Abstract
Early life stress influences adult psychopathology and is associated with an increase in the propensity for drug use/seeking throughout the lifespan. Animal models corroborate that stress exposure exacerbates maladaptive reactivity to stressful stimuli while also shifting the rewarding properties of many drugs of abuse, including nicotine (NIC), a stimulant commonly misused by adolescents. Interestingly, NIC treatment can also normalize some stress-induced behavioral deficits in adult rodents; however, little is known about NIC's therapeutic efficacy following stress experienced during adolescence. The goal of the following experiments was to elucidate NIC's ability to buffer the negative consequences of stress exposure, and to further assess behavioral responsivity while on the drug. Given that stress often occurs in both physical and non-physical forms, we employed the vicarious social defeat stress (VSDS) model which allows for investigation of both physical (PS) and emotional stress (ES) exposure. After 10days, exposure to PS and ES decreased interaction with a social target in the social interaction test (SIT), confirming social avoidance. Groups were further divided and given NIC (0.0 or 160mg/L) in their drinking water. After 1month of NIC consumption, the mice were exposed to the SIT, elevated plus maze (EPM), and the forced swim test (FST), respectively. NIC-treated mice showed a reversal of stress-induced deficits in the EPM and FST. Surprisingly, the mice did not show improvement in the SIT regardless of treatment condition. Together, these data confirm NIC's ability to normalize some stress-induced behavioral deficits; however, NIC's effects on social behavior need further investigation.
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