Abstract:
RATIONALE:Nicotine improves cognitive function in a number of animal models including rats, mice, monkeys, and recently, zebrafish. The zebrafish model allows higher throughput and ease in discovering mechanisms of cognitive improvement. MATERIALS AND METHODS:To further characterize the neural bases of nicotine effects on learning in zebrafish, we determined changes in dopaminergic systems that accompany nicotine-enhanced learning. RESULTS:Nicotine improved learning and increased brain levels of dihydroxyphenylacetic acid (DOPAC), the primary dopamine metabolite. There was a significant correlation between choice accuracy and DOPAC levels. The nicotinic antagonist mecamylamine blocked the nicotine-induced increase in DOPAC concentrations, in line with our previous finding that mecamylamine reversed nicotine-induced learning improvement. CONCLUSIONS:Dopamine systems are related to learning in zebrafish; nicotine exposure increases both learning rates and DOPAC levels; and nicotinic antagonist administration blocks nicotine-induced rises in DOPAC concentrations. Rapid cognitive assessment of drugs with zebrafish could serve as a useful screening tool for the development of new therapeutics for cognitive dysfunction.
journal_name
Psychopharmacology (Berl)journal_title
Psychopharmacologyauthors
Eddins D,Petro A,Williams P,Cerutti DT,Levin EDdoi
10.1007/s00213-008-1287-4subject
Has Abstractpub_date
2009-01-01 00:00:00pages
103-9issue
1-3eissn
0033-3158issn
1432-2072journal_volume
202pub_type
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