Trent F, Tepper J M
Center for Molecular and Behavioral Neuroscience, Rutgers, State University of New Jersey, Newark 07102.
Exp Brain Res. 1991;84(3):620-30. doi: 10.1007/BF00230974.
Extracellular single unit recordings were obtained from antidromically identified nigrostriatal dopaminergic neurons in anesthetized rats to determine the effects of dorsal raphé stimulation on the somatodendritic excitability of substantia nigra dopaminergic neurons. Stimulation of the dorsal raphé with a brief train of pulses delivered 7-2 ms prior to the neostriatal-evoked antidromic response significantly reduced the proportion of neostriatal-evoked antidromic responses that consisted of both initial segment and somatodendritic components without significantly altering the neostriatal-evoked post-stimulus inhibitory period. Raphé stimulation alone facilitated post-stimulus neuronal firing in almost half of the cells examined. The raphé-induced decrease in somatodendritic excitability was blocked by the serotonin antagonist, metergoline (0.5-2.0 mg/kg, i.v.), without significantly affecting the rate or pattern of spontaneous activity. The tryptophan hydroxylase inhibitor, parachlorophenylalanine (400 mg/kg, i.p. for three consecutive days), abolished the decrease in somatodendritic excitability following raphé stimulation which could be re-instated by intravenous administration of 5-HTP. The dopamine antagonists haloperidol (25-100 micrograms/kg, i.v.) and sulpiride (10-30 mg/kg, i.v.) also blocked the effects of dorsal raphé stimulation on somatodendritic invasion. These data suggest that in vivo, serotonin liberated from raphé-nigral terminals facilitates the release of dopamine from nigrostriatal dendrites resulting in a local, autoreceptor-mediated reduction in somatodendritic excitability without affecting the spontaneous firing rate and excitability of the neuron as a whole.
在麻醉大鼠中，通过逆向鉴定黑质纹状体多巴胺能神经元进行细胞外单单位记录，以确定中缝背核刺激对黑质多巴胺能神经元树突体兴奋性的影响。在新纹状体诱发的逆向反应之前7 - 2毫秒给予一串短暂脉冲刺激中缝背核，显著降低了由起始段和树突体成分组成的新纹状体诱发逆向反应的比例，而未显著改变新纹状体诱发的刺激后抑制期。单独的中缝背核刺激在几乎一半被检查的细胞中促进了刺激后神经元放电。中缝背核诱导的树突体兴奋性降低被5-羟色胺拮抗剂美替拉酮（0.5 - 2.0毫克/千克，静脉注射）阻断，而对自发活动的速率或模式没有显著影响。色氨酸羟化酶抑制剂对氯苯丙氨酸（400毫克/千克，腹腔注射，连续三天）消除了中缝背核刺激后树突体兴奋性的降低，静脉注射5-羟色氨酸可恢复这种降低。多巴胺拮抗剂氟哌啶醇（25 - 100微克/千克，静脉注射）和舒必利（10 - 30毫克/千克，静脉注射）也阻断了中缝背核刺激对树突体传入的影响。这些数据表明，在体内，从中缝背核终末释放的5-羟色胺促进黑质纹状体树突释放多巴胺，导致局部、自身受体介导的树突体兴奋性降低，而不影响神经元整体的自发放电速率和兴奋性。
