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PubMed2005

The estrogen receptor alpha gene and breast cancer risk (The Netherlands).

OBJECTIVE: In this study we aimed to investigate whether the PvuII, XbaI and B-variant polymorphisms in the estrogen receptor alpha gene (ER-alpha) are associated with an increased risk of breast cancer in postmenopausal women, and whether the effect of high estradiol (E2) levels on breast cancer risk is altered by these polymorphisms. The selection of these polymorphisms was based on previously published associations with osteoporosis and spontaneous abortions. METHODS: The effect of the three polymorphisms on breast cancer risk was studied using a case-cohort design nested within a large population-based cohort study (n = 9349) in the Netherlands (the DOM-cohort). In total 380 incident breast cancer cases and a subcohort of 422 women were genotyped by RFLP or ASO hybridization methods. RESULTS: Women with the PvuII pp genotype had a 1.5 times non significant increased risk of breast cancer (95% CI: 0.94-2.42; p(trend) = 0.09) compared to women with the PP genotype. The Pp or pp genotype in combination with high E2 levels raised breast cancer risk significantly when compared to women with low E2 levels and the PP genotype (RR=2.26; 95% CI: 1.24-4.13). This interaction was statistically significant on the multiplicative scale (p = 0.01). The XbaI genotype (RR(xx versus XX) = 1.19; 95% CI: 0.73-1.95) and the B' allele (RR(BB'+B'B' versus BB) = 0.87; 95% CI: 0.56-1.33) were not associated with breast cancer risk. CONCLUSION: The results of this study suggest that the PvuII polymorphism in the ER-alpha, or another mutation in linkage disequilibrium with PvuII, in combination with high E2 levels increases breast cancer risk in postmenopausal women.

Aged↗

PubMed2005

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands).

Variants in the metabolic genes NAT1, NAT2, GSTM1 or GSTT1, may cause differences in individual detoxifying capacity of possible carcinogens. We examined the cumulative effect of putative at risk genotypes on breast cancer risk and we examined the extent to which these polymorphisms modify the association between smoking and breast cancer. A case cohort study was conducted in the DOM cohort with 676 breast cancer cases and a random sample of 669 individuals. No effect of the NAT1, NAT2 or GSTM1 genotypes on breast cancer risk was observed. However, women with GSTT1 null genotype had a 30% increased breast cancer risk compared to women with GSTT1 present (RR = 1.30 (95% confidence interval (CI) 1.04-1.64)). Smoking did not influence breast cancer risk nor did genetic variations in NAT1, NAT2 or GSTM1 in combination with smoking. Compared to women who never smoked with GSTT1 present, women with GSTT1 null genotype and who formerly smoked showed an increased breast cancer risk (RR = 2.55 (95% CI 1.10-5.90)), but current smokers who smoked 20 cigarettes or more per day did not (RR = 1.06 (95% CI 0.51-2.18)). Increasing numbers of putative at risk genotypes increased breast cancer risk in a dose dependent manner (p for trend 0.01). The risk was more than doubled in women with all four risk genotypes, RR = 2.45 (95% CI 1.24-4.86), compared to women with zero putative at risk genotypes. In conclusion, the results of this study suggest that presence of three or more putative at risk genotypes increases breast cancer risk.

Arylamine N-Acetyltransferase↗

PubMed2006

Ultrasound and magnetic resonance imaging in sports-related muscle injuries.

PURPOSE: The objective of this study was to evaluate the role of magnetic resonance imaging (MRI) and ultrasonography (US) in the diagnosis of traumatic muscle injuries. MATERIALS AND METHODS: From June 2003 to June 2004, 81 football players with a history of traumatic muscle injuries to the lower limbs were examined. US was performed shortly after the trauma (from 6 to 72 h afterwards) and MRI within a maximum of 5 days. RESULTS: MRI revealed 26 minor and 55 major traumas. MRI and US showed complete concordance in 71 patients (site, type and extent of injury). US produced ten false negative results, including six minor lesions and four major lesions. US had a sensitivity of 87.65% in the correct identification of muscle injuries; its sensitivity was 92.72% for major lesions and 76.92% for minor lesions, 57% for delayed-onset muscle soreness (DOMS), 80% for lengthenings, 83% for contractures, 84% for strains, 87.5% for mild contusions and 100% for severe contusions. CONCLUSIONS: US is the first-line technique for examination of muscle injuries. MRI is able to reveal lesions that may be missed at US and provide a more accurate assessment of site and extent of injury.

