Abstract
The gas molecule nitric oxide (NO) has been shown to modulate autonomic function by acting both peripherally and centrally. Accumulating evidence indicates that the paraventricular nucleus (PVN) of the hypothalamus is an important locus mediating central NO actions on autonomic function, under both physiological and pathological conditions. However, the cellular targets and mechanisms mediating NO actions within the PVN are still poorly understood. By combining in vitro patch-clamp recordings with neuronal tract tracing techniques, we show that neuronal excitability of autonomic-related neurones in the PVN is tonically inhibited by an endogenous NO input. Furthermore, immunohistochemical studies show that approximately 25% of autonomic-related PVN neurones express neuronal nitric oxide synthase, suggesting that at least a proportion of them contribute to the cellular sources of NO within the PVN. In summary, this work suggests that NO modulation of the firing activity of autonomic-related PVN neurones constitutes an efficient mechanism mediated central NO regulation of autonomic function.
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