Kaneda Katsuyuki, Kita Hitoshi
Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis, TN 38163, USA.
J Neurophysiol. 2005 Aug;94(2):1104-14. doi: 10.1152/jn.00255.2005.
The globus pallidus (GP) contains abundant GABAergic synapses and GABA(B) receptors. To investigate whether synaptically released GABA can activate pre- and postsynaptic GABA(B) receptors in the GP, physiological recordings were performed using rat brain slice preparations. Cell-attached recordings from GABA(A) antagonist-treated preparations revealed that repetitive local stimulation induced a GABA(B) antagonist-sensitive pause in spontaneous firings of GP neurons. Whole cell recordings revealed that the repetitive stimulation evoked fast excitatory postsynaptic potentials followed by a slow inhibitory postsynaptic potential (IPSP) in GP neurons. The slow IPSP was insensitive to a GABA(A) receptor antagonist, increased in amplitude with the application of ionotropic glutamate receptor antagonists, and was suppressed by the GABA(B) antagonist CGP55845. The reversal potential of the slow IPSP was close to the potassium equilibrium potential. These results suggest that synaptically released GABA activated postsynaptic GABA(B) receptors and induced the pause and the slow IPSP. On the other hand, in the neurons that were treated to block postsynaptic GABA(B) responses, CGP55845 increased the amplitudes of repetitive local stimulation-induced GABA(A)-mediated inhibitory postsynaptic currents (IPSCs) but not the ionotropic glutamate-mediated excitatory postsynaptic currents. Moreover, the GABA(B) receptor specific agonist baclofen reduced the frequency of miniature IPSCs without altering their amplitude distributions. These results suggest that synaptically released GABA also activated presynaptic GABA(B) autoreceptors, resulting in decreased GABA release in the GP. Together, we infer that both pre- and postsynaptic GABA(B) receptors may play crucial roles in the control of GP neuronal activity.
苍白球（GP）含有丰富的γ-氨基丁酸（GABA）能突触和GABA（B）受体。为了研究突触释放的GABA是否能激活GP中的突触前和突触后GABA（B）受体，使用大鼠脑片标本进行了生理学记录。来自用GABA（A）拮抗剂处理的标本的细胞贴附记录显示，重复局部刺激在GP神经元的自发放电中诱导了对GABA（B）拮抗剂敏感的暂停。全细胞记录显示，重复刺激在GP神经元中诱发了快速兴奋性突触后电位，随后是缓慢抑制性突触后电位（IPSP）。缓慢的IPSP对GABA（A）受体拮抗剂不敏感，随着离子型谷氨酸受体拮抗剂的应用其幅度增加，并被GABA（B）拮抗剂CGP55845抑制。缓慢IPSP的反转电位接近钾平衡电位。这些结果表明，突触释放的GABA激活了突触后GABA（B）受体，并诱导了暂停和缓慢的IPSP。另一方面，在经处理以阻断突触后GABA（B）反应的神经元中，CGP55845增加了重复局部刺激诱导的GABA（A）介导的抑制性突触后电流（IPSCs）的幅度，但不增加离子型谷氨酸介导的兴奋性突触后电流的幅度。此外，GABA（B）受体特异性激动剂巴氯芬降低了微小IPSCs的频率，而不改变其幅度分布。这些结果表明，突触释放的GABA也激活了突触前GABA（B）自身受体，导致GP中GABA释放减少。总之，我们推断突触前和突触后GABA（B）受体可能在GP神经元活动的控制中起关键作用。