Adolescent↗

PubMed1993

Activity of serotonin (5-HT) receptor agonists, partial agonists and antagonists at cloned human 5-HT1A receptors that are negatively coupled to adenylate cyclase in permanently transfected HeLa cells.

The activity of serotonin (5-HT) receptor agonists, partial agonists and antagonists, and various other neurotransmitter receptor antagonists at human 5-HT1A receptors that are negatively coupled to adenylate cyclase in permanently transfected HeLa cells was investigated. 5-HT1A receptor-mediated inhibition of adenylate cyclase was studied by measuring inhibition of cAMP accumulation, induced by forskolin. At 100 microM forskolin produced a 100-fold increase in cAMP formation: 5-HT concentration dependently inhibited the cAMP formation; maximal inhibition was attained at 1 microM 5-HT and represented 90% of the stimulated cAMP formation. Full inhibition was observed with 5-HT1A receptor agonists: N,N-dipropyl-8-hydroxy-2-aminotetralin (8-OH-DPAT) and flesinoxan, and non-selective 5-HT receptor agonists: d-lysergic acid diethylamide (d-LSD), RU 24,969, bufotenine, methysergide and tryptamine. The rank order of potency of the compounds for inhibiting the cAMP formation corresponded to the rank order of the binding affinities of the drugs for the 5-HT1A receptor. Partial inhibition was obtained with submicromolar concentrations of buspirone, spiroxatrine and ipsapirone. A slight inhibition was observed with 1 microM 5-HT receptor agonist CP 93129 and 1 microM 5-HT receptor antagonists mesulergine and BW-501. No inhibition was found with: the 5-HT receptor agonists quipazine, sumatriptan and 1-(2,5-dimethoxy-4-methylphenyl)-2- aminopropane (DOM); the 5-HT receptor antagonist ICS-205,930; and other neurotransmitter receptor antagonists such as pindolol, CGP 20712-A, prazosin, sulpiride and pyrilamine. Spiperone and pindolol fully antagonized the agonist-mediated inhibition of forskolin-stimulated cAMP formation. Partial inhibition of the agonist-mediated inhibition of forskolin-stimulated cAMP formation was apparent with 1 microM ocaperidone and 1 microM ipsapirone. It can be concluded that HeLa cells, permanently expressing human 5-HT1A receptors, are a valid cellular system for studying the negative coupling of 5-HT1A receptors to adenylate cyclase and the action of compounds thereupon.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1984

Hypothalamic neurotransmitter function in experimentally induced hyperprolactinemia.

It is known that animals or patients bearing a prolactin (PRL)-secreting tumor (PST) do not suppress PRL levels after administration of indirectly acting dopamine agonists, namely nomifensine (Nom), and are not responsive to the PRL releasing effect of antidopaminergic drugs and opioid peptides. Since the action of these drugs is mediated through the tuberoinfundibular dopaminergic (TIDA) system, these findings have been taken to indicate that animals and humans bearing prolactinomas have a defective TIDA function. Alternatively, PRL unresponsiveness to these drugs could be due to hyperfunction of TIDA system for the feedback action of high PRL levels. To clarify whether hypo- or hyperfunction of the TIDA system was responsible for such behaviour, we tested the effect of a synthetic opioid peptide (FK 33-824), a DA receptor antagonist, domperidone (Dom), and of Nom on PRL secretion in two experimental models of non-tumoral hyperprolactinemia, i.e. rats bearing ectopic pituitaries since 3 days (TP rats), or treated with ovine PRL (oPRL 250 micrograms, twice daily for 3 days), in which existence of an increased TIDA function has been demonstrated. FK 33-824 (0.5 mg/kg i.p.) increased significantly plasma PRL levels in control rats but failed to do so in TP rats and it elicited a significantly lower PRL response than in controls in rats treated with oPRL. In both experimental models, a PRL secretagogue, e.g. 5-hydroxytryptophan (50 mg/kg i.p.), elicited the same response as in controls, indicating that the pituitary PRL pool was preserved.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Calcium and magnesium in human toenails do not reflect bone mineral density.

