Prenatal ketamine exposure impairs prepulse inhibition via arginine vasopressin receptor 1A-mediated GABAergic neuronal dysfunction in the striatum.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie April 1, 2023 Aeseul Kim, Sun Mi Gu, Haemiru Lee et al. 5 citations
Prenatal exposure to NMDA receptor antagonists like ketamine and methoxetamine in pregnant rats leads to psychosis-like behaviors in their offspring, including hyperactivity and reduced prepulse inhibition (PPI), a measure of sensorimotor gating. These effects are linked to increased expression of the arginine vasopressin receptor 1A (Avpr1a) in the striatum, and artificially overexpressing Avpr1a in the striatum also impairs PPI. Additionally, the treatments raise levels of glutamate decarboxylase 67 (GAD67) and GABA in the striatum, indicating that prenatal NMDA receptor blockade disrupts GABAergic neuron function and sensorimotor gating through Avpr1a regulation.