Tassin J P
INSERM U114, Collège de France, Paris.
Encephale. 1996 Jun;22 Spec No 2:9-12.
After having rapidly recapitulated the various arguments which suggest that meso-subcortical dopaminergic neurons are hyperreactive in the productive form of schizophrenia, we suggest in this article that dysfunction of noradrenergic neurons gives rise to this disorder whether of the productive or deficitary variety. In the specific case of deficitary schizophrenia, noradrenergic transmission appears to be desensitized, most likely following intense and repeated activation. Our results in fact show that activation of noradrenergic neurons inhibits cortical dopaminergic transmission mediated by D1 receptors and enhances the functional role of subcortical dopaminergic neurons. On the basis of these data, the lack of noradrenergic transmission would lead to a cortico/subcortical imbalance in favour of cortical areas. Deficitary schizophrenics would then find themselves stalled in a short-term memory situation without external data they could process. The therapeutic effect of substituted benzamides on negative schizophrenic patients may be explained by the observation that these products increase the release of noradrenaline in the frontal cortex and reactive subcortical dopaminergic neurons by blocking D2-type autoreceptors.
在快速概括了各种表明中脑-皮质下多巴胺能神经元在精神分裂症的阳性形式中反应过度的论据之后，我们在本文中提出，去甲肾上腺素能神经元功能障碍会引发这种疾病，无论是阳性还是阴性类型。在阴性精神分裂症的特定情况下，去甲肾上腺素能传递似乎脱敏，很可能是在强烈且反复激活之后。我们的研究结果实际上表明，去甲肾上腺素能神经元的激活会抑制由D1受体介导的皮质多巴胺能传递，并增强皮质下多巴胺能神经元的功能作用。基于这些数据，去甲肾上腺素能传递的缺乏会导致有利于皮质区域的皮质/皮质下失衡。阴性精神分裂症患者随后会发现自己陷入没有外部数据可供处理的短期记忆状态。取代苯甲酰胺对阴性精神分裂症患者的治疗效果可以通过以下观察来解释，即这些药物通过阻断D2型自身受体增加额叶皮质中去甲肾上腺素的释放并激活皮质下多巴胺能神经元。
