Trovero F, Hervé D, Blanc G, Glowinski J, Tassin J P
INSERM U.114, Chaire de Neuropharmacologie, Collège de France, Paris.
Neurosci Lett. 1991 Jun 24;127(2):198-202. doi: 10.1016/0304-3940(91)90793-s.
The effects of the destruction of mixed dopamine/neurotensin (DA/NT) meso-cortical neurons were investigated by studying the development of denervation supersensitivity of DA (D1) and NT cortical post-synaptic binding sites using respectively [3H]SCH 23390 and [125I]NT as ligands. These neurons were destroyed bilaterally either by injection of 6-hydroxydopamine (6-OHDA) or by an electrolytic coagulation made in the ventral tegmental area (VTA). Five weeks later, both [3H]SCH 23390 and [125I]NT bindings were analysed by quantitative autoradiography on each lesioned animal and on corresponding controls. The chemical lesions of the VTA induced an increase in the density of the cortical NT binding sites but did not affect D1 binding sites. On the contrary, electrolytic lesions induced an increase in D1 binding sites and no change in NT binding sites. One possible explanation of these differences may be that, since chemical lesions of the VTA destroy noradrenergic (NA) ascending pathways while electrolytic lesions spare the cortical NA innervation, the observed modifications of D1 and NT cortical binding sites following their presynaptic denervation are dependent on the presence (increase in D1 receptors) or the absence (increase in NT binding sites) of the cortical NA innervation.
通过分别使用[3H]SCH 23390和[125I]神经降压素（NT）作为配体，研究多巴胺（DA）（D1）和NT皮质突触后结合位点去神经超敏反应的发展，来探究混合多巴胺/神经降压素（DA/NT）中脑皮质神经元破坏的影响。这些神经元通过注射6-羟基多巴胺（6-OHDA）或在腹侧被盖区（VTA）进行电解凝固而被双侧破坏。五周后，通过定量放射自显影对每只损伤动物和相应对照进行[3H]SCH 23390和[125I]NT结合分析。VTA的化学损伤导致皮质NT结合位点密度增加，但不影响D1结合位点。相反，电解损伤导致D1结合位点增加，而NT结合位点没有变化。这些差异的一个可能解释可能是，由于VTA的化学损伤破坏了去甲肾上腺素能（NA）上行通路，而电解损伤保留了皮质NA神经支配，因此在其突触前去神经后观察到的D1和NT皮质结合位点的改变取决于皮质NA神经支配的存在（D1受体增加）或不存在（NT结合位点增加）。