Nail mineral composition is influenced by several physiological and pathological processes. Potentially, nails could be used to monitor alterations in the level of incorporation of specific elements produced by nutritional abnormalities, disease states or chronic exposure to toxic agents. The purpose of this study was to investigate whether the calcium and magnesium content in nail clippings, as measured by instrumental neutron activation analysis (INAA), correlates with bone mineral density (BMD), as measured by quantitative microdensitometry (QMD), and therefore could be interesting as a screening instrument for osteoporosis. The study involved 220 women, who participated in a breast cancer screening project (the DOM-project) in Utrecht, the Netherlands. The correlations found between Ca and Mg measurements and bone mineral densities were very low (correlation coefficients ranging from 0.03 to 0.18). It is concluded that Ca and Mg measurements in nail clippings by INAA cannot be used for screening purposes in the prevention of osteoporosis.

Adult↗

PubMed1987

A comparative study of Norinyl 1/35 versus Norinyl 1/50 in Belgrade, Yugoslavia.

A comparative study of Norinyl 1/35 and Norinyl 1/50 was conducted at the Dom Zdravlja Stari Grad in Belgrade, Yugoslavia. The study sought to evaluate the differences in continuation rates as well as the frequency of selected side effects which might contribute to method discontinuation. The trial included 299 women who were randomly allocated to one of the two oral contraceptives. In the Norinyl 1/35 group, significantly more women (p less than .05) reported a complaint of vaginal discharge as well as an increase in the occurrence of vaginal discharge compared to the Norinyl 1/50 group. There was no significant difference in continuation rates or for particular discontinuation reasons for the Norinyl 1/35 and Norinyl 1/50 groups. No accidental pregnancies were reported during this study. Both oral contraceptives appear to be safe and effective; there appears to be no difference in the acceptability of one oral contraceptive over the other among this group of Yugoslavian women.

Adult↗

PubMed1989

Involvement of 5-HT receptor subtypes in the discriminative stimulus properties of mescaline.

In order to further evaluate the extent to which particular 5-HT receptor subtypes (5-HT1, 5-HT2) might be involved in the behavioral effects of hallucinogenic drugs, rats were trained to discriminate mescaline (10 mg/kg i.p.) from saline and were given substitution (generalization) and combination (antagonism) tests with putatively selective serotonergic and related neuroactive compounds. The mescaline cue generalized to relatively high doses of the 5-HT2 agonists, 2,5-dimethoxy-4-methylamphetamine (DOM), LSD and psilocybin; the extent of generalization to 5-HT1 agonists (8-hydroxy-2-[diethylamino]tetralin (8-OHDPAT), RU-24969 and 8-hydroxy-2-[di-n-propylamino]tetralin (TFMPP] was unclear. Combinations of the training drug and sufficiently high doses of 5-HT2 antagonists (ketanserin, LY-53857, pirenperone) were followed by saline-lever responding; less selective central 5-HT (metergoline), and DA (SCH-23390, haloperidol) antagonists, did not block the mescaline cue. These data suggest that 5-HT2 receptors are involved in the stimulus properties of mescaline.

Animals↗

PubMed1986

Discriminative stimulus properties of the serotonergic agent 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI).

Using a two-lever drug discrimination procedure, six rats were trained to discriminate 0.5 mg/kg of racemic 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) from saline. Once trained, the animals demonstrated a dose-related decrease in discriminative performance upon administration of lower doses of DOI (ED50 = 0.16 mg/kg). DOI-stimulus generalization occurred with the putative 5-HT2 agonist DOM (ED50 = 0.49 mg/kg), but not with the 5-HT1A agonist 8-OH DPAT, or the 5-HT1B agonist TFMPP. Furthermore, the DOI stimulus could be antagonized by pretreatment of the animals with the 5-HT2 antagonist ketanserin. The present results, coupled with the prior demonstration that DOI possesses a significant affinity and selectivity for 5-HT2 binding sites, suggest that the discriminative stimulus effects of DOI may be 5-HT2-mediated.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1995

Gamma-ray mutagenesis measurement in mammalian cells.

