Functional significance of PACAP receptors in regulating secretion and synthesis of vasopressi

含pacap的轴突末端支配大鼠下丘脑视上核（SON）含精氨酸-加压素（AVP）的神经元。PACAP受体（PACAPR） mRNA在含avp神经元SON中高水平表达。虽然腹外侧髓质中含有去甲肾上腺素的神经元产生的通路参与了AVP的调节，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均诱导离体avp神经元中[Ca2+]I的大量增加。当PACAP和NA同时加入时，AVP神经元中[Ca2+]I的升高幅度较大。PKA抑制剂完全抑制pacap诱导的[Ca2+]I的增加，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信号通路在动作电位期间促进Ca2+内流，l型电流可能促进破裂活性的产生。PACAP和NA从相同的轴突末端共同释放，可能协同作用刺激AVP神经元的钙信号，这是由cAMP-PKA通路和l型Ca2+通道介导的。PACAP/NA可能调节avp神经元的功能，参与控制血浆渗透压和血压。

PACAP-containing axon terminals innervate arginine-vasopressin (AVP)-containing neurons in the rat hypothalamic supraoptic nucleus (SON). PACAP receptor (PACAPR) mRNA was expressed at high-levels in SON expressed in AVP-containing neurons. Although the pathway arising from PACAP/NA (noradrenalin)-containing neurons in the ventrolateral medulla is involved in the regulation of 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 [Ca2+]I in isolated AVP-containing neurons. When PACAP and NA were added together, they evoked larger increase in [Ca2+]I in AVP neurons. An inhibitor of PKA completely inhibited the PACAP-induced increase in [Ca2+]I, and partly the NA-induced increase in AVP-containing neurons. We found that T-type calcium channels might contribute to Ca2+ 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 Ca2+ channel. PACAP/NA may regulate the functions of AVP-containing neurons which participate in the control of plasma osmolarity and blood pressure.