found that ethanol exposure potentiates the depolarizing action of GABA in GABAergic cortical interneurons of the embryonic mouse brain. Pharmacological antagonism of the cotransporter NKCC1 mitigated ethanol-induced potentiation of GABA depolarization and prevented aberrant patterns of tangential migration induced by eth

SUBMITTER: Skorput AG 

PROVIDER: S-EPMC6768659 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature