Aromatase activity in the preoptic area differs between aggressive and nonaggressive male house mice

Abstract

Treatment with testosterone (T) or estradiol (E2) facilitates intraspecific aggressive behavior in adult rodents. Brain aromatization of T to E2 appears to be involved in facilitation of fighting behavior. In the present study we measure the in vitro brain aromatase activity (AA) in the preoptic area (POA), amygdaloid nuclei (Am), ventromedial hypothalamus (VMH), and parietal cortex (CTX) from two strains of adult male house mice, which were genetically selected for territorial aggression, based upon their attack latencies (short attack latency: SAL; long attack latency: LAL). The results reveal a higher AA in the POA of nonaggressive LAL males, as compared to aggressive SAL animals. The POA AA is, thus, inversely correlated with aggressiveness. The AA levels in both the VMH and Am do not differ significantly between strains. Furthermore, a differential brain area-specific AA distribution exists: POA > VMH AA in LAL, whereas POA < VMH in SAL. In both selection lines, the Am exhibits the highest levels of AA, as compared to the other investigated areas. Kinetic studies revealed that the aromatase Km is similar in both strains. The results indicate that the strain difference in AA is specific to the POA, but is not necessarily positively correlated with circulating plasma T levels. Other factors, in addition to androgen, are probably involved in the regulation of POA aromatase. We suggest that a higher neural androgen receptor sensitivity exists in the POA of nonaggressive LAL males, resulting in higher adult POA AA, despite lower concentrations of circulating T.

Low sex steroids, high steroid receptors: Increasing the sensitivity of the nonreproductive brain

“…T can act either directly via binding to androgen receptors (ARs), or indirectly via binding to estrogen receptors (ERs) after aromatization into 17 -estradiol (E2) within the brain. Indeed, numerous studies have shown the importance of T, its estrogenic metabolite E2, and the enzyme aromatase (AROM) for the regulation of sexual and aggressive behaviors during the reproductive season (Hutchison, 1971;Schlinger and Callard, 1990;Monaghan and Glickman, 1992;Compaan et al, 1994;Balthazart et al, 1997;Ball and Balthazart, 2004;Scordalakes and Rissman, 2004). Birds have proven to be excellent systems to study seasonal changes in physiology and behavior both in the field and in the laboratory (Ball and Balthazart, 2004).…”

Functional Connectivity among Limbic Brain Areas: Differential Effects of Incubation Temperature and Gonadal Sex in the Leopard Gecko, <i>Eublepharis macularius</i>

“…3), and this functional connection might also help explain the aggressive tendencies of individuals from this temperature. The POA plays an important role in the expression of aggression in rodents [Albert et al, 1986;Compaan et al, 1994], and lesions of the AH-POA continuum abolish agonistic behaviors in male green anole lizards [Wheeler and Crews, 1978]. In all lizards studied to date, both areas also either express the genes for sex steroid receptors [Young et al, 1994] or concentrate sex steroids [Morrell et al, 1979].…”

Predatory aggression, but not maternal or intermale aggression, is associated with high voluntary wheel-running behavior in mice

“…For example, intermale aggression in most rodents is facilitated by testosterone, or its aromatization to estradiol (Compaan et al, 1994), whereas the expression of maternal aggression is facilitated by estradiol, progesterone, and prolactin released during pregnancy and lactation (Bridges, 1996;Mann et al, 1984;Stern and McDonald, 1989), as well as sensory input (including olfactory and tactile stimuli) to the lactating females from pups (Lonstein and Gammie, 2002;Stern and Kolunie, 1993;Svare et al, 1980). Additionally, certain neuromodulators have different effects on maternal and male aggression.…”