Nitric oxide synthase contributes to the maintenance of LTP in the oxytocin–mRFP1 neuron of the rat hypothalamus

Abstract

AbstractOxytocin (OXT) is a neuropeptide hormone that plays a critical role in nociception. Long‐term potentiation (LTP) is a major form of synaptic plasticity in the central nervous system. Recently, LTP has been reported in the hypothalamus; however, data on LTP in hypothalamic OXT‐ergic neurons are unclear. Furthermore, the signaling pathways for hypothalamic OXT‐ergic neuronal LTP and its physiological significance remain unknown. Herein, we aimed to investigate the induction of hypothalamic OXT‐ergic neuronal LTP and its synaptic mechanism using OXT‐monomeric red fluorescent protein 1 transgenic rats to visualize and record from OXT‐ergic neurons. The hypothalamic paraventricular nucleus (PVN) OXT‐ergic neuronal LTP induced by the pairing protocol was dependent on N‐methyl‐D‐aspartate receptor (NMDAR). Furthermore, nitric oxide synthase (NOS) is required to maintain the LTP regardless of the NMDARs. In addition, hypothalamic OXT‐ergic neuronal LTP was not induced in the adjuvant arthritis rat model but increased excitatory postsynaptic currents were detected. LTP in hypothalamic OXT‐ergic neurons in the PVN in the presence of NOS may be involved in neuronal changes during OXT synthesis in chronic inflammation.