Cocaine selectively increases proliferation in the adult murine hippocampus

Cocaine abuse continues to be a significant problem in the USA and elsewhere. Cocaine is an indirect agonist for dopamine, norepinephrine and serotonin with numerous potential downstream effects, including processes and signals associated with adult neurogenesis. Since drug addiction is associated with brain plasticity, we hypothesized that cocaine exposure would alter cellular proliferation in two adult neurogenic regions (the subventricular and subgranular zones). We used bromodeoxyuridine (BrdU) to track newly generated cells in the brains of adult mice after chronic cocaine or saline exposures. No differences were found in the number or migration patterns of BrdU-labeled cells in the forebrain neurogenic areas. However, cocaine produced a significant increase in the number of hippocampal BrdU-labeled cells.

Research highlights▶ Chronic cocaine exposure did not alter aSVZ BrdU labeling in mice. ▶ Chronic cocaine exposure increased SGZ BrdU labeling in mice in a spatio-temporal manner. ▶ BrdU labeling increases were restricted to the dorsal and not ventral SGZ and were noted after 1 and 3, but not 5 days of cocaine abstinence/post-BrdU labeling.