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The Journal of Neurophysiology Vol. 85 No. 4 April 2001, pp. 1351-1356
Copyright ©2001 by the American Physiological Society
1Laboratoire de Neurophysiologie, Centre National de la Recherche Scientifique, Unite Mixte de Recherche 5543, Université Bordeaux II, 33076 Bordeaux Cedex; and 2Institut National de la Santé et de la Recherche Médicale U29, 13273 Marseille Cedex 09, France
Beurrier, Corinne,
Bernard Bioulac,
Jacques Audin, and
Constance Hammond.
High-Frequency Stimulation Produces a Transient Blockade of
Voltage-Gated Currents in Subthalamic Neurons. J. Neurophysiol. 85: 1351-1356, 2001. The effect of
high-frequency stimulation (HFS) of the subthalamic nucleus (STN) was
analyzed with patch-clamp techniques (whole cell configuration,
current- and voltage-clamp modes) in rat STN slices in vitro. A brief
tetanus, consisting of 100-µs bipolar stimuli at a frequency of
100-250 Hz during 1 min, produced a full blockade of ongoing STN
activity whether it was in the tonic or bursting mode. This HFS-induced
silence lasted around 6 min after the end of stimulation, was frequency
dependent, could be repeated without alteration, and was not
synaptically induced as it was still observed in the presence of
blockers of ionotropic GABA and glutamate receptors or in the presence
of cobalt at a concentration (2 mM) that blocks voltage-gated
Ca2+ channels and synaptic transmission. During
HFS-induced silence, the following alterations were observed: the
persistent Na+ current
(INaP) was totally blocked (by 99%),
the Ca2+-mediated responses were strongly reduced
including the posthyperpolarization rebound (
62% in amplitude) and
the plateau potential (76% in duration), suggesting that T- and
L-type Ca2+ currents are transiently depressed by
HFS, whereas the Cs+-sensitive,
hyperpolarization-activated cationic current
(Ih) was little affected. Thus a
high-frequency tetanus produces a blockade of the spontaneous
activities of STN neurons as a result of a strong depression of
intrinsic voltage-gated currents underlying single-spike and bursting
modes of discharge. These effects of HFS, which are completely
independent of synaptic transmission, provide a mechanism for
interrupting ongoing activities of STN neurons.
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