ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012
Corticotropin-releasing factor modulation of forebrain GABAergic transmission has a pivotal role in the expression of anabolic steroid-induced anxiety in the female mouse.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Anabolic-androgenic steroid use and psychopathology in athletes. A systematic review.Current neuropharmacology · 2015Pooled it
- Hyperexcitation of ovBNST CRF neurons during stress contributes to female-biased expression of anxiety-like avoidance behaviors.Science advances · 2024Article
- The Behavioral and Neurochemical Changes Induced by Boldenone and/or Tramadol in Adult Male Rats.Neurochemical research · 2023Article
- Anabolic androgenic steroid abuse in the United Kingdom: An update.British journal of pharmacology · 2020Review
- The Role of Anabolic Androgenic Steroids in Disruption of the Physiological Function in Discrete Areas of the Central Nervous System.Molecular neurobiology · 2018Review
- Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis.Neuropharmacology · 2016Article
- Anabolic steroids alter the physiological activity of aggression circuits in the lateral anterior hypothalamus.Neuroscience · 2016Article
- Mad men, women and steroid cocktails: a review of the impact of sex and other factors on anabolic androgenic steroids effects on affective behaviors.Psychopharmacology · 2016Review
- Maternal testosterone exposure increases anxiety-like behavior and impacts the limbic system in the offspring.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Effects of anabolic-androgens on brain reward function.Frontiers in neuroscience · 2015Review
- The impact of nandrolone decanoate on the central nervous system.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
- Contrasting distribution of physiological cell types in different regions of the bed nucleus of the stria terminalis.Journal of neurophysiology · 2013Article
- The role of PKC signaling in CRF-induced modulation of startle.Psychopharmacology · 2013Article
- Sex-specific effect of the anabolic steroid, 17α-methyltestosterone, on inhibitory avoidance learning in periadolescent rats.Behavioural processes · 2013Article
- Androgenic anabolic steroid exposure during adolescence: ramifications for brain development and behavior.Hormones and behavior · 2013Review
- Estrous cycle variations in GABA(A) receptor phosphorylation enable rapid modulation by anabolic androgenic steroids in the medial preoptic area.Neuroscience · 2012Article
- The Sturm und Drang of anabolic steroid use: angst, anxiety, and aggression.Trends in neurosciences · 2012Review
- The Buzz about anabolic androgenic steroids: electrophysiological effects in excitable tissues.Neuroendocrinology · 2012Review
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2 authors at 1 institution in 1 country.
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Abstract
Increased anxiety is commonly observed in individuals who illicitly administer anabolic androgenic steroids (AAS). Behavioral effects of steroid abuse have become an increasing concern in adults and adolescents of both sexes. The dorsolateral bed nucleus of the stria terminalis (dlBnST) has a critical role in the expression of diffuse anxiety and is a key site of action for the anxiogenic neuromodulator, corticotropin releasing factor (CRF). Here we demonstrate that chronic, but not acute, exposure of female mice during adolescence to AAS augments anxiety-like behaviors; effects that were blocked by central infusion of the CRF receptor type 1 antagonist, antalarmin. AAS treatment selectively increased action potential (AP) firing in neurons of the central amygdala (CeA) that project to the dlBnST, increased the frequency of GABA(A) receptor-mediated spontaneous inhibitory postsynaptic currents (sIPSCs) in dlBnST target neurons, and decreased both c-FOS immunoreactivity (IR) and AP frequency in these postsynaptic cells. Acute application of antalarmin abrogated the enhancement of GABAergic inhibition induced by chronic AAS exposure whereas application of CRF to brain slices of naïve mice mimicked the actions of this treatment. These results, in concert with previous data demonstrating that chronic AAS treatment results in enhanced levels of CRF mRNA in the CeA and increased CRF-IR in the dlBnST neuropil, are consistent with a mechanism in which the enhanced anxiety elicited by chronic AAS exposure involves augmented inhibitory activity of CeA afferents to the dlBnST and CRF-dependent enhancement of GABAergic inhibition in this brain region.
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