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This Article Full Text Full Text (PDF) All Versions of this Article: 99/6/2902    most recent 00402.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Strauss, U. Articles by Gimsa, U. PubMed PubMed Citation Articles by Strauss, U. Articles by Gimsa, U.

Increasing Extracellular Potassium Results in Subthalamic Neuron Activity Resembling That Seen in a 6-Hydroxydopamine Lesion

¹Neurobiology, Department of Neurology and ⁴Institutes of Anatomy and ⁵Physiology, University of Rostock, Rostock, Germany; ²Center for Anatomy, Charite CCM, Berlin, Germany, ³Department of Pharmacology, University of Tennessee Health Science Center, Knoxville, Tennessee; and ⁶Research Unit Behavioural Physiology, Research Institute for the Biology of Farm Animals, Dummerstorf, Germany

Submitted 10 April 2007; accepted in final form 26 March 2008

Abnormal neuronal activity in the subthalamic nucleus (STN) plays a crucial role in the pathophysiology of Parkinson's disease (PD). Although altered extracellular potassium concentration ([K⁺]_o) and sensitivity to [K⁺]_o modulates neuronal activity, little is known about the potassium balance in the healthy and diseased STN. In vivo measurements of [K⁺]_o using ion-selective electrodes demonstrated a twofold increase in the decay time constant of lesion-induced [K⁺]_o transients in the STN of adult Wistar rats with a unilateral 6-hydroxydopamine (6-OHDA) median forebrain bundle lesion, employed as a model of PD, compared with nonlesioned rats. Various [K⁺]_o concentrations (1.5–12.5 mM) were applied to in vitro slice preparations of three experimental groups of STN slices from nonlesioned control rats, ipsilateral hemispheres, and contralateral hemispheres of lesioned rats. The majority of STN neurons of nonlesioned rats and in slices contralateral to the lesion fired spontaneously, predominantly in a regular pattern, whereas those in slices ipsilateral to the lesion fired more irregularly or even in bursts. Experimentally increased [K⁺]_o led to an increase in the number of spontaneously firing neurons and action potential firing rates in all groups. This was accompanied by a decrease in the amplitude of post spike afterhyperpolarization (AHP) and the amplitude and duration of the posttrain AHP. Lesion effects in ipsilateral neurons at physiological [K⁺]_o resembled the effects of elevated [K⁺]_o in nonlesioned rats. Our data suggest that changed potassium sensitivity due to conductivity alterations and delayed clearance may be critical for shaping STN activity in parkinsonian states.