Nicotine enhances GABAergic inhibition of oxytocin mRNA-expressing neuron in the hypothalamic paraventricular nucleus in vitro in rats

摘要: We recently found that extracellular administration of nicotine indirectly excited hypothalamic paraventricular nucleus (PVN) corticotropin-releasing hormone (CRH) mRNA-expressing neurons. In this study, we studied the effect on PVN oxytocin (OT) neuron in vitro rats, by whole-cell patch-clamp recording technique, immunohistochemistry methods and single-cell reverse-transcription multiplex polymerase chain reaction (SC-RT-mPCR) Our results showed 79.3% (73/92) 92 putative magnocellular neurons co-expressed GAPDH mRNA OT mRNA. Under current-clamp conditions, local micro application (1-300μM) induced a decrease spontaneous firing rate accompanied with hyperpolarization membrane potential 76.7% (56/73) The inhibition activity was dose-dependent. half-inhibitory concentration (IC50) is 2.9μM. sensitive to GABAA receptor antagonist, SR95531 (10μM) tetrodotoxin (TTX, 1μM). addition, significant increase frequency inhibitory postsynaptic potentials (sIPSPs), but without changes sEPSPs amplitude OT-mRNA expressing Biocytin staining confirmed nicotine-sensitive were These demonstrated enhances GABAergic inhibition, resulting findings suggested modulated secretion via enhancement both presynaptic action drive quantal GABA release.