Application of conventional in vitro mutagenesis testing has so far failed to result in marked reduction of the total incidence of cancer. At least part of the reason may lie in the frequent use of a cell target too small to yield adequate sensitivity, and in failure to take into account the effects of cell killing in the assessment of mutagenic action. A single theoretical analysis fits the results of experimental data on gamma-irradiation applied to single marker gene testing in bacteria and to cytogenetic analysis of irradiated mammalian cells, and permits determination of the mean mutagenic dose, DoM, without complication due to cell killing. Cytogenetic monitoring of human lymphocytes which can detect mutagenic effects of gamma-radiation down to doses of < 0.1 Gy (10 rad) will also furnish an estimate of repair effectiveness at these low levels and may well be a useful tool in a program for prevention of cancer and other genetic disease.

Animals↗

PubMed1985

Domperidone in defective and insufficient lactation.

The clinical use of anti-dopaminergic drugs to stimulate plasma PRL levels, to induce lactogenesis and maintain an adequate lactation has been widely suggested, taking into consideration the main inhibitory role of hypothalamic dopamine on PRL secretion. We therefore studied the effects of domperidone (DOM), a direct anti-dopaminergic drug with a low tendency to be secreted in the milk and which does not cross the blood-brain barrier, on inducing lactogenesis in 8 puerperal women with a history of defective lactogenesis (group A) and inducing galactopoiesis in 9 puerperal women who showed 2 weeks after delivery an insufficient lactation (group B). A placebo treatment was performed in 7 and 8 puerperal women with the same characteristics of group A and B, respectively. PRL plasma levels were assayed in basal conditions and after suckling from the 2nd to the 5th day of puerperium in group A and through a 10-day treatment in group B. In both groups domperidone-treated subjects always showed baseline PRL levels and daily milk yield significantly higher than those of the placebo group (P less than 0.01). The lack of any side-effects and the positive results suggest a high usefulness of such a drug in inducing and/or maintaining successful breast feeding, which is at present considered so important for a healthy development of infants.

Adult↗

PubMed1982

Is domperidone a selective peripheral dopamine-receptor antagonist in vivo?

The ability of domperidone (DOM) to antagonize dopamine (DA) receptor agonist-induced hypothermia or hyperactivity was investigated in rats. Apomorphine (APO) or RDS-127 (2-di-n-propylamino-4,7-dimethoxyindane), two DA receptor agonists, produced dose-dependent hypothermia following subcutaneous (s.c.) administration. Also, RDS-127 produced hypothermia following lateral ventricular (i.c.v.) administration. The hypothermia produced by apomorphine or RDS-127 (given s.c. or i.c.v.) was antagonized by pretreatment with pimozide (0.25 mg/kg, i.p.) or domperidone (0.2, 1.0 and 5.0 mg/kg, i.p.). The hyperactivity produced by apomorphine was unaffected by pretreatment with domperidone. These data suggested that central DA receptors mediating temperature regulation, but not those mediating locomotor activity are accessible to peripherally administered domperidone. Therefore, domperidone may not be useful to differentiate hypothalamic (central) vs peripheral sites of action for DA receptor agonists in the rat.

Animals↗

PubMed1992

Pharmacological characterization of regulation of phosphoinositide metabolism by recombinant 5-HT2 receptors of the rat.

Transfection of 5-HT2 receptor cDNA in 293 cells induced the expression of a protein binding domain, exhibiting the classical 5-HT2 receptor transduction mechanism. Both [3H]DOB and [3H]spiperone high affinity binding sites were present in membranes of sense but not of antisense, 5-HT2 receptor cDNA transfected cells. Addition of 1 microM 5-HT induced a time-dependent increase of phosphoinositide (PI) metabolism in sense but not in antisense, 5-HT2 receptor cDNA transfected cells. Graded concentrations of 5-HT and of different serotonergic agonists showed different potencies (DOI greater than 5-HT greater than quipazine greater than DOM greater than alpha-methyl-5-HT greater than 8-OH-DPAT greater than 2-methyl-5-HT greater than CGS-12066B) in stimulating turnover of PI in cells transfected with cDNA encoding for 5-HT2 receptors of the rat. The ability of different antagonists to inhibit 5-HT-stimulated turnover of PI bore a direct relationship with their potency to inhibit 5-HT2 receptor binding in cells transfected with 5-HT2 receptor cDNA (spiperone greater than ketanserin greater than ritanserin greater than mianserin greater than haloperidol). Preincubation of transfected 293 cells with pertussis toxin failed to modify either 5-HT- or DOI-induced activation of metabolism of PI. Pretreatment of transfected 293 cells with DOI (100 nM) for 2 hr or more, significantly reduced activation of turnover of PI elicited by graded doses of 5-HT. When the transfected 293 cells were exposed to DOI (100 nM) for 12 hr and the challenge was performed after a 2-hr wash-out period, the desensitization of the response to 5-HT was virtually abolished.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

