Cocaine in adolescent rats produces residual memory impairments that are reversible with time

Rats received injections (subcutaneous) of either 10 or 20 mg/kg cocaine on postnatal days 26-33, while lab chow-fed and pair-fed controls received saline. Spatial memory in a Morris water maze was assessed on four different occasions commencing 10 days postcocaine and ending approximately 12 months later. To determine whether there existed long-term changes in cholinergic processes, maze performance was evaluated following 1 mg/kg scopolamine challenge 4 months postcocaine. Subjects survived under standard laboratory housing conditions until they died. Results from the first assessment indicated a working memory deficit in the low-dose cocaine group and a long-term memory impairment in the high-dose cocaine group. These decrements neither were permanent nor were exacerbated by age-related processes in that cocaine-treated subjects performed at control levels on subsequent assessments. An exception to this was the results derived from the third assessment indicating that animals previously treated with 20 mg/kg cocaine were impaired when challenged with scopolamine. Examination of mortality rates revealed that cocaine-treated rats died significantly sooner than lab chow-fed control subjects. Taken together, these data indicate that cocaine during adolescence causes residual, but not permanent, deleterious effects on memory that may be mediated by alterations in cholinergic neurochemistry. More provocatively, the results showed that cocaine during adolescence shortened the lifespan of rats. This latter finding suggests that cocaine during adolescence may produce residual physiological effects that last well into adulthood.