Brain Nerve Growth Factor Unbalance Induced by Anabolic Androgenic Steroids in Rats


Medicine & Science in Sports & Exercise:
doi: 10.1249/MSS.0b013e31826c60ea
Basic Sciences

Purpose: Anabolic androgenic steroids (AAS) are synthetic androgen-like compounds that are abused in sport communities despite their adverse effects. Nerve growth factor (NGF) influences neuronal differentiation and survival, and it also mediates higher brain functions such as learning and memory. Changes in NGF expression have been implicated in neurodegenerative disorders, including Alzheimer disease. Hence, we decided to study the effect of chronic AAS exposure on brain NGF profile, NGF-dependent cholinergic function, and related behavioral performance.

Methods: Male Wistar rats were injected for 4 wk with either nandrolone or stanozolol at daily doses (5.0 mg·kg−1, s.c.) that are considered equivalent to those abused by humans. NGF levels and NGF receptor (TrkA and p75NTR) expression were measured in the hippocampus and in the basal forebrain. Choline acetyltransferase expression was evaluated in basal forebrain. Spatial learning and memory were assessed using the Morris water maze.

Results: AAS treatment caused region-specific changes in the expression of NGF and its receptors. Both nandrolone and stanozolol increased NGF levels in the hippocampus and reduced NGF levels in the basal forebrain, reduced p75NTR expression in the hippocampus, and failed to affect TrkA expression in the basal forebrain. Finally, AAS treatment reduced the expression of choline acetyltransferase in the basal forebrain and impaired the behavioral performance in the Morris water maze.

Conclusion: The evidence that supraphysiological doses of AAS cause neurotrophic unbalance and related behavioral disturbances raises the concern that AAS abuse in humans may affect mechanisms that lie at the core of neuronal plasticity.

Author Information

1Department of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, ITALY; 2Department of Biomedical Sciences, University of Foggia, Foggia, ITALY; 3IRCCS Neuromed, Pozzilli, ITALY; and 4Department of Physiology and Pharmacology, Sapienza University of Rome, Rome, ITALY

Address for correspondence: Sergio Scaccianoce, Department of Physiology and Pharmacology, Sapienza University of Rome, Piazzale Aldo Moro, 500185 Rome, Italy; E-mail:

Submitted for publication May 2012.

Accepted for publication July 2012.

©2013The American College of Sports Medicine