Waszczak B L, Walters J R
J Neurosci. 1986 Jan;6(1):120-6. doi: 10.1523/JNEUROSCI.06-01-00120.1986.
Previous reports from this laboratory have described an ability of iontophoretically applied dopamine to attenuate the inhibitory effects of iontophoresed GABA on neurons of the substantia nigra pars reticulata. This finding raised the question of whether endogenous dopamine, released from dendrites of neighboring pars compacta dopamine neurons, might act as a neuromodulator which diminishes the inhibition of pars reticulata neurons evoked by either GABA iontophoresis or electrical stimulation of the striatonigral GABAergic pathway. Extracellular, single-unit activity of pars reticulata neurons was recorded in male rats anesthetized with chloral hydrate. In one set of studies, d-amphetamine, a drug reported to release dopamine from nigral dendrites, was administered intravenously (1.6 mg/kg) during regular, intermittent iontophoretic pulses of GABA. As had been previously observed with iontophoresed dopamine, i.v. amphetamine significantly lessened the inhibition of reticulata neurons produced by GABA application. This change was reflected by a decrease in GABA's inhibitory potency by 22% relative to the control level of inhibition achieved prior to amphetamine administration. Amphetamine caused no decreases in GABA's effectiveness, however, in animals that had previously received treatments that depleted or destroyed nigral dopamine stores, i.e., in rats pretreated with reserpine and alpha-methyl-p-tyrosine, or in rats with 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway. In a second set of experiments, amphetamine or dopamine was delivered iontophoretically while monitoring the GABA-mediated (bicuculline-reversible) inhibition of reticulata neurons that can be elicited by striatal stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
本实验室之前的报告描述了通过离子电渗法施加多巴胺来减弱离子电渗法施加的GABA对黑质网状部神经元抑制作用的能力。这一发现提出了一个问题，即从邻近的致密部多巴胺能神经元树突释放的内源性多巴胺是否可能作为一种神经调质，减少由GABA离子电渗法或纹状体黑质GABA能通路电刺激所诱发的网状部神经元的抑制作用。在用水合氯醛麻醉的雄性大鼠中记录网状部神经元的细胞外单单位活动。在一组研究中，在定期、间歇性的GABA离子电渗脉冲期间静脉注射（1.6mg/kg）d-苯丙胺，据报道该药物可从黑质树突释放多巴胺。正如之前用离子电渗多巴胺所观察到的那样，静脉注射苯丙胺显著减轻了GABA施加对网状部神经元的抑制作用。这种变化表现为相对于苯丙胺给药前达到的对照抑制水平，GABA的抑制效力降低了22%。然而，在先前接受过耗尽或破坏黑质多巴胺储备治疗的动物中，即在用利血平和α-甲基-p-酪氨酸预处理的大鼠中，或在黑质纹状体多巴胺通路有6-羟基多巴胺损伤的大鼠中，苯丙胺并未降低GABA的有效性。在第二组实验中，在监测由纹状体刺激所诱发的、GABA介导的（荷包牡丹碱可逆的）网状部神经元抑制作用时，通过离子电渗法递送苯丙胺或多巴胺。（摘要截短于250词）
