Activation of V_1a vasopressin receptors facilitates neuronal excitability in the medial nucleus of central amygdala (CeM) V_1a receptor activation excites about 80% CeM neurons by opening a cationic conductance and about 20% CeM neurons by suppressing an inwardly rectifying K⁺ (Kir) channel The cationic conductance activated by V_1a receptors is identified as TRPC5 channels PLCβ-mediated depletion of PIP₂ is involved in V_1a receptor-elicited excitation of CeM neurons Intracellular Ca²⁺ release and PKC are unnecessary for V_1a receptor-mediated excitation of CeM neurons ABSTRACT: Arginine vasopressin (AVP) serves as a hormone in the periphery to modulate water homeostasis and a neuromodulator in the brain to regulate a diverse range of functions including anxiety, social behaviour, cognitive activities and nociception. The amygdala is an essential brain region involved in modulating defensive and appetitive behaviours, pain and alcohol use disorders. Whereas activation of V_1a receptors in the medial nucleus of the central amygdala (CeM) increases neuronal excitability, the involved ionic and signalling mechanisms have not been determined. We found that activation of V_1a receptors in the CeM facilitated neuronal excitability predominantly by opening TRPC5 channels, although AVP excited about one fifth of the CeM neurons via suppressing an inwardly rectifying K⁺ (Kir) channel. G proteins and phospholipase Cβ (PLCβ) were required for AVP-elicited excitation of CeM neurons, whereas intracellular Ca²⁺ release and the activity of protein kinase C were unnecessary. Prevention of the depletion of phosphatidylinositol 4,5-bisphosphate (PIP₂ ) blocked AVP-induced excitation of CeM neurons, suggesting that PLCβ-mediated depletion of PIP₂ is involved in AVP-mediated excitation of CeM neurons. Our results may provide a cellular and molecular mechanism to explain the anxiogenic effects of AVP in the amygdala.

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