Interactions between the dopaminergic and GABAergic neural systems in the lateral anterior hypothalamus of aggressive AAS-treated hamsters

@article{Schwartzer2009InteractionsBT,
  title={Interactions between the dopaminergic and GABAergic neural systems in the lateral anterior hypothalamus of aggressive AAS-treated hamsters},
  author={Jared J. Schwartzer and Lesley Ricci and Richard Melloni},
  journal={Behavioural Brain Research},
  year={2009},
  volume={203},
  pages={15-22}
}
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30 Citations
Highly Influential Citations
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Background Citations
16
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30 Citations

Dopamine activity in the lateral anterior hypothalamus modulates AAS-induced aggression through D2 but not D5 receptors.
TLDR
Results indicate that D5 receptors in the LAH modulate non-GABAergic pathways that indirectly influence aggression control, while D2 receptors have a direct influence on AAS-induced aggression.
Anabolic steroids alter the physiological activity of aggression circuits in the lateral anterior hypothalamus
Dopamine D2 receptors act upstream of AVP in the latero-anterior hypothalamus to modulate adolescent anabolic/androgenic steroid-induced aggression in Syrian hamsters.
TLDR
Behavioral data indicate that interactions between AVP and DA neural systems within the LAH modulate the control of aggression following adolescent exposure to AAS and that DA D2 receptor signaling functions upstream of AVP in theLAH to control this behavioral response.
Anterior hypothalamic dopamine D2 receptors modulate adolescent anabolic/androgenic steroid-induced offensive aggression in the Syrian hamster
TLDR
The findings identify a neuroanatomical locus where D2 receptor antagonism suppresses adolescent AAS-induced aggression in the absence of alterations to general mobility, and identify a brain region implicated in the control of aggression.
&ggr;-Aminobutyric acid neural signaling in the lateroanterior hypothalamus modulates aggressive behavior in adolescent anabolic/androgenic steroid-treated hamsters
TLDR
These data identify a neuroanatomical locus where GABAA receptor activation functions to enhance aggression in adolescent AAS-treated animals, while also promoting the display of mature forms of aggression and suppressing juvenile play behaviors.
Adolescent exposure to anabolic/androgenic steroids and the neurobiology of offensive aggression: A hypothalamic neural model based on findings in pubertal Syrian hamsters
The Role of Anabolic Androgenic Steroids in Disruption of the Physiological Function in Discrete Areas of the Central Nervous System
TLDR
The molecular mechanisms underlying the behavioral alterations following AAS abuse is unclear and remains ambiguous as additional long-term studies aimed to understand the precise mechanisms are required.
Valproate selectively suppresses adolescent anabolic/androgenic steroid-induced aggressive behavior: implications for a role of hypothalamic γ-aminobutyric acid neural signaling
TLDR
Preclinical evidence is provided that the anticonvulsant valproate selectively suppresses adolescent, AAS-induced aggression and that this suppression is modulated, in part, by GABA neural signaling within the LAH.
Cortical control of aggression: GABA signalling in the anterior cingulate cortex
Effect of muscimol and picrotoxin injection in am and ac nucleus of amygdala on aggressive behavior
TLDR
It can be deduced that GABA system in the ac nucleus of amygdale is more potent than the am nucleus; and both ac and am nuclei of amygdala modulate aggressive behavior mediated by GABAA receptors.
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References

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Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters
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TLDR
Increased density of Fos-immunoreactivity was found in experimental animals within the medial amygdaloid nucleus, ventrolateral hypothalamus, bed nucleus of the stria terminalis and dorsolateral part of the midbrain central gray, suggesting that these areas are integrated in a neural network centered on the anterior hypothalamus and involved in the consummation of offensive aggression.
Adolescent anabolic androgenic steroids reorganize the glutamatergic neural circuitry in the hypothalamus
Alterations in anterior hypothalamic vasopressin, but not serotonin, correlate with the temporal onset of aggressive behavior during adolescent anabolic-androgenic steroid exposure in hamsters (Mesocricetus auratus).
TLDR
It is indicated that relatively short-term adolescent AAS exposure alters aggression and AH 5-HT and AVP development, yet only alterations in AH AVPDevelopment correlate with temporal onset of the aggressive behavioral phenotype during adolescent Aas exposure.
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TLDR
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Chronic anabolic-androgenic steroid treatment during adolescence increases anterior hypothalamic vasopressin and aggression in intact hamsters
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TLDR
It is indicated that adolescent AAS exposure has short-term, reversible effects on both aggression and AH-AVP, correlating AH- aVP with the aggressive/nonaggressive behavioral phenotype during AAS withdrawal.
Serotonin-1B receptor activity and expression modulate the aggression-stimulating effects of adolescent anabolic steroid exposure in hamsters.
TLDR
Data support a role for site-specific alterations in 5HT1B signaling and expression in adolescent AAS-induced aggression and show significant decreases in the area covered by 5 HT1B-containing neuronal puncta and increases in the number of 5HT2B- containing neuronal somata in select brain regions implicated in aggression control.
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