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Received for publication August 23, 2004.
Revised January 28, 2005.
Accepted for publication January 28, 2005.
6* nAChR sites and function in mice
-Conotoxin MII-sensitive nicotinic receptors (nAChRs) are distinct from other subtypes in their relatively restricted localization to the striatum and some other brain regions. The effect of nicotine treatment on nAChR subtypes has been extensively investigated, with the exception of changes in -conotoxin MII-sensitive receptor expression. We therefore determined the consequence of chronic nicotine administration on this subtype and its function. Nicotine was given in drinking water to provide a chronic yet intermittent treatment. Consistent with previous studies, nicotine exposure increased 125I-epibatidine and 125I-A85380, but not 125I--bungarotoxin, receptors in cortex and striatum. Unexpectedly, we observed a decrease (30%) in striatal 125I--conotoxin MII sites, which was due to a decrease in Bmax. This decline was more robust in older (>8 month) compared to younger (2-4 month) mice, suggesting age is important for nicotine-induced disruption of nAChR phenotype. Immunoprecipitation experiments using nAChR subunit-directed antibodies indicate that alterations in subunit-immunoreactivity with nicotine treatment agree with changes observed in the receptor binding studies. To determine the relationship between striatal nAChR sites and function, we measured nicotine-evoked 3H-dopamine release. A decline was obtained with nicotine treatment that was due to a selective decrease in -conotoxin MII-sensitive but not -resistant dopamine release. These results may explain earlier findings that nicotine treatment decreased striatal nAChR-mediated dopamine function, despite an increase in 3H-nicotine (4*) sites. The present data suggest that the 6* nAChR subtype represents a key factor in the control of dopamine release from striatum, which adapts to chronic nicotine treatment by down-regulation of 6* receptor sites and function.
Key words:
Nicotinic cholinergic, Func. analysis receptor/ion channel mutants, Immunocytochemistry, Receptor binding studies
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