Phillipson O T, Emson P C, Horn A S, Jessell T
Brain Res. 1977 Nov 4;136(1):45-58. doi: 10.1016/0006-8993(77)90130-5.
The dopamine (DA)-sensitive adenylate cyclase in the substantia nigra was assayed in rats which had been subjected to 3 different kinds of brain lesion: (1) unilateral 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle; (2) unilateral lesions of the descending strio-nigral and pallido-nigral projections; (3) total lesions of the serotoninergic raphe-nigral pathway. Lesions of the medial forebrain bundle causing 97% depletion of striatal DA, 72% depletion of nigral tyrosine hydroxylase, and no change in nigral glutamate decarboxylase (GAD), resulted in no change in basal or DA-stimulated cyclic AMP production ipsilateral to the injection. Lesions of the globus pallidus, causing 70% and 79% reductions in GAD and substance P respectively in the ipsilateral nigra, produced a reduction in basal cyclic AMP production and abolished the normal increase in cyclic AMP produced by DA on the side of the lesion. Lesions to the dorsal and median raphe nuclei did not affect the normal DA-sensitive adenylate cyclase response in the nigra. The results suggest that one of the neurotransmitter functions of DA in this brain region may be to modulate the release of psi-aminobutyric acid (GABA) or substance P from synaptic terminals afferent to the nigra.
在遭受三种不同类型脑损伤的大鼠中检测黑质中对多巴胺（DA）敏感的腺苷酸环化酶：（1）内侧前脑束的单侧6-羟基多巴胺（6-OHDA）损伤；（2）纹状体-黑质和苍白球-黑质下行投射的单侧损伤；（3）5-羟色胺能中缝-黑质通路的完全损伤。内侧前脑束损伤导致纹状体DA耗竭97%，黑质酪氨酸羟化酶耗竭72%，黑质谷氨酸脱羧酶（GAD）无变化，注射同侧的基础或DA刺激的环磷酸腺苷（cAMP）生成无变化。苍白球损伤导致同侧黑质中GAD和P物质分别减少70%和79%，使基础cAMP生成减少，并消除了损伤侧DA引起的cAMP正常增加。背侧和中缝核损伤不影响黑质中正常的对DA敏感的腺苷酸环化酶反应。结果表明，DA在该脑区的神经递质功能之一可能是调节从传入黑质的突触终末释放γ-氨基丁酸（GABA）或P物质。
