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Locally released vasopressin increases presympathetic PVN neuronal activity

In addition to neurohypophysial secretion, vasopressin (VP) is locally released within the supraoptic and paraventricular (PVN) nuclei, autoregulating VP neuronal activity. Here, we tested the hypothesis that locally produced VP can also influence presympathetic PVN neuronal activity. Patch‐clamp recordings from presympathetic PVN‐RVLM neurons show that focal application of VP (1μM) depolarized, and increased the firing activity of PVN‐RLVM neurons (∼450%, P< 0.01). The effect persisted in the presence of the GABAA and glutamate receptor blockers BIC (20 μM) and KYN (1 mM), respectively. In the voltage‐clamp mode, VP activated an inward current of ∼6–10 pA. VP effects were blocked by the manning compound (1 μM), a V1a receptor antagonist. The expression of V1a receptors in PVN‐RVLM neurons was further confirmed by immunohistochemical studies. Importantly, the V1a receptor antagonist per se induced membrane hyperpolarization (∼4 mV) and reduced the ongoing firing activity of PVN‐RVLM neurons (∼75%, P< 0.02). In summary, our results indicate that locally produced VP tonically excites presympathetic PVN neurons, and suggest that activity‐dependent VP release from magnocellular neurosecretory neurons may constitute an important intercellular signaling pathway in the generation of homeostatic patterns of neuroendocrine and autonomic activities by the PVN. Supported by NIH HL68725.