Göthert M, Weinheimer G
Naunyn Schmiedebergs Arch Pharmacol. 1979 Dec;310(1):93-6. doi: 10.1007/BF00499879.
Rat brain cortex slices preincubated with 3H-5-hydroxytryptamine were superfused with physiological salt solution and stimulated electrically, or they were superfused with Ca2+-free solution containing 25 mM K+ and stimulated by introduction of 1.3 mM CaCl2 for 2 min. After blockade of neuronal 5-hydroxy-tryptamine (5-HT) uptake with clomipramine or paroxetine, the 3H overflow evoked by both methods of stimulation was decreased by unlabelled 5-HT and increased by methiothepin. The inhibition caused by 5-HT was antagonized by simultaneous administration of methiothepin. The inhibition by 5-HT of Ca2+-induced overflow was also observed in the presence of tetrodotoxin. These results suggest that 5-HT regulates its own release from central serotoninergic neurones by activating presynaptic 5-HT autoreceptors, thus decreasing the availability of Ca2+ for stimulus-release coupling.
用3H - 5 - 羟色胺预孵育的大鼠脑皮质切片，用生理盐溶液进行灌流并电刺激，或者用含25 mM钾的无钙溶液灌流，并通过加入1.3 mM氯化钙刺激2分钟。用氯米帕明或帕罗西汀阻断神经元5 - 羟色胺（5 - HT）摄取后，两种刺激方法诱发的3H溢出量被未标记的5 - HT降低，被甲硫噻平增加。5 - HT引起的抑制作用可被同时给予甲硫噻平所拮抗。在存在河豚毒素的情况下，也观察到5 - HT对钙离子诱导的溢出的抑制作用。这些结果表明，5 - HT通过激活突触前5 - HT自身受体来调节其从中枢5 - 羟色胺能神经元的释放，从而降低钙离子用于刺激 - 释放偶联的可用性。
