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J Physiol Volume 553, Number 1, 169-182, November 15, 2003 DOI: 10.1113/jphysiol.2003.050799
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J Physiol (2003), 553.1 pp. 169-182
© Copyright 2003 D 2003 The Physiological Society
DOI: 10.1113/jphysiol.2003.050799

Spontaneous voltage oscillations in striatal projection neurons in a rat corticostriatal slice

R. Vergara, C. Rick*, S. Hernández-López*, J. A. Laville, J. N. Guzman, E. Galarraga, D. J. Surmeier* and J. Bargas

Department of Biophysics, Instituto de Fisiología Celular UNAM, Mexico City 04510, Mexico and *Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago 60611, USA

In a rat corticostriatal slice, brief, suprathreshold, repetitive cortical stimulation evoked long-lasting plateau potentials in neostriatal neurons. Plateau potentials were often followed by spontaneous voltage transitions between two preferred membrane potentials. While the induction of plateau potentials was disrupted by non-NMDA and NMDA glutamate receptor antagonists, the maintenance of spontaneous voltage transitions was only blocked by NMDA receptor and L-type Ca2+ channel antagonists. The frequency and duration of depolarized events, resembling up-states described in vivo, were increased by NMDA and L-type Ca2+ channel agonists as well as by GABAA receptor and K+ channel antagonists. NMDA created a region of negative slope conductance and a positive slope crossing indicative of membrane bistability in the current-voltage relationship. NMDA-induced bistability was partially blocked by L-type Ca2+ channel antagonists. Although evoked by synaptic stimulation, plateau potentials and voltage oscillations could not be evoked by somatic current injection - suggesting a dendritic origin. These data show that NMDA and L-type Ca2+ conductances of spiny neurons are capable of rendering them bistable. This may help to support prolonged depolarizations and voltage oscillations under certain conditions.



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