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GABA and the GABAB receptor agonist baclofen activated a potassium conductance in acutely dissociated hippocampal CA3 neurons. Baclofen-activated current required internal GTP, was purely potassium selective, and showed strong inward rectification. As with acetylcholine-activated current in atrial myocytes, external Cs+ blocked inward but not outward current in a highly voltage-dependent manner, whereas Ba2+ blocked with no voltage dependence. Unlike the cardiac current, however, the baclofen-activated current showed no intrinsic voltage-dependent relaxation. With fast solution exchange, current was activated by baclofen or GABA with a lag of ∼50 msec followed by an exponential phase (time constant ∼225 msec at saturating agonist concentrations); deactivation was preceded by a lag of ∼150 msec and occurred with a time constant of ∼1 sec. GABA activated the potassium conductance with a half maximally effective concentration (EC50) of 1.6 μm, much lower than that for activation of GABAA receptor-activated chloride current in the same cells (EC50 ∼25 μm). At low GABA concentrations, activation of the GABAB current had a Hill coefficient of 1.4–2.1, suggesting cooperativity in the receptor-to-channel pathway. Although the maximal conductance activated by GABABreceptors is much smaller than that activated by GABAAreceptors, its higher sensitivity to GABA and slower time course make it well suited to respond to low concentrations of extra-synaptic GABA.

GABABReceptor-Activated Inwardly Rectifying Potassium Current in Dissociated Hippocampal CA3 Neurons

GABA_BReceptor-Activated Inwardly Rectifying Potassium Current in Dissociated Hippocampal CA3 Neurons