The 5HT2 antagonist pirenperone reverses disruption of FR-40 by hallucinogenic drugs.

Indolealkylamine and phenethylamine hallucinogens disrupted responding maintained under a fixed-ratio 40 (FR-40) schedule of reinforcement. LSD, DMT, mescaline and DOM produced dose-dependent decreases in number of reinforcers and increases in 10-sec periods of non-responding (pause-intervals). The 5HT agonist quipazine, as well as the LSD congener lisuride, altered response patterns in a similar manner. The effects of these drugs were examined after pretreatment with pirenperone, an antagonist with specificity toward the 5HT2 receptor with reference to the 5HT1 receptor. The dose-response curves for the phenethylamine hallucinogens were shifted significantly to the right and to a greater degree than were those for the indolealkylamine hallucinogens. Pirenperone also antagonized the effects of quipazine to a degree similar to that observed with the phenethylamine-type hallucinogens. Pirenperone did not significantly shift the dose-response pattern to lisuride. These data suggest that the behavioral disruption induced by these hallucinogens and quipazine relates at least in part to an effect on 5HT2 receptors, while the effects of lisuride do not involve a significant interaction at the 5HT2 receptor.

Animals↗

PubMed1989

Stimulus effects of N-monoethyl-1-(3,4-methylenedioxyphenyl)-2-aminopropane (MDE) and N-hydroxy-1-(3,4-methylenedioxyphenyl)-2-aminopropane (N-OH MDA) in rats trained to discriminate MDMA from saline.

Tests of stimulus generalization were conducted using rats trained to discriminate 1.5 mg/kg of N-monomethyl-1-(3,4-methylenedioxyphenyl)-2-aminopropane HCl (MDMA) from saline in order to determine if two structurally related analogs (MDE and N-OH MDA) would produce similar stimulus effects. The MDMA-stimulus (MDMA, ED50 value = 0.76 mg/kg) generalized both to MDE (ED50 value = 0.73 mg/kg) and N-OH MDA (ED50 value = 0.47 mg/kg). Administration of (+)amphetamine resulted in partial generalization (maximum of 49% MDMA-appropriate responding) in the MDMA-trained animals. Taken together with our previous studies showing that MDMA substitutes for the phenylisopropylamine stimulant (+)amphetamine, but that neither MDE nor N-OH MDA substitute for (+)amphetamine or for the phenylisopropylamine hallucinogen 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM), the present results [i.e., MDMA-stimulus generalization to MDE, N-OH MDA, but not to (+)amphetamine] suggest that 1) MDMA produces effects other than those that may be considered amphetamine-like, and 2) MDE and N-OH MDA are MDMA-like agents with even less of an amphetamine-like component of action than MDMA itself.

3,4-Methylenedioxyamphetamine↗

PubMed1991

3,4-Methylenedioxyamphetamine (MDA) analogues exhibit differential effects on synaptosomal release of 3H-dopamine and 3H-5-hydroxytryptamine.

