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Prolonged stimulation of presynaptic nicotinic acetylcholine receptors in the rat interpeduncular nucleus has differential effects on transmitter release
Author(s) -
Covernton Patrick O.J.,
Lester Robin A.J.
Publication year - 2002
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(02)00036-9
Subject(s) - nicotine , neuroscience , stimulation , glutamate receptor , acetylcholine , inhibitory postsynaptic potential , nicotinic agonist , chemistry , acetylcholine receptor , bicuculline , receptor , gabaa receptor , biology , pharmacology , biochemistry
Alterations in nicotinic acetylcholine (nAChR) receptor number can be induced by chronic exposure to nicotine possibly by stabilization of the desensitized state(s) of the receptor. Since within the central nervous system (CNS), many nAChRs are localized presynaptically, we have investigated the physiological consequences of prolonged nicotine applications on spontaneous transmitter release. In the presence of glutamate receptor antagonists, bicuculline‐sensitive spontaneous GABA inhibitory synaptic currents (IPSCs) could be readily resolved in whole‐cell recordings from neurons in the interpeduncular nucleus (IPN) maintained as brain slices. Nicotine (300 nM) caused a marked enhancement in the frequency of spontaneous events. During a 15 min exposure to nicotine, the time course of changes in IPSC frequency could be divided into two groups. In most neurons, there was a fast increase in event frequency followed by a decline to a lower steady‐state level that remained above baseline. In the remaining neurons, the effect of nicotine was more slowly developing and outlasted the application. Interestingly, the rapid effect was associated with a shift to higher amplitude events, whereas, no change in the IPSC amplitude histogram was observed during the slow onset effect. These data show that prolonged stimulation of presynaptic nicotinic receptors can have different outcomes that could potentially contribute to the diverse effects of nicotine on central information processing.