Effects of neonatal methamphetamine treatment on adult stress-induced corticosterone release in rats

In rats, neonatal (+)-methamphetamine (MA) exposure and maternal separation stress increase corticosterone during treatment and result in learning and memory impairments later in life. Early-life stress also changes later responses to acute stress. We tested the hypothesis that neonatal MA exposure would alter adult corticosterone after acute stress or MA challenge. Rats were treated with MA (10 mg/kg × 4/day), saline, or handling on postnatal (P) days 11–15 or 11–20 (days that lead to learning and memory impairments at this dose). As adults, corticosterone was measured before and after 15 min forced swim (FS) or 15 min forced confinement (FC), counterbalanced, and after an acute MA challenge (10 mg/kg) given last. FS increased corticosterone more than FC; order and stress type interacted but did not interact with treatment; treatment interacted with FS but not with FC. In the P11-15 regimen, MA-treated rats showed more rapid increases in corticosterone after FS than controls. In the P11-20 regimen, MA-treated rats showed a trend toward more rapid decrease in corticosterone after FS. No differences were found after MA challenge. The data do not support the hypothesis that neonatal MA causes changes in adult stress responsiveness to FS, FC, or an acute MA challenge.

► Developmental methamphetamine or stress cause learning and memory deficits.
► Rats given methamphetamine on P11-15 or P11-20 were given forced swim, forced confinement, or methamphetamine as adults.
► Forced swim increased corticosterone more than forced confinement; acute methamphetamine was intermediate.
► Minor interactions were found between neonatal methamphetamine and force swim-induced corticosterone increases.
► The hypothesis that early methamphetamine alters adult corticosterone release in response to acute stress was not confirmed.