ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Chronic exposure to anabolic androgenic steroids alters neuronal function in the mammalian forebrain via androgen receptor- and estrogen receptor-mediated mechanisms.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Nandrolone Abuse Prior to Head Trauma Mitigates Endoplasmic Reticulum Stress, Mitochondrial Bioenergetic Deficits, and Markers of Neurodegeneration.Molecular neurobiology · 2025Article
- Anabolic-androgenic steroid use is associated with psychopathy, risk-taking, anger, and physical problems.Scientific reports · 2022Article
- No association between psychiatric symptoms and doses of anabolic steroids in a cohort of male and female bodybuilders.Drug testing and analysis · 2022Article
- Occurrence, ecological risk assessment and source apportionment of pharmaceuticals, steroid hormones and xenoestrogens in the Ghanaian aquatic environments.Toxicology reports · 2022Article
- Anabolic-androgenic steroid abuse and cognitive impairment: Testosterone IMPAIRS biconditional task performance in male rats.Behavioural brain research · 2020Article
- Differential protein expression profile in the hypothalamic GT1-7 cell line after exposure to anabolic androgenic steroids.PloS one · 2017Article
- Anabolic steroids alter the physiological activity of aggression circuits in the lateral anterior hypothalamus.Neuroscience · 2016Article
- Article
- The impact of nandrolone decanoate on the central nervous system.Current neuropharmacology · 2015Review
- Neurotoxicity by synthetic androgen steroids: oxidative stress, apoptosis, and neuropathology: A review.Current neuropharmacology · 2015Review
- Sex and exercise interact to alter the expression of anabolic androgenic steroid-induced anxiety-like behaviors in the mouse.Hormones and behavior · 2014Article
- New knockout model confirms a role for androgen receptors in regulating anxiety-like behaviors and HPA response in mice.Hormones and behavior · 2014Article
- The impact of tonic GABAA receptor-mediated inhibition on neuronal excitability varies across brain region and cell type.Frontiers in neural circuits · 2014Review
- Sex-specific effect of the anabolic steroid, 17α-methyltestosterone, on inhibitory avoidance learning in periadolescent rats.Behavioural processes · 2013Article
- The Sturm und Drang of anabolic steroid use: angst, anxiety, and aggression.Trends in neurosciences · 2012Review
- Corticotropin-releasing factor modulation of forebrain GABAergic transmission has a pivotal role in the expression of anabolic steroid-induced anxiety in the female mouse.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Anabolic androgenic steroid abuse: multiple mechanisms of regulation of GABAergic synapses in neuroendocrine control regions of the rodent forebrain.Journal of neuroendocrinology · 2012Review
- The Buzz about anabolic androgenic steroids: electrophysiological effects in excitable tissues.Neuroendocrinology · 2012Review
- Chronic exposure to anabolic androgenic steroids alters activity and synaptic function in neuroendocrine control regions of the female mouse.Neuropharmacology · 2011Article
- Chronic anabolic androgenic steroid exposure alters corticotropin releasing factor expression and anxiety-like behaviors in the female mouse.Psychoneuroendocrinology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Anabolic androgenic steroids (AAS) can promote detrimental effects on social behaviors for which GABA type A (GABA(A)) receptor-mediated circuits in the forebrain play a critical role. While all AAS bind to androgen receptors (AR), they may also be aromatized to estrogens and thus potentially impart effects via estrogen receptors (ER). Chronic exposure of wild-type male mice to a combination of chemically distinct AAS increased action potential (AP) frequency, selective GABA(A) receptor subunit mRNAs, and GABAergic synaptic current decay in the medial preoptic area (mPOA). Experiments performed with pharmacological agents and in AR-deficient Tfm mutant mice suggest that the AAS-dependent enhancement of GABAergic transmission in wild-type mice is AR-mediated. In AR-deficient mice, the AAS elicited dramatically different effects, decreasing AP frequency, spontaneous IPSC amplitude and frequency and the expression of selective GABA(A) receptor subunit mRNAs. Surprisingly, in the absence of AR signaling, the data indicate that the AAS do not act as ER agonists, but rather suggest a novel in vivo action in which the AAS inhibit aromatase and impair endogenous ER signaling. These results show that the AAS have the capacity to alter neuronal function in the forebrain via multiple steroid signaling mechanisms and suggest that effects of these steroids in the brain will depend not only on the balance of AR- versus ER-mediated regulation for different target genes, but also on the ability of these drugs to alter steroid metabolism and thus the endogenous steroid milieu.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.