Cerebrospinal Fluid and Behavioral Changes After Methyltestosterone Administration

Daly, Robert C.; Su, Tung‐Ping; Schmidt, Peter J.; Pickar, David; Murphy, Dennis L.; Rubinow, David R.

doi:10.1001/archpsyc.58.2.172

Cited by 77 publications

(52 citation statements)

References 40 publications

(39 reference statements)

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“…In vivo studies on human males have furthermore shown that administration of methyl-testosterone negatively influences levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) in cerebrospinal fluid (Daly et al, 2001). Since MHPG is a degradation product of norepinephrine by MAO-A, this finding is consistent with the idea of a direct effect of MAO activity on testosterone.…”

Section: Introductionsupporting

confidence: 55%

A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior

Sjöberg

Ducci²,

Barr³

et al. 2007

Neuropsychopharmacol

122

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A functional VNTR polymorphism in the promoter of the monoamine oxidase A gene (MAOA-LPR) has previously been shown to be an important predictor of antisocial behavior in men. Testosterone analogues are known to interact with the MAOA promoter in vitro to influence gene transcription as well as in vivo to influence CSF levels of the MAO metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) in human males. We examined the possible joint effects of testosterone (measured in CSF) and MAOA-LPR genotype on antisocial personality disorder and scores on the Brown-Goodwin Aggression scale in 95 unrelated male criminal alcoholics and 45 controls. The results confirm that MAOA genotype and CSF testosterone interact to predict antisocial behaviors. The MAOA/testosterone interaction also predicted low levels of CSF MHPG, which tentatively suggests the possibility that the interaction may be mediated by a direct effect on gene transcription. If replicated these findings offer plausible explanations for previous inconsistencies in studies of the relationship between testosterone and male human aggression, as well as for how MAOA genotype may influence aggressive behavior in human males.

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Section: Introductionsupporting

confidence: 55%

A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior

Sjöberg

Ducci²,

Barr³

et al. 2007

Neuropsychopharmacol

122

View full text Add to dashboard Cite

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“…Similarly, Tricker et al [175], O'Connor et al [121] and Fingerhood [59] reported no increases in angry behavior [121,175] or subjective drug responses ("feel the drug", "feel high"; [59]). However, other studies have observed increased aggression [42,72,98,140,163], positive mood including sexual arousal and manic scores [5,42,72,140,163], as well as changes in cognitive [42] and psychomotor function [72].…”

Section: • Just Say No: Aas Reinforcement and Dependence In Humansmentioning

confidence: 92%

“…By contrast, AAS increase serotonin levels in cerebral cortex [99], and 5HT2 receptors in Acb [94]. In male volunteers receiving injections of methyltestosterone, levels of the serotonin metabolite 5-hydroxyindolacetic acid in cerebrospinal fluid increased, and this was correlated with activation symptoms: energy, sexual arousal, diminished sleep [42]. Most significantly, Grimes and Melloni [69] have shown that changes in the serotonergic system persist long after steroid is discontinued.…”

