Hardin H, Bernard A, Rajas F, Fevre-Montange M, Derrington E, Belin M F, Didier-Bazes M
INSERM CJF 90-10, Faculté de Médecine A. Carrel, Lyon, France.
Brain Res Mol Brain Res. 1994 Oct;26(1-2):1-8. doi: 10.1016/0169-328x(94)90067-1.
We have investigated the role of serotonergic neurons on the astrocytes catabolism of glutamate by analyzing glutamine synthetase (GS) and glutamate dehydrogenase (GDH) expression in the hippocampus after the degeneration of serotonergic neurons by a specific neurotoxin (5,7-DHT). 5,7-DHT caused reactive gliosis with hypertrophy (increase in glial fibrillary acidic protein (GFAP) expression) but not proliferation of astrocytes. Glutamate metabolism appeared preferentially regulated by a control of GDH expression rather than GS since the expression of GDH was specifically and significantly induced in the hippocampus whereas the level of GS remained unchanged. The inhibition of serotonin synthesis (by para-chlorophenylalanine (p-CPA) administration) produced no significant increase of GDH level. This suggests that serotonin is not the principal factor involved in this control of GDH expression.
我们通过分析特定神经毒素（5,7 - 二氢麦角隐亭，5,7 - DHT）导致血清素能神经元变性后海马体中谷氨酰胺合成酶（GS）和谷氨酸脱氢酶（GDH）的表达，研究了血清素能神经元在星形胶质细胞谷氨酸分解代谢中的作用。5,7 - DHT导致反应性胶质增生伴肥大（胶质纤维酸性蛋白（GFAP）表达增加），但星形胶质细胞未增殖。谷氨酸代谢似乎主要受GDH表达调控而非GS，因为海马体中GDH的表达被特异性且显著诱导，而GS水平保持不变。抑制血清素合成（通过给予对氯苯丙氨酸（p - CPA））未使GDH水平显著升高。这表明血清素不是参与这种GDH表达调控的主要因素。
