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Vol. 284, Issue 2, 768-776, February 1998
Departments of
Pharmacology (D.W.S., H.H.Y.),
Neurology (H.H.Y.)
and
Program in Neuroscience (H.H.Y.), University of Connecticut Health
Center, Farmington, Connecticut
This study compared the interaction between ethanol and
-aminobutyric acid (GABA)-mediated current responses elicited in several immortalized cell lines and stably transfected cells, as well
as in cultured and acutely dissociated rat cerebellar Purkinje cells.
Only cell lines that were found previously to possess functional
GABAA receptors were examined in this study. Under
identical recording conditions, ethanol (10-200 mM) exerted no effect
on GABA-induced currents in any of the cell lines or stably transfected
cells tested in this study. However, GABA responses monitored in both
primary culture and acutely dissociated Purkinje cells were
significantly potentiated by ethanol (25 and 50 mM). Mouse pancreatic
cells (RINm5F) were insensitive to both diazepam and ethanol suggesting
the expression of a GABAA receptor isoform lacking a subunit. Immortalized neuroblastoma IMR-32 cells displayed GABA
responses that could be distinguished based on differential sensitivity
to diazepam. However, none of the IMR-32 cells displayed GABA responses
that were sensitive to modulation by ethanol. GABA responses in the
stably transfected cell lines, PA3 (
1
12L) and
WSS-1 (122), were also unaffected by exposure to ethanol. In
Purkinje cells acutely dissociated from the neonatal cerebellum, the
ethanol-induced potentiation of GABA-induced current response could be
observed before postnatal day 7, when only the 2S but not the 2L splice variant is expressed. This indicates
that the 2L subunit is not necessary for an
ethanol-induced potentiation of GABAA receptor-mediated
response to become manifest. In addition, the results point to inherent
differences that should be taken into account in interpreting
comparative data between native and recombinant GABAA
receptors.
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