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The Journal of Neurophysiology Vol. 84 No. 6 December 2000, pp. 2758-2766
Copyright ©2000 by the American Physiological Society
Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institutet, S-17177 Stockholm, Sweden
Büschges, A.,
M. A. Wikström,
S. Grillner, and
A. El Manira.
Roles of High-Voltage-Activated Calcium Channel Subtypes in a
Vertebrate Spinal Locomotor Network. J. Neurophysiol. 84: 2758-2766, 2000. Lamprey spinal cord
neurons possess N-, L-, and P/Q-type high-voltage-activated (HVA)
calcium channels. We have analyzed the role of the different HVA
calcium channels subtypes in the overall functioning of the spinal
locomotor network by monitoring the influence of their specific
agonists and antagonists on synaptic transmission and on
N-methyl-D-aspartate (NMDA)-elicited fictive locomotion. The N-type calcium channel blocker 
-conotoxin GVIA (-CgTx) depressed synaptic transmission from excitatory and
inhibitory interneurons. Blocking L-type and P/Q-type calcium channels
with nimodipine and -agatoxin, respectively, did not affect synaptic transmission. Application of -CgTx initially decreased the frequency of the locomotor rhythm, increased the burst duration, and subsequently increased the coefficient of variation and disrupted the motor pattern.
These effects were accompanied by a depression of the synaptic drive
between neurons in the locomotor network. Blockade of L-type channels
by nimodipine also decreased the frequency and increased the duration
of the locomotor bursts. Conversely, potentiation of L-type channels
increased the frequency of the locomotor activity and decreased the
duration of the ventral root bursts. In contrast to blockade of N-type
channels, blockade or potentiation of L-type calcium channels had no
effect on the stability of the locomotor pattern. The P/Q-type calcium
channel blocker -agatoxin IVA had little effect on the locomotor
frequency or burst duration. The results indicate that rhythm
generation in the spinal locomotor network of the lamprey relies on
calcium influx through L-type and N-type calcium channels.
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