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Vol. 283, Issue 3, 1396-1411, 1997
-Aminobutyric Acid Release from CA1 Neurons of Rat Hippocampal
Slices1
Department of Pharmacology and Experimental Therapeutics (M.A.,
E.F.R.P., C.T.F.B., E.X.A.), University of Maryland School of Medicine,
Baltimore, MD 21201;
Department of Basic and Clinical Pharmacology
(E.X.A.),
Institute of Biomedical Sciences and Lab. Mol. Pharmacol. II,
Institute of Biophysics Carlos Chagas Filho (C.T.F.B., E.X.A.), Center
of Health Sciences, Federal University of Rio de Janeiro, RJ
21941-590, Brazil
In the present study we investigated electrophysiologically the
nicotinic responses of pyramidal neurons and interneurons visualized by
infrared-assisted videomicroscopy and fluorescence in the CA1 field of
hippocampal slices obtained from 8- to 24-day-old rats. Application of
nicotinic agonists to CA1 neurons evoked at least four types of
nicotinic responses. Of major interest was the ability of these
agonists to induce the release of 
-aminobutyric acid (GABA) from
interneurons. Slowly decaying ACh whole-cell currents and GABA-mediated
postsynaptic currents could be recorded from pyramidal neurons and
interneurons, whereas fast-decaying nicotinic currents and fast current
transients were recorded only from interneurons. Nicotinic responses
were sensitive to blockade by d-tubocurarine (10 µM),
which indicated that they were mediated by nicotinic acetylcholine
receptors (nAChRs). The slowly decaying currents, the postsynaptic
currents and the fast current transients were insensitive to blockade
by the 
-7 nAChR-specific antagonist methyllycaconitine (up to 1 µM) or -bungarotoxin (100 nM). On the other hand, the slowly
decaying nicotinic currents recorded from the interneurons were blocked
by the 4
2 nAChR-specific antagonist dihydro--erythroidine, and
the fast-desensitizing nicotinic currents were evoked by the -7
nAChR-specific agonist choline. In experimental conditions similar to
those used to record nicotinic responses from neurons in slice
(i.e., in the absence of tetrodotoxin), we observed that
nicotinic agonists can also induce the release of GABA from hippocampal
neurons in culture. In summary, these results provide direct evidence
for more than one subtype of functional nAChR in CA1 neurons and
suggest that activation of nAChRs present in GABAergic interneurons can
evoke inhibitory activity in CA1 pyramidal neurons, thereby modulating processing of information in the hippocampus.
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