Casali T A, Gomez R S, Moraes-Santos T, Gomez M V
Departamento de Farmacologia, ICB, UFMG-Belo, Horizonte-Minas, Gerais, Brasil.
Neuropharmacology. 1995 Jun;34(6):599-603. doi: 10.1016/0028-3908(95)00019-3.
In this paper, the effect of calcium channel blockers on acetylcholine release induced by tityustoxin and ouabain in rat brain cortical slices is described. Cadmium, a non-specific blocker of calcium channels, inhibited the release of ACh induced by tityustoxin. L-type calcium channel blockers (verapamil, nifedipine and diltiazen) had no effect on the release of ACh induced by tityustoxin. The release of ACh was also unaffected by nickel, a T-type calcium channel blocker, and the conotoxins GVIA and MVIIC, blockers of N and Q-type calcium channels. Agatoxin IVA, a specific blocker of the P-type calcium channel, inhibited the release of ACh induced by tityustoxin by 50%. The spontaneous release of ACh as well as ouabain-induced release of ACh was unaffected by any of the calcium channel blockers studied. It is concluded that ACh release induced by tityustoxin is mediated by Ca2+ influx via P-type calcium channels.
本文描述了钙通道阻滞剂对大鼠脑皮质切片中由巴西蝰蛇毒素和哇巴因诱导的乙酰胆碱释放的影响。镉作为一种非特异性钙通道阻滞剂，抑制了巴西蝰蛇毒素诱导的乙酰胆碱释放。L型钙通道阻滞剂（维拉帕米、硝苯地平和地尔硫䓬）对巴西蝰蛇毒素诱导的乙酰胆碱释放没有影响。镍作为一种T型钙通道阻滞剂，以及芋螺毒素GVIA和MVIIC作为N型和Q型钙通道阻滞剂，对乙酰胆碱的释放也没有影响。P型钙通道的特异性阻滞剂阿加毒素IVA可使巴西蝰蛇毒素诱导的乙酰胆碱释放减少50%。所研究的任何一种钙通道阻滞剂均未影响乙酰胆碱的自发释放以及哇巴因诱导的乙酰胆碱释放。结论是，巴西蝰蛇毒素诱导的乙酰胆碱释放是由Ca2+通过P型钙通道内流介导的。
