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Reciprocally connected glutamatergic subthalamic and GABAergic globus pallidus neurons have recently been proposed to act as a generator of low-frequency oscillatory activity in Parkinson's disease. To determine whether GABA(A) receptor-mediated synaptic potentials could theoretically generate rebound burst firing in subthalamic neurons, a feature that is central to the proposed oscillatory mechanism, we determined the equilibrium potential of GABA(A) current (E(GABA(A))) and the degree of hyperpolarization required for rebound firing using perforated-patch recording. In the majority of neurons that fired rebounds, E(GABA(A)) was equal to or more hyperpolarized than the hyperpolarization required for rebound burst firing. These data suggest that synchronous activity of pallidal inputs could underlie rhythmic bursting activity of subthalamic neurons in Parkinson's disease.

Original publication




Journal article


J Neurophysiol

Publication Date





3169 - 3172


Animals, Bicuculline, Carbonic Anhydrase Inhibitors, Chlorides, Electric Impedance, Ethoxzolamide, GABA Antagonists, GABA-A Receptor Antagonists, In Vitro Techniques, Male, Neurons, Patch-Clamp Techniques, Periodicity, Phosphinic Acids, Propanolamines, Rats, Rats, Sprague-Dawley, Receptors, GABA-A, Sensory Thresholds, Subthalamus, Synaptic Transmission, Temperature, gamma-Aminobutyric Acid