Simasko Steven M, Wiens Jason, Karpiel Adrienne, Covasa Mihai, Ritter Robert C
Program in Neuroscience, Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164, USA.
Am J Physiol Regul Integr Comp Physiol. 2002 Dec;283(6):R1303-13. doi: 10.1152/ajpregu.00050.2002. Epub 2002 Aug 1.
Imaging fluorescent measurements with fura 2 were used to examine cytosolic calcium signals induced by sulfated CCK octapeptide (CCK-8) in dissociated vagal afferent neurons from adult rat nodose ganglia. We found that 40% (184/465) of the neurons responded to CCK-8 with a transient increase in cytosolic calcium. The threshold concentration of CCK-8 for inducing the response varied from 0.01 to 100 nM. In most neurons (13/16) the response was eliminated by removing extracellular calcium. Depleting intracellular calcium stores with thapsigargin slightly augmented the response. Most neurons were unresponsive to nonsulfated CCK-8. The response was eliminated by the CCK-A receptor antagonist lorglumide. Low concentrations of JMV-180 had no effect; however, high concentrations of JMV-180 reduced responses to CCK-8. These results demonstrate that CCK acts at the low-affinity site of the CCK-A receptor to trigger the entry of extracellular calcium into vagal afferent neurons. Increased cytosolic calcium may participate in acute activation of vagal afferent neurons, or it may initiate long-term changes, which modulate future neuronal responses to sensory stimuli.
使用fura 2进行荧光成像测量，以检测成年大鼠结状神经节中解离的迷走传入神经元中由硫酸化胆囊收缩素八肽（CCK-8）诱导的胞质钙信号。我们发现40%（184/465）的神经元对CCK-8有反应，胞质钙短暂增加。诱导该反应的CCK-8阈值浓度在0.01至100 nM之间变化。在大多数神经元（13/16）中，去除细胞外钙可消除该反应。用毒胡萝卜素耗尽细胞内钙储存会略微增强该反应。大多数神经元对非硫酸化CCK-8无反应。该反应被CCK-A受体拮抗剂洛谷胺消除。低浓度的JMV-180无作用；然而，高浓度的JMV-180会降低对CCK-8的反应。这些结果表明，CCK作用于CCK-A受体的低亲和力位点，以触发细胞外钙进入迷走传入神经元。胞质钙增加可能参与迷走传入神经元的急性激活，或者它可能引发长期变化，从而调节未来神经元对感觉刺激的反应。
