Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

Abstract

Repeated exposure to anabolic/androgenic steroids (AAS) during adolescence stimulates high levels of offensive aggression in Syrian hamsters. The current study investigated whether adolescent AAS exposure activated neurons in areas of hamster forebrain implicated in aggressive behavior by examining the expression of FOS, i.e., the protein product of the immediate early gene c-fos shown to be a reliably sensitive marker of neuronal activation. Adolescent AAS-treated hamsters and sesame oil-treated littermates were scored for offensive aggression and then sacrificed 1 day later and examined for the number of FOS immunoreactive (FOS-ir) cells in regions of the hamster forebrain important for aggression control. When compared with non-aggressive, oil-treated controls, aggressive AAS-treated hamsters showed persistent increases in the number of FOS-ir cells in select aggression regions, namely the anterior hypothalamus and lateral septum. However, no differences in FOS-ir cells were found in other areas implicated in aggression such as the ventrolateral hypothalamus, bed nucleus of the stria terminals, central and/or medial amygdala or in nonaggression areas such as the samatosensory cortex and the suprachiasmatic nucleus. These results suggest that adolescent AAS exposure may constitutively activate neurons in select forebrain areas critical for the regulation of aggression in hamsters. A model for how persistent activation of neurons in one of these brain regions (i.e., the anterior hypothalamus) may facilitate the development of the aggressive phenotype in adolescent-AAS exposed animals is presented.

Topography of estradiol‐modulated genomic responses in the songbird auditory forebrain

“…E2 did not increase the number of vocalizations, so the increase in ZENK-IR cannot be attributed to the birds' own vocal behavior (see also Maney et al, 2003Maney et al, , 2006. This result is consistent with other reports of steroidinduced IEG expression (Insel, 1990;Hyder et al, 1994;Johansson-Steensland et al 2002;Dimeo and Wood, 2006;Ricci et al, 2007;Tremere et al, 2009). Like Tremere et al (2009), who administered E2 locally in NCM in zebra finches, we found that E2 was as effective as song stimulation at inducing ZENK-IR and that song presentation did not enhance it further.…”

Neurobiological Mechanisms of Aggression and Stress Coping: A Comparative Study in Mouse and Rat Selection Lines

“…This is in contrast with other studies showing a positive relationship between the display of aggression and lateral septum activation [Halasz et al, 2002a;Ricci et al, 2007]. Moreover, a pharmacologically induced decrease in aggression was associated with a decrease in neuronal activation of the lateral septum [Trainor et al, 2006].…”

Glutamate and the aggression neural circuit in adolescent anabolic steroid-treated Syrian hamsters (Mesocricetus auratus).

“…In a number of previous reports, we have shown that in the Syrian hamster administration of AAS throughout the developmental period of adolescence produces hamsters with escalated levels of offensive aggressive behavior (Carrillo et al, 2(X)9; Grimes & Melloni, 2002;Melloni et al, 1997;Ricci et al, 2007). One putative mechanism through which adolescent AAS exposure facilitates the development of aggression is through alterations in the neural circuitry modulating this behavior.…”

“…It is interesting to note that an investigation of the onset of the neurodevelopmental effects of AAS on LAH-glutamate revealed that AAS-mediated increases in the number of glutamate fibers occur following 2 weeks exposure to AAS (Carrillo et al, 2011a). Not surprisingly is that this is the .same time point when heightened levels of aggressive behavior are first observed in adolescent AAS-treated hamsters (Grimes, Ricci, & Melloni, 2007;Melloni, Connor, Hang, Harrison, & Ferris, 1997). Together these data support the notion that adolescent AAS exposure underiies neurodevelopmental changes in LAH-glutamate, and that these changes may play a role in the emergence of the elevated aggressive phenotype.…”