Aminergic and peptidergic innervation of neuroendocrine cells and its signal transduction system

虽然在调节精氨酸后叶加压素（AVP）的过程中，可调用腹外侧髓质中含有去甲肾上腺素的神经元PACAP (Pituitary Adenylate cyase - activating Polypeptide) INA （noradrenaline alin）所产生的通路，但PACAP与NA共存的确切作用机制和生理意义仍有待进一步研究。PACAP和NA均可诱导离体avp神经元[Ca^<2+>]i大幅升高。当PACAP和NA同时作用时，AVP神经元[Ca^<2+>]i升高幅度较大。PKA（蛋白激酶A）抑制剂完全抑制pacap诱导的[Ca^<2+>]i的增加，并部分抑制na诱导的avp神经元的增加。我们发现t型钙通道可能通过cAMP-PKA信号通路参与动作电位期间Ca^<2+>内流，l型电流可能参与破裂活动的产生。PACAP和NA从同一轴突末端共同释放，可能协同作用刺激AVP神经元钙信号通路，该通路由cAMP-PKA通路和l型Ca^<2+>通道介导。我们推测PACAP/NA可调节avp神经元的功能，而avp神经元参与控制血浆渗透压和血压。

Although the pathway arising from PACAP (Pituitary Adenylate Cydase-Activating Polypeptide) INA (Noradrenalin)-containing neurons in the ventrolateral medulla is invoked in the regulation of arginine vasopressin (AVP), the precise mechanism of action and physiological significance of the coexistence of PACAP and NA still need to be investigated. Both PACAP and NA induced large increases in the [Ca^<2+>]i in isolated AVP-containing neurons. When PACAP and NA were added together, they evoked larger increase in [Ca^<2+>]i in AVP neurons. An inhibitor of PKA (protein kinase A) completely inhibited the PACAP-induced increase in [Ca^<2+>]i, and partly the NA-induced increase in AVP-containing neurons. We found that T-type calcium channels might contribute to Ca^<2+> influx during action potentials through cAMP-PKA signaling pathway and L-type currents might contribute to the generation of bursting activity. PACAP and NA, co-released from the same axon terminals, may act synergistically to stimulate calcium signaling in AVP neurons, which is mediated by both cAMP-PKA pathway and L-type Ca^<2+> channel. It is hypothesized that PACAP/NA regulate the functions of AVP-containing neurons which participate in the control of plasma osmolarity and blood pressure.