The active phase-related increase in corticosterone and aggression are linked.

Recently we demonstrated that corticosterone exerts an acute facilitatory effect on aggression in male rats. Corticosterone production reaches a maximum at the onset of the dark period, while male rats are more aggressive in the dark. Here we present evidence demonstrating that the corticosterone increase at the beginning of the dark period is causally linked to the increase in aggressiveness. We measured plasma corticosterone and quantified aggressive behaviour of male territorial rats at various time points of the day-night transition. Low aggression levels were observed in the full light period when plasma concentrations of corticosterone were low. An increase in plasma corticosterone occurred just prior to the dark phase, when aggressive responding was the highest. Aggressive behaviour remained high in the early dark period when corticosterone was still high. We found that blocking the high affinity mineralocorticoid receptor (MR) with spironolactone (5 or 10 mg/kg) during the early dark period dramatically and specifically reduced territorial aggression.

Time- and region-dependent effect of adrenalectomy on neuropeptide gene expression in rat hippocampus and striatum.

Seven days after removal of the adrenals in rats, the messenger RNA levels of preproenkephalin (ENK), preprodynorphin (DYN), cholecystokinin (CCK), and neuropeptide Y (NPY) were measured in hippocampus, striatum, and hypothalamus. Adrenalectomy (ADX) in the morning, when endogenous corticosterone levels were low, resulted 7 days later in a decrease of ENK mRNA and DYN mRNA levels in the hippocampus (41.3 +/- 4.3 and 41.9 +/- 5.7%, respectively) and in the striatum (32.1 +/- 6.6 and 31.2 +/- 12.9%, respectively), but no change was observed in the ENK mRNA content of the hypothalamus. When ADX was performed in the evening the opioid mRNA levels were not changed in these brain areas 7 days after ADX. Pretreatment with a single dose of corticosterone before surgery in the morning produced high corticosterone levels similar to those in the evening and prevented the decrease of ENK mRNA in the hippocampus. The decrease in hippocampal DYN mRNA and in striatal ENK mRNA and DYN mRNA persisted. CCK mRNA and NPY mRNA were not changed in any of the experimental groups in any of the three examined brain areas. This study demonstrates that ADX decreases opioid gene expression in the rat hippocampus and striatum. The effect of ADX on hippocampal ENK mRNA levels that persists for at least 7 days postsurgery is independent of the circulating corticosterone level at the time of surgery.