Nitric Oxide and Neurotransmission in Magnocellular Neurons of the Rat Supraoptic Nucleus

Abstract

The importance of Nitric oxide (NO) as a neurotransmitter acting on magnocellular neurons of the supraoptic nucleus (nmSON) became evident when the expression of nitric oxide synthase (NOS), oxytocin (OT) and vasopresin (VP) RNAm levels were increased by treating the cells with hyperosmotic solution. Currently, it is well known that NO has an indirect effect on the nmSON activity by acting on the synaptic transmission in the nucleus. NO plays an inhibitory effect on the nmSON by enhancing the frequency of IPSCs (inhibitory post synaptic currents) which could be blocked by GABAA receptor antagonists. On the other hand, the glutamate transmission in nmSON seems not to be modulated by NO. In addition, L-NAME, a NOS inhibitor, increased the frequency of action potentials induced by hypertonic solutions, suggesting an endogenous production of NO during osmotic stress. In fact, transient potential receptors vanilloid (TRPV) found in nmSON, which are cation channels activated by osmomechano stimuli, had been postulated as mediators of the neuronal hyperactivity induced by osmotic stress. This was confirmed by observations that TRPV gene knockout mice exhibit insufficient vasopressin secretion when facing a hyperosmotic challenged. Thus, in this work we aim to investigate the effects of NO on the evoked synaptic currents in the rat nmSON, as well as, the osmosensitive mechanisms influenced by TRPV channels which acts in contraposition of NO on the electrical activity of the nmSON.