Sex Differences in Brain Aromatase Activity: Genomic and Non-Genomic Controls

Aromatization of testosterone into estradiol in the preoptic area plays a critical role in the activation of male copulation in quail and in many other vertebrate species. Aromatase expression in quail and in other birds is higher than in rodents and other mammals, which has facilitated the study of the controls and functions of this enzyme. Over relatively long time periods (days to months), brain aromatase activity (AA), and transcription are markedly (four- to sixfold) increased by genomic actions of sex steroids. Initial work indicated that the preoptic AA is higher in males than in females and it was hypothesized that this differential production of estrogen could be a critical factor responsible for the lack of behavioral activation in females. Subsequent studies revealed, however, that this enzymatic sex difference might contribute but is not sufficient to explain the sex difference in behavior. Studies of AA, immunoreactivity, and mRNA concentrations revealed that sex differences observed when measuring enzymatic activity are not necessarily observed when one measures mRNA concentrations. Discrepancies potentially reflect post-translational controls of the enzymatic activity. AA in quail brain homogenates is rapidly inhibited by phosphorylation processes. Similar rapid inhibitions occur in hypothalamic explants maintained in vitro and exposed to agents affecting intracellular calcium concentrations or to glutamate agonists. Rapid changes in AA have also been observed in vivo following sexual interactions or exposure to short-term restraint stress and these rapid changes in estrogen production modulate expression of male sexual behaviors. These data suggest that brain estrogens display most if not all characteristics of neuromodulators if not neurotransmitters. Many questions remain however concerning the mechanisms controlling these rapid changes in estrogen production and their behavioral significance

Chronic noise exposure in the spontaneously hypertensive rat

Introduction: Epidemiological studies have suggested an association between the relative risk for developing cardiovascular disease (CVD) and long-term exposure to elevated levels of transportation noise. The contention is that this association is largely owing to an increase in stress-related biomarkers that are thought to be associated with CVD. Animal models have demonstrated that acute noise exposure is capable of triggering a stress response; however, similar studies using chronic noise models are less common. Materials and Methods: The current study assessed the effects of intermittent daily exposure to broadband 80 kHz bandwidth noise of 87.3 dBA for a period of 21 consecutive days in spontaneously hypertensive rats. Results: Twenty-one days of exposure to noise significantly reduced body weight relative to the sham and unhandled control groups; however, noise had no statistically significant impact on plasma adrenocorticotropic hormone (or adrenal gland weights). Noise was associated with a significant, albeit modest, increase in both corticosterone and aldosterone concentrations following the 21 days of exposure. Interleukin 1 and interleukin 6 levels were unchanged in the noise group, whereas both tumour necrosis factor alpha and C-reactive protein were significantly reduced in noise exposed rats. Tail blood sampling for corticosterone throughout the exposure period showed no appreciable difference between the noise and sham exposed animals, largely due to the sizeable variation for each group as well as the observed fluctuations over time. Discussion: The current pilot study provides only modest support that chronic noise may promote stress-related biological and/or developmental effects. More research is required to verify the current findings and resolve some of the unexpected observations