Durán-Vázquez A, Drucker-Colín R
Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, D.F., Mexico.
Brain Res. 1997 Jan 2;744(1):171-4. doi: 10.1016/s0006-8993(96)01203-6.
Recently, we have shown that rapid eye movement sleep deprivation (REM-SD) in animals with lesions of the nigro-striatal pathway facilitates turning behavior and such increase still occurred even in the presence of dopaminergic grafts. The objective of this work was to determine which DA receptors are preferentially involved. The results showed that the D2 receptor antagonist sulpiride decreases significantly turning behavior of lesioned animals, with no effect whatsoever of the D1 antagonist SCH 23390. When lesioned animals were REM sleep deprived, the D1 but not the D2 receptor antagonist prevented the increase of turning induced by REM-SD. This work suggests that the increase of post-synaptic supersensitivity induced by REM-SD in nigro-striatal lesioned animals is mediated by D1 receptors.
最近，我们发现，黑质纹状体通路受损的动物快速眼动睡眠剥夺（REM-SD）会促进其旋转行为，而且即使存在多巴胺能移植，这种增加仍然会出现。这项工作的目的是确定哪些多巴胺受体优先参与其中。结果表明，D2受体拮抗剂舒必利显著降低了受损动物的旋转行为，而D1拮抗剂SCH 23390则没有任何作用。当对受损动物进行REM睡眠剥夺时，D1受体拮抗剂而非D2受体拮抗剂可阻止REM-SD诱导的旋转增加。这项研究表明，REM-SD在黑质纹状体受损动物中诱导的突触后超敏反应的增加是由D1受体介导的。
