(+)-methamphetamine corticosterone in plasma increases and BDNF in brain more than forced swim or isolation in neonatal rats

(+)-Methamphetamine (MA) administered on postnatal days (P) 11-15 (four times/day) results in increased corticosterone that overlaps the stress hyporesponsive period (SHRP; P2-14) and leads to later learning and memory deficits. Elevated corticosterone during the SHRP results in neurotrophin changes and long-term effects on learning. We determined whether two known stressors could mimic the effects of MA [10 (mg/kg)/dose] administration in neonatal rats. Stressors were four 15-min sessions of forced swim or isolation (confinement in forced swim tubes without water). Saline and weighed-only controls were included and all five treatments were represented within each litter. Corticosterone in plasma and brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in neostriatum and hippocampus were examined after one or four treatments on P11 or P15 (0.5, 1.75, 6.5, or 24 h after first dose). MA increased corticosterone and BDNF; forced swim and isolation also increased corticosterone, but to a lesser extent than M, and neither stressor increased BDNF. NGF was unaffected by saline treatment, but there was a minor reduction in NGF in the forced swim group compared with the weighed-only group. The data show that M is more potent at releasing corticosterone and increasing BDNF than short-term, repeated episodes of forced swim or isolation. The possible relationship between these changes and the long-term cognitive effects of developmental M administration are discussed.