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Volume 16, Number 16,
Issue of August 15, 1996
pp. 4971-4982
Copyright ©1996 Society for Neuroscience
Multiple Actions of 1S,3R-ACPD in Modulating Endogenous Synaptic
Transmission to Spinal Respiratory Motoneurons
Received Feb. 20, 1996; revised May 22, 1996; accepted May 28, 1996.
Xiao-Wei Dong1,
Didier Morin1, and
Jack L. Feldman1, 2
Systems Neurobiology Laboratory, Departments of
1 Physiological Science and 2 Neurobiology,
University of California at Los Angeles, Los Angeles, California
90095-1527
To determine physiological roles of metabotropic glutamate
receptors (mGluRs) affecting breathing, we examined the effects of
(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) on
synaptic transmission and excitability of phrenic motoneurons (PMNs) in
an in vitro neonatal rat brainstem/spinal cord preparation.
The effects of 1S,3R-ACPD were multiple, including reduction of
inspiratory-modulated synaptic currents and increase of neuronal
excitability via an inward current (Iacpd)
associated with a decrease of membrane conductance. The mechanism
underlying synaptic depression was examined. We found that 1S,3R-ACPD
reduced the frequency but not the amplitude of miniature excitatory
postsynaptic currents. The current induced by exogenous AMPA was not
significantly affected by 1S,3R-ACPD. These results suggest that
1S,3R-ACPD-induced reduction of inspiratory synaptic currents is
mediated by presynaptic mGluRs. We also examined the ionic basis for
Iacpd. We found that
Iacpd had a reversal potential of
approximately 100 mV, close to the estimated
EK+ ( 95 mV). Elevating
extracellular [K+] to 9 mM reduced the Iacpd
reversal potential to 75 mV. The K+ channel blocker
Ba2+ induced an inward current with a
reversal potential at 93 mV associated with a decrease of membrane
conductance, closely resembling the effect of 1S,3R-ACPD. Moreover,
Ba2+ occluded 1S,3R-ACPD effects. In the presence
of Ba2+, Iacpd and
the 1S,3R-ACPD-induced decrease of membrane conductance were
diminished. Our data indicate that the dominant component of
Iacpd results from the blockade of a
Ba2+-sensitive resting K+
conductance. We conclude that the activation of mGluRs affects the
inspiratory-modulated activity of PMNs via distinct mechanisms at pre-
and postsynaptic sites.
Key words:
1S,3R-ACPD;
metabotropic glutamate receptors;
synaptic
transmission;
presynaptic;
excitability;
potassium channels;
brainstem;
spinal cord;
phrenic motoneurons;
respiration
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