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

尽管在精氨酸加压素（AVP）的调节中涉及到延髓腹外侧区含去甲肾上腺素（NA）神经元的PACAP（腺苷酸环化酶激活肽）通路，但PACAP和NA共存的确切作用机制和生理意义仍需进一步研究。PACAP和NA均诱导分离的含AVP神经元内[Ca^<2+>]i大幅增加。当PACAP和NA共同作用时，可引起AVP神经元内[Ca^<2+>]i明显增加。PKA（蛋白激酶A）抑制剂可完全抑制PACAP诱导的[Ca^2+]i增加，部分抑制NA诱导的AVP神经元[Ca^2 +] i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过程中的Ca^2+内流，而L型电流可能参与动作电位爆发活动的产生。在AVP神经元中，由同一轴突终末共同释放的PACAP和NA可协同激活cAMP PKA通路和L型Ca^2+通道介导的钙信号。推测PACAP/NA调节含AVP神经元的功能，这些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.