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Received for publication August 18, 2005.
Revised October 13, 2005.
Accepted for publication November 3, 2005.
7 nicotinic acetylcholine receptors of noradrenaline release in rat hippocampal slices: interaction with glutamate and GABA systems and effect of nicotine withdrawal
Nicotinic acetylcholine receptors (nAChR) can modulate transmitter release. Striatal [3H]dopamine ([3H]DA) release is regulated by presynaptic nAChR on dopaminergic terminals and 
7 nAChR on neighbouring glutamatergic afferents. Here, we explored the role of 7 nAChR in the modulation of [3H]noradrenaline ([3H]NA) release from rat hippocampal slices. The nicotinic agonist anatoxin-a (AnTx) evoked monophasic [3H]NA release (EC50=1.2 µM) that was unaffected by -conotoxin-MII or dihydro-beta-erythroidine, antagonists of 3/6
2* and 2* nAChR respectively. In contrast AnTx-evoked striatal [3H]DA release was biphasic (EC50=138.9 nM; 7.1 µM) and blocked by these antagonists. At a high AnTx concentration (25 µM), 7 nAChR antagonists (methyllycaconitine, -conotoxin-ImI) and glutamate receptor (GluR) antagonists (kynurenic acid, DNQX) partially inhibited [3H]NA release . The 7 nAChR-selective agonist choline evoked [3H]NA release (Emax=33% of that of AnTx) that was blocked by GluR antagonists, supporting a model in which 7 nAChR trigger glutamate release that subsequently stimulates [3H]NA release. A GABAergic component was also revealed: choline-evoked [3H]NA release was partially blocked by the GABAA receptor antagonist bicuculline, and co-application of bicuculline and DNQX fully abolished this response. These findings support 7 nAChR on GABAergic neurones that can promote GABA release that, in turn, leads to [3H]NA release, probably by disinhibition. To investigate the impact of chronic nicotine exposure on this model, rats were exposed for 14 days to nicotine (4 mg/kg/day) with or without 3 or 7 days withdrawal. 7 nAChR responses were selectively and transiently up-regulated after 3 days withdrawal. This functional up-regulation could contribute to the withdrawal effects of nicotine.
Key words:
Dopamine, Nicotinic cholinergic, GABAA, GABAC, Glutamate, Drug tolerance/dependence
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