There is a major problem in biological research, especially in neuroscience and psychology, with a lack of representation of both sexes in experiments. Countless tests are published using data solely from male model organisms, meaning that whatever conclusions are drawn from the results about the disease or phenotype or genes at hand may only be applicable to male brains, yet these conclusions are made to be all-encompassing, regardless of sex. However, as seen in both papers this week, this is not the case as even simple modulations to the brain such as exposure to cocaine can have drastically different results for male and female rats. Namely, Holly et al.’s findings – which I personally found more compelling in their simplicity – demonstrated that female rats have longer “binge” periods when given the option of self-administration of cocaine and have greater extracellular density of dopamine in the nucleus accumbens, especially when stressed. This experiment offers multiple lanes of further research, including differential stress behaviors between males and females when exposed to other pharmacological manipulations (perhaps ketamine to investigate schizophrenic phenotypes), the possibly protecting effects of testosterone or other hormones more expressed in males (and vice versa for estradiol), or perhaps manipulation of the levels of the opposite hormone in the opposite sex and testing said modulations. These modulations can also be used to study the effects of cocaine on BDNF expression as found in the Vassoler et al paper. As they found a greater expression of BDNF in cocaine-exposed male rats, perhaps the parallels between BDNF, testosterone, estradiol, and dopamine expression in response to cocaine exposure may be a valid course of action for study, specifically if one has protecting or enhancing effects on another, and if cessation of expression of one induces differential behavioral and phenotypic results.