title: Developmental and withdrawal effects of adolescent AAS exposure on the glutamatergic system in hamsters.
abstract: In the Syrian hamster (Mesocricetus auratus) glutamate activity has been implicated in the modulation of adolescent anabolic-androgenic steroid (AAS)-induced aggression. The current study investigated the time course of adolescent AAS-induced neurodevelopmental and withdrawal effects on the glutamatergic system and examined whether these changes paralleled those of adolescent AAS-induced aggression. Glutamate activity in brain areas comprising the aggression circuit in hamsters and aggression levels were examined following 1, 2, 3, and 4 weeks of AAS treatment or 1, 2, 3, and 4 weeks following the cessation of AAS exposure. In these studies glutamate activity was examined using vesicular glutamate transporter 2 (VGLUT2). The onset of aggression was observed following 2 weeks exposure to AAS and continued to increase showing maximal aggression levels after 4 weeks of AAS treatment. This aggressive phenotype was detected after 2 weeks of withdrawal from AAS. The time-course of AAS-induced changes in latero-anterior hypothalamus (LAH)-VGLUT2 closely paralleled increases in aggression. Increases in LAH-VGLUT2 were first detected in animals exposed to AAS for 2 weeks and were maintained up to 3 weeks following the cessation of AAS treatment. AAS treatment also produced developmental and long-term alterations in VGLUT2 expression within other aggression areas. However, AAS-induced changes in glutamate activity within these regions did not coincide with changes in aggression. Together, these data indicate that adolescent AAS treatment leads to alterations in the glutamatergic system in brain areas implicated in aggression control, yet only alterations in LAH-glutamate parallel the time course of AAS-induced changes in the aggressive phenotype.
authors.affiliation: Behavioral Neuroscience Program, Department of Psychology, Northeastern University, Boston, MA 02155, USA.
authors.forename: Maria
authors.initials: M
authors.lastname: Carrillo
authors.forename: Lesley A
authors.initials: LA
authors.lastname: Ricci
authors.forename: Richard H
authors.initials: RH
authors.lastname: Melloni
mesh_terms: D000293:Adolescent; D000374:Aggression / Q000187:drug effects / Q000502:physiology*; D045930:Anabolic Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D000728:Androgens / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism / Q000502:physiology; D006224:Cricetinae; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D018698:Glutamic Acid / Q000502:physiology*; D006801:Humans; D007031:Hypothalamus / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism / Q000502:physiology; D008297:Male; D009277:Nandrolone / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives / Q000494:pharmacology; D000077603:Nandrolone Decanoate; D009474:Neurons / Q000378:metabolism / Q000502:physiology; D013375:Substance Withdrawal Syndrome / Q000378:metabolism* / Q000523:psychology; D013739:Testosterone / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors; D050599:Vesicular Glutamate Transport Protein 2 / Q000378:metabolism
chemical_list: D045930:Anabolic Agents; D000728:Androgens; D050599:Vesicular Glutamate Transport Protein 2; D018698:Glutamic Acid; D013739:Testosterone; D009277:Nandrolone; D000077603:Nandrolone Decanoate; C016131:testosterone 17 beta-cypionate; C001371:boldenone undecylenate