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Vol. 284, Issue 3, 904-913, March 1998
-Bungarotoxin-Sensitive Nicotinic Acetylcholine Receptors In Rat
Hippocampal Neurons1
Department of Pharmacology and Experimental Therapeutics,
University of Maryland School of Medicine, Baltimore, Maryland (H.M.,
M.A., E.F.R.P., K.L.S., E.X.A.) and
Department of Clinical and Basic
Pharmacology, Institute of Biomedical Sciences, Federal University of
Rio de Janeiro, Rio de Janeiro, RJ 21944, Brazil (E.X.A.)
In our study, evidence is provided that strychnine, a competitive
antagonist at glycine-gated Cl
channels, is also a potent
competitive antagonist at native 
-7-containing, -bungarotoxin-sensitive nicotinic acetylcholine receptor (nAChRs). To address the effects of strychnine on two types of nicotinic responses, the whole-cell mode of the patch-clamp technique was applied
to rat hippocampal neurons in culture. Type IA and type II nicotinic
currents evoked by acetylcholine (ACh) were inhibited by strychnine in
a concentration-dependent manner with IC50s of 1.2 and 38 µM, respectively. Strychnine (2 µM) decreased the peak amplitude of
the -bungarotoxin-sensitive type IA current in a voltage-independent
manner and prolonged the decay phase of this current. The
concentration-response curve for ACh in evoking type IA current showed
a parallel shift to the right in the presence of strychnine (2 µM);
the EC50 for ACh was increased from 0.4 to 0.8 mM. These
findings suggest that strychnine acts as a competitive antagonist of
ACh at the 7 nAChRs that subserve type IA current. In contrast, the
inhibition by strychnine of type II current was strongly voltage
dependent, and the decay phase of this current was markedly accelerated
by the toxin, suggesting an open-channel blockade by strychnine of the
4
2 nAChRs subserving type II currents. Preexposure of the neurons
to strychnine enhanced its ability to decrease the peak amplitude of
type II currents, indicating that the toxin may also act on 42
nAChR channels that are not open. It is concluded that strychnine is a
potent competitive antagonist of ACh at neuronal 7 nAChRs and a
noncompetitive antagonist at the 42 nAChR.
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