Parenti M, Tirone F, Olgiati V R, Groppetti A
Brain Res. 1983 Dec 5;280(2):317-22. doi: 10.1016/0006-8993(83)90061-6.
After degeneration of serotoninergic neurons induced by either transection of the ascending neuronal pathways originating from the nucleus raphe dorsalis or intraventricular 5,6-dihydroxytryptamine administration, the number of binding sites for [3H]D-Ala2, Met5-enkephalinamide was significantly reduced. This decrease in binding sites does not seem to be related to the opiate receptors present on dopaminergic terminals, nor is it due to a simple decrease in serotoninergic neuronal tone, since after p-chlorophenylalanine (100 mg/kg X 4 days) the number of striatal binding sites for the opiate ligand was not diminished. On the other hand, shortly after mechanical interruption of the raphe-striatal serotoninergic fibers, at a time when the metabolic processes are still functioning in the lesioned neurons, morphine still increased the striatal content of 5-hydroxyindoleacetic acid. These results suggest the presence of opiate receptors on striatal serotoninergic terminals, where they may modulate the presynaptic activity of these neurons.
在通过切断源自中缝背核的上行神经通路或脑室内注射5,6-二羟基色胺诱导血清素能神经元变性后，[3H]D-Ala2, Met5-脑啡肽酰胺的结合位点数量显著减少。结合位点的这种减少似乎与多巴胺能终末上存在的阿片受体无关，也不是由于血清素能神经元张力的简单降低，因为在给予对氯苯丙氨酸（100mg/kg×4天）后，阿片配体的纹状体结合位点数量并未减少。另一方面，在中缝-纹状体血清素能纤维机械中断后不久，即在受损神经元的代谢过程仍在起作用时，吗啡仍增加了纹状体中5-羟吲哚乙酸的含量。这些结果表明纹状体血清素能终末上存在阿片受体，它们可能在这些部位调节这些神经元的突触前活性。
