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Anabolic Steroids Modulate the NPYergic Circuitry of the Hypothalamus in Adolescent Rats: A Molecular and Behavioral Approach
Author(s) -
RamosPratts Keyla Mariel,
SantiagoGascot Maria Elisa,
Parrilla Jeffrey,
BarretoEstrada Jennifer,
RoigLopez Jose Luis
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.639.3
Subject(s) - medicine , endocrinology , neuropeptide y receptor , hypothalamus , anabolism , androgen , androgen receptor , population , receptor , antagonist , messenger rna , neuropeptide , biology , hormone , gene , biochemistry , environmental health , prostate cancer , cancer
The abuse of anabolic steroids has increased at alarming rates among adolescents, however, little is known about their behavioral consequences in this population. Given that neuropeptide Y (NPY) and the androgen receptor (AR) are highly expressed in the hypothalamus, we aimed to assess the effects of 17a‐methyltestosterone (17a‐meT) in the behavioral and molecular aspects of the NPYergic circuit in this brain region. Male pubertal rats were chronically exposed to 17a‐meT. Animals were sacrificed and brain punches were done at the mPOA, VMN, and the extra‐hypothalamic BNST. NPY protein levels and mRNA expression for NPY and its receptors were determined by RIA and Real Time‐PCR, respectively. An increase in NPY was observed in the VMN, a region associated with male sexual motivation, while no changes were observed in the mPOA. Preliminary results showed a 3‐fold increase of NPY mRNA in the mPOA in AAS‐treated rats, and an 8‐fold decrease in the VMN. This effect was accompanied by a decrease in mRNA expression of receptors NPY Y2, Y5, and AR in the VMN. In the BNST, a 3‐fold decrease in NPY mRNA, and an increase in NPY Y1, Y2, and Y5 was observed. At the behavioral level, AAS‐treated rats increased the incentive sexual motivation. Our results suggest an interaction between synthetic androgens and neuropeptide systems to control behavior. NIH‐NCRR (2P20RR016470‐09), NIH‐EARDA (G11HD046326), RCMI (G12RR030551).