Engelbrecht A H, Russell V A, Taljaard J J
Department of Chemical Pathology, University of Stellenbosch, Tygerberg Hospital, R.S.A.
Neurochem Res. 1994 Sep;19(9):1119-23. doi: 10.1007/BF00965144.
The aim of the present study was to investigate whether a disturbance of the central noradrenergic (NA) system could cause changes in gamma-aminobutyric acidB (GABAB) receptors in the rat frontal cortex. Manipulation of the NA projection to the frontal cortex was achieved by bilateral lesion of the locus coeruleus with 6-hydroxydopamine (6-OHDA) or chronic treatment with the NA reuptake blocker and antidepressant drug, desipramine. Precautions were taken to ensure that the GABAB receptor assay was performed optimally and was not confounded by the presence of endogenously generated GABA. The results show conclusively that manipulation of the NA projection did not result in any significant change in the number (Bmax) or affinity (Kd) of GABAB receptors in the frontal cortex. These results do not support the hypothesis that hypoactivity of the central NA system can lead to changes in cortical GABAB receptors and that antidepressant drugs act by increasing GABAB receptor binding in the frontal cortex.
本研究的目的是调查中枢去甲肾上腺素能（NA）系统的紊乱是否会导致大鼠额叶皮质中γ-氨基丁酸B（GABAB）受体的变化。通过用6-羟基多巴胺（6-OHDA）双侧损毁蓝斑或用NA再摄取阻滞剂及抗抑郁药地昔帕明进行慢性治疗，来对投射至额叶皮质的NA进行操控。已采取预防措施以确保GABAB受体测定能以最佳方式进行，且不会因内源性生成的GABA的存在而受到干扰。结果确凿地表明，对NA投射的操控并未导致额叶皮质中GABAB受体的数量（Bmax）或亲和力（Kd）发生任何显著变化。这些结果并不支持以下假说，即中枢NA系统功能减退会导致皮质GABAB受体发生变化，以及抗抑郁药通过增加额叶皮质中GABAB受体结合而起作用。