The effect of various analogues of the neurotoxic amphetamine derivative, MDA (3,4-methylenedioxyamphetamine) on carrier-mediated, calcium-independent release of 3H-5-HT and 3H-DA from rat brain synaptosomes was investigated. Both enantiomers of the neurotoxic analogues MDA and MDMA (3,4-methylenedioxymethamphetamine) induce synaptosomal release of 3H-5-HT and 3H-DA in vitro. The release of 3H-5-HT induced by MDMA is partially blocked by 10(-6) M fluoxetine. The (+) enantiomers of both MDA and MDMA are more potent than the (-) enantiomers as releasers of both 3H-5-HT and 3H-DA. Eleven analogues, differing from MDA with respect to the nature and number of ring and/or side chain substituents, also show some activity in the release experiments, and are more potent as releasers of 3H-5-HT than of 3H-DA. The amphetamine derivatives (+/-)fenfluramine, (+/-)norfenfluramine, (+/-)MDE, (+/-)PCA, and d-methamphetamine are all potent releasers of 3H-5-HT and show varying degrees of activity as 3H-DA releasers. The hallucinogen DOM does not cause significant release of either 3H-monoamine. Possible long-term serotonergic neurotoxicity was assessed by quantifying the density of 5-HT uptake sites in rats treated with multiple doses of selected analogues using 3H-paroxetine to label 5-HT uptake sites. In the neurotoxicity study of the compounds investigated, only (+)MDA caused a significant loss of 5-HT uptake sites in comparison to saline-treated controls. These results are discussed in terms of the apparent structure-activity properties affecting 3H-monoamine release and their possible relevance to neurotoxicity in this series of MDA congeners.

3,4-Methylenedioxyamphetamine↗

PubMed1994

Methylenedioxyamphetamine: a selective effect on cortical content and turnover of 5-HT.

This study examined the effects of the hallucinogen, MDA, on brain content of monoamines and their metabolites in the rabbit. A single 1.8 mg/kg dose of MDA produced 30 to 64% increases in the 5-HT content of frontal cortex from 30 to 120 min after injection and a decrease in 5-HT turnover from 30 min to 8 h, but had no effect in hippocampus, caudate nucleus, or hypothalamus. A single 3.6 mg/kg dose of MDA also reduced the turnover of 5-HT in frontal cortex, but this was accompanied by a decrease in 5-HIAA with no increase in 5-HT. The 1.8 and 3.6 mg/kg doses of MDA had no significant or consistent effects on the contents of DA, DOPAC, HVA, and NE in any brain area examined. Chronic administration of MDA (3.6 mg/kg/day for 4 days) failed to produce any evidence of a neurotoxic action on 5-HT neurons. Higher doses could not be employed because the LD50 of MDA was approximately 5 mg/kg. This study has demonstrated that behaviorally effective and nonneurotoxic doses of MDA produce increases in the content and decreases in turnover of 5-HT in frontal cortex that resemble those of other hallucinogens such as LSD and DOM.

3,4-Methylenedioxyamphetamine↗

PubMed1994

Serotonergic control of androgen-induced dominance.

The present study investigates the role of serotonergic systems in anabolic steroid-induced aggression. An animal model of aggressive dominance was used to assess the chronic effects of testosterone propionate. When rats that had become dominant following administration of testosterone propionate received serotonergic agonists with selectivity for the 5-HT1A receptor (8-OH-DPAT, buspirone, gepirone), the 5-H1B receptor (eltoprazine, TFMPP), or the 5-HT2A/2C receptor (DOM), a dose-dependent decrease in dominance was demonstrated. Pretreatment with three serotonergic antagonists (pizotyline, pirenpirone, and pindolol) blocked agonist-induced reductions in dominance in varying degrees. Nonserotonergic agonists with CNS depressant effects were also tested in dominant animals. The benzodiazepine, chlordiazepoxide, did not reduce dominance except at doses that interfered with motor behavior. The opioid agonist, morphine, dose dependently decreased dominance, but this effect was reversible with administration of the serotonergic antagonist, pirenpirone, suggesting the antidominant effect of morphine had a serotonergic component. Biochemical experiments demonstrated that following chronic testosterone propionate, there was a decrease in levels of 5-HT and 5-HIAA in the hippocampus but not in the striatum or the frontal cortex. Chronic testosterone propionate also caused an increase in the affinity of [3H]8-OH-DPAT for the 5-HT1A receptor but no corresponding change in the density of 5-HT1A binding sites in the hippocampus. There was also no change in the properties of the 5-HT2 receptor in the frontal cortex following chronic testosterone propionate. These data suggest that serotonergic systems may play an important role in the control of anabolic steroid-induced aggressive dominance.

Aggression↗