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Synaptically Released GABA Activates Both Pre- and Postsynaptic GABA_B Receptors in the Rat Globus Pallidus

¹Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis, Tennessee; and ²The Japan Society for the Promotion of Science, Tokyo, Japan

Submitted 10 March 2005; accepted in final form 25 April 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, CGP55845increased 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.

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