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在记录神经元放电频率的实验中,发现麻醉或麻痹大鼠给予DA受体拮抗剂SPD,使VTA,SNC和DA神经元放电频率增加.但随着剂量的增加,SPD选择性地使VTA的DA神经元放电完全抑制,可被DA受体激动剂APO所翻转.提示这种抑制作用可能是DI.但SPD不抑制SNCDA神经元放电.在计数自发放电的神经元数目的实验中,观察到:慢性给予SPD21d后,大鼠VTA部位自发放电的DA神经元数目减少,有量效关系.可被APO所翻转.相反,同样给药并不影响SNC部位自发放电的DA神经元数目.当急性给予SPD时,VTA自发放电的DA神经元数目也减少,而SNC自发放电的DA细胞数不受影响.在行为实验中,SPD能抑制APO引起的定型活动,但SPD本身引起的僵住症很弱,仅能维持15min,并且无剂量依赖关系.上述结果提示:SPD选择性抑制VTADA神经元,而对SNCDA神经元的抑制作用很弱,引起的锥体外系副作用弱,可能发展成为新一代的非经典安定剂.
In the experiment of recording neuronal firing frequency, it was found that DA receptor antagonist SPD was administered to anesthetized or paralyzed rats to increase the discharge frequency of VTA, SNC and DA neurons. However, as the dose increased, SPD selectively made VTA. DA neuronal firing is completely inhibited and can be reversed by the DA receptor agonist APO. It is suggested that this inhibitory effect may be DI. However, SPD does not inhibit the SNCDA neuron discharge. In the experiment of counting the number of spontaneously discharged neurons, it was observed that : After chronic administration of SPD for 21 days, the number of DA neurons spontaneously discharged at the VTA site of the rat is reduced and has a dose-effect relationship. It can be reversed by APO. Conversely, the same dose does not affect the number of DA neurons spontaneously discharged at the SNC site. When SPD was given, the number of DA neurons spontaneously discharged by VTA was also decreased, while the number of DA cells spontaneously discharged by SNC was not affected. In behavioral experiments, SPD could inhibit stereotyped activity caused by APO, but the catalepsy caused by SPD itself was very high. Weak, can only be maintained for 15 min, and there is no dose-dependent relationship. The above results suggest that SPD selectively inhibits VTADA neurons, but the inhibitory effect on SNCDA neurons is weak, resulting in weak extrapyramidal side effects, may develop into a new generation of Non-classical stabilizers .