title: Anabolic steroids alter the physiological activity of aggression circuits in the lateral anterior hypothalamus.
abstract: Syrian hamsters exposed to anabolic/androgenic steroids (AAS) during adolescence consistently show increased aggressive behavior across studies. Although the behavioral and anatomical profiles of AAS-induced alterations have been well characterized, there is a lack of data describing physiological changes that accompany these alterations. For instance, behavioral pharmacology and neuroanatomical studies show that AAS-induced changes in the vasopressin (AVP) neural system within the latero-anterior hypothalamus (LAH) interact with the serotonin (5HT) and dopamine (DA) systems to modulate aggression. To characterize the electrophysiological profile of the AAS aggression circuit, we recorded LAH neurons in adolescent male hamsters in vivo and microiontophoretically applied agonists and antagonists of aggressive behavior. The interspike interval (ISI) of neurons from AAS-treated animals correlated positively with aggressive behaviors, and adolescent AAS exposure altered parameters of activity in regular firing neurons while also changing the proportion of neuron types (i.e., bursting, regular, irregular). AAS-treated animals had more responsive neurons that were excited by AVP application, while cells from control animals showed the opposite effect and were predominantly inhibited by AVP. Both DA D2 antagonists and 5HT increased the firing frequency of AVP-responsive cells from AAS animals and dual application of AVP and D2 antagonists doubled the excitatory effect of AVP or D2 antagonist administration alone. These data suggest that multiple DA circuits in the LAH modulate AAS-induced aggressive responding. More broadly, these data show that multiple neurochemical interactions at the neurophysiological level are altered by adolescent AAS exposure.
authors.affiliation: Behavioral Neuroscience Program, Department of Psychology, Northeastern University, Boston, MA 02115, United States.
authors.forename: T R
authors.initials: TR
authors.lastname: Morrison
authors.affiliation: Department of Physical Therapy, Rehabilitation, and Movement Sciences, Northeastern University, Boston, MA 02115, United States.
authors.forename: R W
authors.initials: RW
authors.lastname: Sikes
authors.affiliation: Behavioral Neuroscience Program, Department of Psychology, Northeastern University, Boston, MA 02115, United States. Electronic address: r.melloni@neu.edu.
authors.forename: R H
authors.initials: RH
authors.lastname: Melloni
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000374:Aggression / Q000187:drug effects* / Q000502:physiology; D045930:Anabolic Agents / Q000633:toxicity*; D000818:Animals; D065127:Dopamine D2 Receptor Antagonists / Q000494:pharmacology; D007026:Hypothalamic Area, Lateral / Q000187:drug effects* / Q000503:physiopathology; D007032:Hypothalamus, Anterior / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D008647:Mesocricetus; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000378:metabolism; D012457:Salicylamides / Q000494:pharmacology; D012701:Serotonin / Q000008:administration & dosage / Q000378:metabolism; D013256:Steroids / Q000633:toxicity*; D014667:Vasopressins / Q000008:administration & dosage / Q000378:metabolism
chemical_list: D045930:Anabolic Agents; D065127:Dopamine D2 Receptor Antagonists; D017448:Receptors, Dopamine D2; D012457:Salicylamides; D013256:Steroids; D014667:Vasopressins; D012701:Serotonin; C045989:eticlopride
keywords: aggression; development; dopamine; hypothalamus; serotonin; vasopressin