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The Journal of Neuroscience, November 15, 1998, 18(22):9216-9226
Regulation of Intrinsic and Synaptic Properties of Neonatal Rat
Trigeminal Motoneurons by Metabotropic Glutamate Receptors
Christopher A.
Del Negro and
Scott
H.
Chandler
Department of Physiological Science, University of California at
Los Angeles, Los Angeles, California 90095-1586
We studied how metabotropic glutamate receptor (mGluR) activation
modifies the synaptic and intrinsic membrane properties of neonatal rat
trigeminal motoneurons using the broad-spectrum mGluR agonist
(1S,3R)-1-amino-1,3-cyclopentane-dicarboxylic acid [(1S,3R)-ACPD],
group I/II antagonist (±)- -methyl-4-carboxy-phenylglycine (MCPG),
and group III agonist L-2-amino-4-phosphonobutanoate
(L-AP4). (1S,3R)-ACPD depressed excitatory transmission to
trigeminal motoneurons presynaptically and postsynaptically via
presynaptic inhibition and by reducing the currents carried by
ionotropic glutamate receptors selective for AMPA. (1S,3R)-ACPD
also depolarized trigeminal motoneurons and increased input resistance
by suppressing a Ba2+-sensitive leakage
K+ current. These effects were not mimicked by
L-AP4 (100-200 µM). High-threshold
Ca2+ currents were also suppressed by (1S,3R)-ACPD.
Repetitive stimulation of excitatory premotoneurons mimicked the
postsynaptic effects of (1S,3R)-ACPD. The postsynaptic effects of
(1S,3R)-ACPD and repetitive stimulation were both antagonized by MCPG,
suggesting that mGluRs were similarly activated in both experiments. We
conclude that mGluRs can be recruited endogenously by glutamatergic
premotoneurons and that mGluR-mediated depression of excitatory
transmission, combined with increased postsynaptic excitability,
enhances the signal-to-noise ratio of oral-related
synaptic input to trigeminal motoneurons during rhythmical jaw movements.
Key words:
(1S,3R)-ACPD; MCPG; leakage K+
currents; Ca2+ currents; mEPSCs; mGluR
Copyright © 1998 Society for Neuroscience 0270-6474/98/18229216-11$05.00/0
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