Anabolic androgenic steroids (AAS) are synthetic derivates of testosterone. There are approximately 60 different AAS compounds that can be classified in three classes based upon their chemical structure and metabolites. Even short exposure to AAS can produce mood and behavioral symptoms. In previous experiments, we found that class I and II AAS induce hedonic and rewarding effects in adult mice. Recently, NIDA reported that 1.4 – 2.2% of adolescents ever tried steroids. In this study, we aimed to determine if AAS have hedonic properties in adolescent male mice. Animals received alternate androgen injections in a conditioned place preference (CPP) for 10 days. In addition, anxiety behaviors were measured. Androgens tested were testosterone propionate (TP) and 17α‐methyltestosterone (17α‐meT), class I and class III AAS, respectively. Three doses were tested (0.075, 0.75 and 7.5 mg/kg) for each drug. We have found a shift in place preference in animals treated with 17α‐meT in all doses tested, while TP showed no effect. In exploratory‐based anxiety, using light‐dark transitions, we found an increase in this parameter only with 17α‐meT (7.5 mg/kg). Body and gonadal weight were not affected in any of the AAS treatments. Our results suggest that developmental age, hormonal environment and AAS metabolism are important modulators of hedonia and reward.

Anabolic androgenic steroids (AAS) can affect brain regions associated with cognitive processes through steroid sensitive regions in the amygdala and hippocampus. We aim to assess the effect of acute exposure to AAS in adolescent female rats (PN‐40) on emotional memory using the Inhibitory Avoidance Task (IAT). On day 1 (D‐1), animals were placed into the illuminated side of the chamber and the latency to enter to the dark side of the chamber was recorded. On day 2 (D‐2), rats were injected with a high dose of 17α‐methyltestosterone (7.5 mg/kg) during the diestrus phase of the estrus cycle. They received an electric foot shock (0.3mA, 3 sec) in the dark side of the chamber. On day 3 (D‐3), each animal was placed into the illuminated side of the chamber and the latency to enter the dark compartment was recorded. In addition, gene a tendency of AAS to decrease the latency to move to the dark side of the chamber on D‐3. Similarly, AAS elicited a tendency to spend more time in the open arms of the EPM. Ou ralized anxiety was determined using the Elevated Plus Maze (EPM). Our results suggest that acute exposure to AAS in adolescent female rats affects emotional memory decreasing inhibitory avoidance learning and decreasing generalized anxiety.

Anabolic androgenic steroids (AAS) are a class of steroid hormones derived from testosterone, being abused by adolescents, and known to affect anxiety, learning, and memory. The neural system underlying these behaviors includes the amygdala (AMY), a forebrain region that is known to express neuropeptide Y (NPY). NPY is one of the most abundant peptides in the brain and it plays a role in the regulation of energy homeostasis, anxiety and cognitive processes. Therefore, we aimed to assess NPY modulation in the AMY and in cognitive behavioral processes after chronic exposure to AAS in pubertal rats. Female and male pubertal rats were exposed to 17α‐methyltestosterone for two weeks. Food intake and body weight were measured during AAS exposure. For general anxiety and emotional memory, we used the Elevated Plus Maze (EPM) and the Passive Avoidance Task (PAT), respectively. Using RIA, we found a significant decrease in NPY levels in females, while there was no modulation in males. AAS in females showed an increase in body weight at the first and second weeks of AAS exposure, and an increase in food intake in the second week. In males, these differences were observed in the first, but not in the second week. Anxiety was not altered in male or female animals. Females but not males, showed a significant impairment of passive avoidance learning. Taken together, our results suggest that AAS can differentially modulate emotional memory and energy metabolism, maybe through NPY‐related neural circuits. Supported by RCMI (G12RR030551), NCRR‐NIH (P20RR016470).