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

Ricci, Lesley A.; Grimes, Jill M.; Melloni, Richard H.

doi:10.1016/j.bbr.2006.10.025

Cited by 33 publications

(29 citation statements)

References 79 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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.…”

Section: Discussionsupporting

confidence: 93%

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

Sanford

Lange

Maney

2009

Developmental Neurobiology

View full text Add to dashboard Cite

Sex steroids facilitate dramatic changes in behavioral responses to sociosexual signals and are increasingly implicated in the sensory processing of those signals. Our previous work demonstrated that in female white-throated sparrows, which are seasonal breeders, genomic responses in the auditory forebrain are selective for conspecific song over frequency-matched tones only when plasma estradiol (E2) reaches breeding levels. Here, we sought to map this E2-dependent selectivity in the best-studied area of the auditory forebrain, the caudomedial nidopallium (NCM). Nonbreeding females with low endogenous levels of E2 were treated with E2 or a placebo and exposed to conspecific song, tones, or no sound playback. Immunoreactive protein product of the immediate early gene zenk (egr-1) was then quantified within seven distinct subregions, or domains, of NCM. We report three main findings: (1) regardless of hormone treatment, the zenk response is significantly higher in dorsal than in ventral NCM, and higher in medial than in lateral NCM; (2) E2-dependent selectivity of the response is limited to the rostral and medial domains of NCM; in the more caudal domains, song induces more zenk expression than tones regardless of hormone treatment; (3) even when no sound stimuli were presented, E2 treatment significantly increased zenk expression in the rostral, but not the caudal, domains of NCM. Together, the latter two findings suggest that E2-dependent plasticity in NCM is concentrated in rostral NCM, which is hodologically and neurochemically distinct from caudal NCM. Activity in rostral NCM may therefore be seasonally regulated in this species.

show abstract

Section: Discussionsupporting

confidence: 93%

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

Sanford

Lange

Maney

2009

Developmental Neurobiology

View full text Add to dashboard Cite

show abstract

“…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].…”

Section: Neuronal Circuits/neuronal Activationcontrasting

confidence: 55%

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

Veenema¹,

Neumann²

2007

Brain Behav Evol

131

View full text Add to dashboard Cite

Aggression causes major health and social problems and constitutes a central problem in several psychiatric disorders. There is a close relationship between the display of aggression and stress coping strategies. In order to gain more insight into biochemical pathways associated with aggression and stress coping, we assessed behavioral and neurobiological responses in two genetically selected rodent models, namely wild house mice selectively bred for a short (SAL) and long (LAL) attack latency and Wistar rats bred for high (HAB) or low (LAB) anxiety-related behavior. Compared to their line counterparts, the SAL mice and the LAB rats display a high level of intermale aggression associated with a proactive coping style. Both the SAL mice and the LAB rats show a reduced hypothalamic-pituitary-adrenal (HPA) axis response to non-social stressors. However, when exposed to social stressors (resident-intruder, sensory contact), SAL mice show an attenuated HPA response, whereas LAB rats show an elevated HPA response. In both rodent lines, the display of aggression is associated with high neuronal activation in the central amygdala, but reduced neuronal activation in the lateral septum. Furthermore, in the lateral septum, SAL mice have a reduced vasopressinergic fiber network, and LAB rats show a decreased vasopressin release during the display of aggression. Moreover, the two lines show several indications of an increased serotonergic neurotransmission. The relevance of these findings in relation to high aggression and stress coping is discussed. In conclusion, exploring neurobiological systems in animals sharing relevant behavioral characteristics might be a useful approach to identify general mechanisms of action, which in turn can improve our understanding of specific behavioral symptoms in human psychiatric disorders.

show abstract

“…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.…”

Section: Discussionmentioning

confidence: 92%

“…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.…”

mentioning

confidence: 89%

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

Carrillo¹,

Ricci²,

Melloni³

2011

Behavioral Neuroscience

View full text Add to dashboard Cite

Adolescent exposure to anabolic androgenic steroids (AAS) alters the development and activity of the glutamate neural system in the latero-anterior hypothalamus (LAH) in hamsters (Mesocricetus auratus); that is, an important neural component of the adolescent AAS-induced aggressive response. In this article, we used retrograde tracing to investigate glutamate-specific alterations in the connections between the LAH and several other nuclei implicated in adolescent AAS-induced aggression. Briefly, hamsters were treated with AAS or sesame-oil control during adolescence and then microinjected with retrograde tracer into the medial amygdala (MeA), lateral septum (LS), or bed nucleus of the stria terminalis (BNST). Brains were then processed for vesicular glutamate transporter 2 (VGLUT2) and examined for AAS-induced changes in the number VGLUT2 cells containing retrograde tracer (VGLUT2/tracer) within the LAH. It is interesting to note that while aggressive AAS-treated hamsters injected retrograde tracer into the MeA showed a significant reduction in the number of VGLUT2/tracer cells in the LAH, aggressive AAS-treated hamsters injected tracer into the BNST showed a significant increase in the number of VGLUT2/tracer cells in the LAH when compared with controls. Last, AAS hamsters injected with tracer into the LS had a comparable number of LAH-VGLUT2/tracer cells to controls. The current results indicate that glutamate likely functions as the major aggression output system from the LAH and that adolescent AAS treatment significantly alters the neural circuitry modulating aggression. Moreover, increases in the number of glutamate projections from the LAH to the BNST in AAS hamsters identify the BNST as an area particularly important for the regulation of AAS-induced aggression.

show abstract

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

Cited by 33 publications

References 79 publications

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

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

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

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

Contact Info

Product

Resources

About