Crunelli V, Bernasconi S, Samanin R
Psychopharmacology (Berl). 1979;66(1):79-85. doi: 10.1007/BF00431994.
Intraventricular injection of 5,7-dihydroxytryptamine, selective destruction of descending serotoninergic neurons by 5,6-dihydroxytryptamine or electrolytic and chemical lesions of the nucleus raphe dorsalis did not affect the electroconvulsive threshold in rats. No effect was observed after the systemic administration of drugs known to increase central serotonin transmission, such as quipazine, m-chlorophenylpiperazine, and moderate doses of d-fenfluramine, whereas p-chlorophenylalanine, an inhibitor of serotonin synthesis, decreased seizure susceptibility. The anticonvulsant activity of carbamazepine was not modified in animals with the same experimental lesions. The results, in relation to the high selectivity of the experimental procedures employed to deplete brain and spinal cord serotonin, do not bear out any involvement of serotonin in the tonic component of electrically induced convulsions or in the action of carbamazepine.
脑室内注射5,7 - 二羟基色胺、用5,6 - 二羟基色胺选择性破坏下行5 - 羟色胺能神经元或对中缝背核进行电解和化学损伤，均不影响大鼠的电惊厥阈值。全身给予已知可增强中枢5 - 羟色胺传递的药物，如喹哌嗪、间氯苯哌嗪和中等剂量的右旋芬氟拉明后，未观察到任何影响，而5 - 羟色胺合成抑制剂对氯苯丙氨酸则降低了惊厥易感性。卡马西平的抗惊厥活性在具有相同实验损伤的动物中未发生改变。鉴于所采用的耗尽脑和脊髓5 - 羟色胺的实验程序具有高度选择性，这些结果并不支持5 - 羟色胺参与电诱导惊厥的强直成分或卡马西平的作用。
