Impaired synaptic plasticity in the prefrontal cortex of mice with developmentally decreased number of interneurons.

摘要: Interneurons are inhibitory neurons, which protect neural tissue from excessive excitation. They interconnected with glutamatergic pyramidal neurons in the cerebral cortex and regulate their function. Particularly prefrontal (PFC), interneurons have been strongly implicated regulating pathological states display deficits PFC. The aim of this study is to investigate adaptations adult system, when defects interneuron development do not allow adequate numbers reach cortex. To end, we used a mouse model that displays ~50% fewer cortical due Rac1 protein loss Nkx2.1/Cre expressing cells (Rac1 conditional knockout (cKO) mice), examine how developmental may affect basal synaptic transmission, plasticity neuronal morphology Despite decrease number interneurons, as examined by recording field excitatory postsynaptic potentials (fEPSPs) layer II networks, altered PFC cKO mice. However, there decreased paired-pulse ratio (PPR) long-term potentiation (LTP), response tetanic stimulation, synapses Furthermore, expression N-methyl-d-aspartate (NMDA) subunits dendritic altered, changes could underlie LTP Finally, find treating mice diazepam early postnatal life can reverse observed non-treated Therefore, our data show disruption GABAergic inhibition alters function PFC, an effect be reversed enhancement during period.