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Journal of Neuroscience, Vol 13, 2680-2688, Copyright © 1993 by Society for Neuroscience
Evidence for "preterminal" nicotinic receptors on GABAergic axons in the rat interpeduncular nucleus
C Lena, JP Changeux and C Mulle
URA CNRS D1284, Departement des Biotechnologies, Institut Pasteur, Paris, France.
Presynaptic nicotinic ACh receptors (nAChRs) are abundant in the nervous
system, where they are thought to regulate the release of various
neurotransmitters. Whole-cell recordings performed on rat interpeduncular
nucleus neurons using the thin-slice technique showed that nicotine
dramatically increased the frequency of postsynaptic GABAergic currents.
This effect was observed at low micromolar concentration of agonist; it was
mimicked by cytisine, dimethylphenylpiperazinium, and ACh in the presence
of eserine. It was blocked by hexamethonium, dihydro-beta-erythroidine, and
mecamylamine. The presynaptic action was suppressed in the presence of TTX.
A comparable effect of nicotine was found using a preparation of acutely
isolated neurons that had retained synaptic terminals attached to their
cell body as evidenced by immunoreactivity to synaptophysin and presence of
spontaneous GABAergic and glutamatergic synaptic activity. Nicotinic
agonists increased the frequency of GABAergic postsynaptic currents, an
effect blocked by curare and mecamylamine. This action was also suppressed
in the presence of TTX. These data suggest the presence of nAChRs at a
preterminal level on axons of intrinsic GABAergic neurons. We propose that,
in contrast to presynaptic nAChRs, activation of these "preterminal" nAChRs
can trigger a spike discharge and thus have a generalized action on the
GABAergic afferent.
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