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Vol. 289, Issue 3, 1564-1574, June 1999
Department of Molecular Physiology and Biophysics, Vanderbilt
University Medical School, Nashville, Tennessee
The objective of this study was to identify factors that influence
ethanol (EtOH) inhibition of the
N-methyl-D-aspartate receptor (NMDAR) in
primary cultured cerebellar granule cells. Several factors
contributing to the inhibitory effects of EtOH on NMDAR function were
assessed using both whole-cell and perforated patch-clamp recordings.
The NMDAR subunit composition was examined by Western blot analysis
using NR2 subunit-specific antibodies and pharmacological manipulation
with the NR2B-specific antagonist infenprodil. Western blot analysis
indicated that NMDAR subunit composition changed from a combination of
NR2A and NR2B containing NMDARs to primarily NR2A with increasing days
in vitro (DIV). Although the NR2B subunit was detectable until 21 DIV,
there was a significant decrease in ifenprodil sensitivity after 7 DIV.
EtOH sensitivity did not change with an increasing DIV. A high
concentration of glycine reversed EtOH inhibition of steady-state, but
not peak, NMDA-induced current during whole-cell recordings.
Significant glycine reversal of effects of a low concentration of EtOH
on peak current was observed under perforated patch-clamp conditions. A
30-s EtOH pretreatment significantly enhanced EtOH inhibition of
NMDA-induced peak current. Collectively, these results indicate that
EtOH sensitivity of the NMDAR in primary cultured cerebellar granule
cells is not related to subunit composition nor ifenprodil sensitivity,
involves a kinetic interaction with glycine, and can be enhanced by a
slowly developing transduction mechanism that occurs within tens of seconds.
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