Ram J L, Shukla U A, Parti R, Goines R L
J Neurobiol. 1984 May;15(3):197-206. doi: 10.1002/neu.480150303.
Serotonin [5-hydroxytryptamine (5-HT)] enhances acetyl choline (ACh)-elicited contractures of Aplysia buccal muscles E1 and I5 . The possible role of external calcium in regulating the magnitude of ACh contracture in the presence and absence of 5-HT was investigated. Superfusion of E1 with zero calcium medium caused ACh contractures to fail within one to two minutes. Recovery of ACh contracture upon restoring normal medium occurred within two to four minutes. In the absence of 5-HT, ACh contracture decreased proportionally to external [Ca++] in the concentration range of 0-10 mM; however, the amount of enhancement of ACh contracture following 5-HT treatment did not decrease with external [Ca++] as long as [Ca++] was above a threshold concentration that varied from preparation to preparation. For most preparations, the enhancement of ACh contracture by 5-HT was dependent on the presence of external calcium during 5-HT treatment. Calcium influx into muscles E1 and I5 increased approximately two and a half fold in the presence of 10(-6) M 5-HT. A model in which 5-HT brings about calcium "loading" of an ACh releasable intracellular storage site is discussed.
血清素[5-羟色胺(5-HT)]可增强海兔颊肌E1和I5由乙酰胆碱(ACh)引发的挛缩。研究了在存在和不存在5-HT的情况下,细胞外钙在调节ACh挛缩幅度方面可能发挥的作用。用零钙培养基对E1进行灌流,会导致ACh挛缩在1至2分钟内失效。恢复正常培养基后,ACh挛缩在2至4分钟内恢复。在不存在5-HT的情况下,在0-10 mM的浓度范围内,ACh挛缩与细胞外[Ca++]成比例降低;然而,只要[Ca++]高于不同标本中各不相同的阈值浓度,5-HT处理后ACh挛缩的增强量就不会随细胞外[Ca++]的降低而减少。对于大多数标本,5-HT对ACh挛缩的增强作用取决于5-HT处理期间细胞外钙的存在。在存在10(-6) M 5-HT的情况下,流入肌肉E1和I5的钙增加了约两倍半。文中讨论了一个模型,即5-HT导致ACh可释放的细胞内储存位点发生钙“负载”。