Iravani M M, Kruk Z L
Department of Pharmacology, Queen Mary and Westfield College, London, United Kingdom.
Synapse. 1997 Jan;25(1):93-102. doi: 10.1002/(SICI)1098-2396(199701)25:1<93::AID-SYN11>3.0.CO;2-#.
Fast cyclic voltammetry at a carbon fibre microelectrode was used to measure 5-HT signals following electrical or chemical stimulation in rat substantia nigra pars reticulata slices. Chemical stimulation with (+)-amphetamine or veratrine gave signals which were indistinguishable from those of exogenous 5-HT. Electrical stimulation of sufficient duration gave voltammetric signals which were characteristic of 5-HT. Release of dopamine was not detected following either chemical or electrical stimulation. The 5-HT signals were attenuated by TTX and enhanced by fluvoxamine. It was not possible to demonstrate regulation of 5-HT release in the SNr by 5-HT1B autoreceptors using CGS 12066A or methiothepin. Signal following electrical stimulation were not enhanced by either benztropine or GBR12909, or modified in the presence of either quinpirole or sulpiride. We conclude that 5-HT release can be detected voltammetrically in the SNr; 5-HT release is likely to be from axon terminals, but somatodendritic DA release could not be detected.
在大鼠黑质网状部切片中，采用碳纤维微电极快速循环伏安法，在电刺激或化学刺激后测量5-羟色胺（5-HT）信号。用（+）-苯丙胺或藜芦碱进行化学刺激产生的信号与外源性5-HT的信号无法区分。足够长时间的电刺激产生了具有5-HT特征的伏安信号。化学刺激或电刺激后均未检测到多巴胺释放。5-HT信号被河豚毒素（TTX）减弱，被氟伏沙明增强。使用CGS 12066A或甲硫噻平无法证明5-HT1B自身受体对黑质网状部（SNr）中5-HT释放的调节作用。电刺激后的信号既未被苯海索也未被GBR12909增强，在喹吡罗或舒必利存在的情况下也未改变。我们得出结论，在SNr中可以通过伏安法检测到5-HT释放；5-HT释放可能来自轴突终末，但无法检测到树突体多巴胺释放。
