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

尽管延髓腹外侧区含有PACAP(垂体腺苷环化酶激活多肽)的INA(去甲肾上腺素)神经元参与精氨酸加压素(AVP)的调节，但PACAP和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均可引起含AVP神经元[Ca~(2+)]i显著升高。PACAP和NA合用时，AVP神经元[Ca~(2+)&gt；]i有较大幅度的升高。蛋白激酶A(PKA)抑制剂可完全抑制PACAP引起的[Ca~(2+)]i升高和NA引起的含AVP神经元[Ca~(2+)]i的升高。我们发现，在动作电位过程中，T型钙通道可能通过cAMP-PKA信号通路参与钙内流，L型电流可能参与爆发活动的产生。从同一轴突终末共同释放的PACAP和NA可能通过cAMP-PKA通路和L型钙通道协同刺激AVP神经元上的钙信号。推测PACAP/NA调节AVP神经元的功能，AVP神经元参与血浆渗透压和血压的控制。

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.