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alpha 2-Adrenergic receptors in brain are important presynaptic modulators of central noradrenergic function (autoreceptors) and postsynaptic mediators of many of the widespread effects of catecholamines and related drugs. alpha 2-Adrenergic agonists are currently used as antihypertensives and preanesthetic agents, but new subtype-selective alpha 2-adrenoceptor agonists and antagonists have additional therapeutic application potential. Three genes encoding specific alpha 2-adrenoceptor subtypes (alpha 2A, alpha 2B, and alpha 2C) have been isolated and characterized. RNA blotting indicates that all three are expressed in rat brain. This study used in situ hybridization with 35S-labeled RNA probes to map the distribution of alpha 2-adrenoceptor subtype gene expression in rat brain. alpha 2A mRNA was most abundant in the locus coeruleus, but was also widely distributed in the brain stem, cerebral cortex, septum, hypothalamus, hippocampus and amygdala. alpha 2B mRNA was observed only in the thalamus. alpha 2C mRNA was mainly localized to the basal ganglia, olfactory tubercle, hippocampus, and cerebral cortex. These mRNA distributions largely agree with previous findings on the alpha 2-adrenoceptor distributions in the rat brain, but suggest that the localization patterns for each receptor subtype are unique. The expression of alpha 2A mRNA in noradrenergic neurons indicates that this subtype mediates presynaptic autoreceptor functions. Furthermore, the localization of alpha 2A mRNA in noradrenergic projection areas suggests that this receptor may also have an important role in mediating postsynaptic effects. The precise physiological and pharmacological roles of the alpha 2-adrenoceptor subtypes are still largely unknown, but it is expected that in situ hybridization coupled to various methods to identify the transmitter phenotypes of the subtype-expressing neurons will help to clarify these important issues in the near future.

Abstract Site-, context- and dose-dependent actions of intrahypothalamic cortisol administration on the agonistic behaviors of adult male golden hamsters (n = 128 dyads) were examined. When cortisol-treated animals were tested in paired encounters with aggressive cholesterol-treated opponents, chronic (>/= 24 h) cortisol treatment (1 mm implants) induced significant (P < 0.05) submission in three medial hypothalamic areas (anterior hypothalamic area > medial preoptic area > ventromedial hypothalamus), but aggression in the paraventricular nucleus or third ventricle. In contrast, chronic cortisol treatment in the anterior hypothalamic area resulted in high levels of aggression during paired encounters with submissive opponents, and during territorial aggression tests with juvenile male intruders. Acute (>/= 20 min) cortisol treatment in the anterior hypothalamic area (100 nl injections) induced significant submission after 10(-2) M, but significant aggression after 10(-6) M microinjections in paired encounters with aggressive vehicle-injected opponents. These findings suggest glucocorticoid-sensitive mechanisms within the anterior hypothalamus modulate aggressive responding during intrasexual social encounters.

The agonistic behaviors of adult male golden hamsters (N = 108 dyads) were examined 5 min after stereotaxic microinjection of adrenal and gonadal steroids into the anterior hypothalamus. Flank marks, attacks, bites, and retreats were scored over a 15 min test period during which steroid-injected animals were paired in a neutral arena with vehicle-injected conspecifics. Animals microinjected with either 10(-6) M cortisol or 10(-6) M beta-estradiol displayed significantly (p less than 0.05) higher levels of flank marking than other steroid-treated animals. Animals microinjected with 10(-6) M cortisol displayed significantly higher levels of aggression than their opponents. In contrast, the behavior of the vehicle-injected animals paired with 10(-6) M cortisol-treated opponents was characterized by submissive responding. This profile of the 10(-6) M cortisol treatment, i.e., promoting aggression in a steroid-treated animal while eliciting submission from its vehicle-treated opponent, was not observed in pairs in which steroid-injected animals were treated with equimolar concentrations of testosterone, dihydrotestosterone, progesterone, beta-estradiol, or deoxycorticosterone. These findings suggest steroids exert immediate effects on agonistic responding in the anterior hypothalamus of male hamsters. The immediate action(s) of cortisol appear to include facilitating aggression and flank marking, while the immediate action(s) of beta-estradiol appears to be confined to the communicative aspect of agonistic responding in this species.