Bianchi L, Sharp T, Bolam J P, Della Corte L
Dipartimento di Farmacologia Preclinica e Clinica, Università di Firenze, Italy.
Neuroreport. 1994 Jun 2;5(10):1233-6. doi: 10.1097/00001756-199406020-00019.
In order to test the hypotheses that stimulation of non-N-methyl-D-aspartate (NMDA) receptors in the neostriatum causes the release of gamma-aminobutyric acid (GABA) from nigrostriatal neurones, dual microdialysis was carried out in the neostriatum and substantia nigra of freely moving rats. Application of kainic acid to the neostriatum caused a dose-dependent release of GABA both locally and, at the same time, from the ipsilateral substantia nigra. These effects were blocked by the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX). Direct application of kainic acid to the substantia nigra caused a DNQX-sensitive local release of GABA. It is concluded that excitatory amino acid receptor stimulation of the neostriatum releases GABA from striatonigral neurones and that stimulation of the substantia nigra causes the release from striatonigral terminals and/or the collaterals of nigrofugal neurones.
为了验证新纹状体中非N-甲基-D-天冬氨酸(NMDA)受体的刺激会导致黑质纹状体神经元释放γ-氨基丁酸(GABA)这一假说,在自由活动大鼠的新纹状体和黑质中进行了双重微透析实验。向新纹状体施加 kainic 酸会导致局部以及同时从同侧黑质中出现剂量依赖性的GABA释放。这些效应被非NMDA受体拮抗剂6,7-二硝基喹喔啉-2,3-二酮(DNQX)阻断。直接向黑质施加kainic酸会导致对DNQX敏感的局部GABA释放。得出的结论是,新纹状体的兴奋性氨基酸受体刺激会使纹状体黑质神经元释放GABA,并且黑质的刺激会导致从纹状体黑质终末和/或黑质传出神经元的侧支释放GABA。