Interactions between the dopaminergic and GABAergic neural systems in the lateral anterior hypothalamus of aggressive AAS-treated hamsters.
Adolescent exposure to anabolic-androgenic steroids (AAS) produces alterations to various neurochemical systems resulting in an elevated aggressive response. Both the GABAergic and dopaminergic neural systems are implicated in aggression control and are altered in the presence of AAS. The present studies provide a detailed report of the interaction between D2 receptors and GABAergic neurons in the lateral subdivision of the anterior hypothalamus (LAH), a brain region at the center of aggression control. Male Syrian hamsters were administered AAS throughout adolescence and their brains were processed for double-label immunofluorescence of GAD67 and D2 receptors. Results indicate an increase in the number of D2-ir and GAD67-ir cells in the LAH of AAS-treated animals. Although there were several cells in the LAH colocalized with both GAD67 and D2 receptors, there were no significant increases in the number of double-labeled GAD67/D2-ir neurons. Together, the data suggest the possibility of multiple GABAergic systems in the LAH allowing for differential inhibition of various neural systems. Given these changes in the number of GABAergic cells, it is likely that adolescent AAS exposure also alters the expression of GABAA receptors in brain areas innervated by the LAH. Thus, hamster brains were processed for immunohistochemistry and quantified for changes in GABAA-ir. Interestingly, adolescent exposure to AAS produced a significant decrease in the number of GABAA-ir elements in the LAH of aggressive hamsters. Taken together, results from the current studies provide a putative mechanism whereby dopamine stimulates aggression through removal of GABA inhibition in the LAH of AAS-treated animals.
Schwartzer
Jared J
JJ
Behavioral Neuroscience Program, Department of Psychology, 125 Nightingale Hall, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, United States.
Ricci
Lesley A
LA
Melloni
Richard H
RH
D000374:Aggression / Q000502:physiology*; D045930:Anabolic Agents / Q000494:pharmacology; D000728:Androgens / Q000494:pharmacology; D000818:Animals; D006224:Cricetinae; D004298:Dopamine / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007031:Hypothalamus / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D008647:Mesocricetus; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D011897:Random Allocation; D017448:Receptors, Dopamine D2 / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D045930:Anabolic Agents; D000728:Androgens; D017448:Receptors, Dopamine D2; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; D004298:Dopamine