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The Journal of Neurophysiology Vol. 86 No. 4 October 2001, pp. 1816-1825
Copyright ©2001 by the American Physiological Society
1Department of Electronic Engineering, Graduate School of Engineering, Osaka University, Suita 565-0871; 2Division of Biophysical Engineering, Graduate School of Engineering Science, Osaka University; and 3Core Research for Evolutional Science and Technology/Murakami Laboratory, Center for Advanced Research Projects, Osaka University, Toyonaka 560-8531, Japan
Otsuka, Takeshi,
Fujio Murakami, and
Wen-Jie Song.
Excitatory Postsynaptic Potentials Trigger a Plateau Potential in
Rat Subthalamic Neurons at Hyperpolarized States. J. Neurophysiol. 86: 1816-1825, 2001. The subthalamic
nucleus (STN) directly innervates the output structures of the basal
ganglia, playing a key role in basal ganglia function. It is therefore
important to understand the regulatory mechanisms for the activity of
STN neurons. In the present study, we aimed to investigate how the
intrinsic membrane properties of STN neurons interact with their
synaptic inputs, focusing on their generation and the properties of the
long-lasting, plateau potential. Whole cell recordings were obtained
from STN neurons in slices prepared from postnatal day 14 (P14) to P20 rats. We found that activation of glutamate receptor-mediated excitatory synaptic potentials (EPSPs) evoked a plateau potential in a
subpopulation of STN neurons (n = 13/22), in a
voltage-dependent manner. Plateau potentials could be induced only when
the cell was hyperpolarized to more negative than about
75 mV.
Plateau potentials, evoked with a depolarizing current pulse, again
only from a hyperpolarized state, were observed in about half of STN neurons tested (n = 162/327). Only in neurons in which
a plateau potential could be evoked by current injection did EPSPs
evoke plateau potentials. L-type Ca2+ channels,
Ca2+-dependent K+ channels,
and TEA-sensitive K+ channels were found to be
involved in the generation of the potential. The stability of the
plateau potential, tested by the injection of a negative pulse current
during the plateau phase, was found to be robust at the early phase of
the potential, but decreased toward the end. As a result the early part
of the plateau potential was resistant to membrane potential
perturbations and would be able to support a train of action
potentials. We conclude that excitatory postsynaptic potentials, evoked
in a subpopulation of STN neurons at a hyperpolarized state, activate
L-type Ca2+ and other channels, leading to the
generation of a plateau potential. Thus about half of STN neurons can
transform short-lasting synaptic excitation into a long train of output
spikes by voltage-dependent generation of a plateau potential.
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