Section: Serotoninmentioning

confidence: 99%

Anabolic–androgenic steroid dependence? Insights from animals and humans

Wood

2008

Frontiers in Neuroendocrinology

132

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Anabolic-androgenic steroids (AAS) are drugs of abuse. They are taken in large quantities by athletes and others to increase performance, with negative health consequences. As a result, in 1991 testosterone and related AAS were declared controlled substances. However, the relative abuse and dependence liability of AAS have not been fully characterized. In humans, it is difficult to separate the direct psychoactive effects of AAS from reinforcement due to their systemic anabolic effects. However, using conditioned place preference and self-administration, studies in animals have demonstrated that AAS are reinforcing in a context where athletic performance is irrelevant. Furthermore, AAS share brain sites of action and neurotransmitter systems in common with other drugs of abuse. In particular, recent evidence links AAS with opioids. In humans, AAS abuse is associated with prescription opioid use. In animals, AAS overdose produces symptoms resembling opioid overdose, and AAS modify the activity of the endogenous opioid system. KeywordsAnabolic agents; Testosterone; self-administration; hamsters; drug dependence • Breakfast of champions: Recent history and prevalence of AAS useAnabolic-androgenic steroids (AAS) are a hot topic. A search of the Google news archive in March 2007 reveals 47,500 news stories on "steroids" in 2006, a 400% increase since their debut in the archive in 2002. In 2006, "steroids" even surpassed trend-setters such as "Paris Hilton" (38,500 stories) or "spinach" (42,700 stories). Current media attention on AAS abuse has been driven by accusations of steroid use among professional athletes in baseball, track, and cycling. However, public recognition of AAS use in sports dates back nearly 20 years, when Ben Johnson tested positive for stanozolol at the Seoul Olympics in 1988 [77]. Eastern Block athletes had been using steroids since the 1950's, and the International Olympic Committee banned steroid use from Olympic competition in 1976. However, the ability to reliably detect androgen metabolites in urine samples was limited until the advent of gas chromatography-mass spectroscopy [89]. Johnson's drug test spurred the United States Congress to pass the Anabolic Steroid Control Act of 1991 which declared steroids as Address all reprint requests and correspondence to Ruth I. Wood, Department of Cell and Neurobiology, Keck School of Medicine at the University of Southern California, 1333 San Pablo St., BMT 401, Los Angeles, CA 90033. Telephone (323) 442-1980, Fax: (323) 442-3466, e-mail: riw@usc.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain....

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“…During a cycle, adult men are reported to self-administer AAS at concentrations that reflect 10-100× therapeutic replacement doses of testosterone (therapeutic doses: 10-40 mg/day) (for review, Clark et al, 2006). Although assessments of circulating levels of AAS in chronic steroid users is hindered by the lack of reagents to detect AAS metabolites as well as the inability to accurately monitor illicit users, cerebrospinal levels of 17α-MeT from adult male volunteers given a brief (3 day) administration of a moderate dose (240 mg/day) of this AAS were measured to be as high as 898 nmol/L (Daly et al, 2001). Adolescents and women are reported to take AAS at levels equivalent to or even exceeding those administered by men (Franke and Berendonk, 1997).…”

Section: Neurosteroid and Anabolic Androgenic Steroid Levels In The Cnsmentioning

confidence: 99%

Steroid modulation of GABAA receptor-mediated transmission in the hypothalamus: Effects on reproductive function

Henderson

2007

Neuropharmacology

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The hypothalamus, the seat of neuroendocrine control, is exquisitely sensitive to gonadal steroids. For decades it has been known that androgens, estrogens and progestins, acting through nuclear hormone receptors, elicit both organizational and activational effects in the hypothalamus and basal forebrain that are essential for reproductive function. While changes in gene expression mediated by these classical hormone pathways are paramount in governing both sexual differentiation and the neural control of reproduction, it is also clear that steroids impart critical control of neuroendocrine functions through nongenomic mechanisms. Specifically, endogenous neurosteroid derivatives of deoxycorticosterone, progesterone and testosterone, as well and synthetic anabolic androgenic steroids that are self-administered as drugs of abuse, elicit acute effects via allosteric modulation of γ-aminobutyric acid type A receptors. GABAergic transmission within the hypothalamus and basal forebrain is a key regulator of pubertal onset, the expression of sexual behaviors, pregnancy and parturition. Summarized here are the known actions of steroid modulators on GABAergic transmission within the hypothalamus/basal forebrain, with a focus on the medial preoptic area and the supraoptic/paraventricular nuclei that are known to be central players in the control of reproduction.

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Cerebrospinal Fluid and Behavioral Changes After Methyltestosterone Administration

Cited by 77 publications

References 40 publications

A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior

A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior

Anabolic–androgenic steroid dependence? Insights from animals and humans

Steroid modulation of GABAA receptor-mediated transmission in the hypothalamus: Effects on reproductive function

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