Ikarashi Y, Yuzurihara M, Takahashi A, Shiobara T, Maruyama Y
Department of Neuropsychopharmacology (Tsumura), Gunma University, School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511,
Brain Res. 1999 Jan 16;816(1):238-40. doi: 10.1016/s0006-8993(98)01163-9.
In order to investigate whether changes in acetylcholine (ACh) release induced by GABA receptors are due to a direct or indirect effect on cholinergic neurons in the striatum, GABAA and GABAB receptor bindings were assayed in the striatum microinjected with ethylcholine mustard aziridinium ion (AF64A), a cholinergic neurotoxin. Intra-striatal injection of a selective concentration of AF64A (10 nmol) reduced GABAA receptor binding without significantly altering GABAB receptor binding. Treatment with a higher, less selective concentration of AF64A (20 nmol) reduced all markers examined. These results suggest that GABAA, but not GABAB receptors, are located on cholinergic neurons in the striatum, and that GABA can directly modulate ACh release through stimulation of GABAA receptors. Findings further suggest that GABA can also indirectly modulate ACh release through stimulation of GABAB receptors located on non-cholinergic neuronal elements in the striatum.
为了研究γ-氨基丁酸(GABA)受体诱导的乙酰胆碱(ACh)释放变化是由于对纹状体胆碱能神经元的直接作用还是间接作用,在注射了胆碱能神经毒素氮芥乙胆碱吖丙啶离子(AF64A)的纹状体中检测了GABAA和GABAB受体结合情况。纹状体内注射选择性浓度的AF64A(10 nmol)可降低GABAA受体结合,而不会显著改变GABAB受体结合。用更高、选择性更低浓度的AF64A(20 nmol)处理会降低所有检测的标志物。这些结果表明,GABAA受体而非GABAB受体位于纹状体的胆碱能神经元上,并且GABA可通过刺激GABAA受体直接调节ACh释放。研究结果进一步表明,GABA还可通过刺激位于纹状体非胆碱能神经元成分上的GABAB受体间接调节ACh释放。