| Popis: |
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 behaviors, cognitive activities and nociception. The amygdala is an essential brain region involved in modulating defensive and appetitive behaviors, 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 signaling 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 Ca(2+) release and the activity of protein kinase C were unnecessary. Prevention of the depletion of phosphatidylinositol 4,5-bisphosphate (PIP(2)) blocked AVP-induced excitation of CeM neurons suggesting that PLCβ-mediated depletion of PIP(2) 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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