Anabolic steroids have long-lasting effects on male social behaviors (original) (raw)
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Hormones and Behavior, 2008
Anabolic androgenic steroids (AAS) are synthetic derivatives of testosterone used by over half a million adolescents in the United States for their tissue-building potency and performance-enhancing effects. AAS also affect behavior, including reports of heightened aggression and changes in sexual libido. The expression of sexual and aggressive behaviors is a function of complex interactions among hormones, social context, and the brain, which is extensively remodeled during adolescence. Thus, AAS may have different consequences on behavior during adolescence and adulthood. Using a rodent model, these studies directly compared the effects of AAS on the expression of male sexual and aggressive behaviors in adolescents and adults. Male Syrian hamsters were injected daily for 14 days with either vehicle or an AAS cocktail containing testosterone cypionate (2 mg/kg), nandrolone decanoate (2 mg/kg), and boldenone undecylenate (1 mg/kg), either during adolescence (27-41 days of age) or in adulthood (63-77 days of age). The day after the last injection, males were tested for either sexual behavior with a receptive female or agonistic behavior with a male intruder. Adolescent males treated with AAS showed significant increases in sexual and aggressive behaviors relative to vehicle-treated adolescents. In contrast, AAS-treated adults showed significantly lower levels of sexual behavior compared with vehicle-treated adults and did not show heightened aggression. Thus, adolescents, but not adults, displayed significantly higher behavioral responses to AAS, suggesting that the still-developing adolescent brain is more vulnerable than the adult brain to the adverse consequences of AAS on the nervous system and behavior.
Pharmacology Biochemistry and Behavior, 2011
Early abuse and anabolic androgenic steroids (AAS) both increase aggression. We assessed the behavioral and neurochemical consequences of AAS, alone or in combination with social subjugation (SS), an animal model of child abuse. On P26, gonadally intact male rats began SS consisting of daily pairings with an adult male for 2 weeks followed by daily injections of the AAS, testosterone on P40. As adults, males were tested for sexual and aggressive behaviors towards females in various hormonal conditions and inter-male aggression in a neutral setting using home or opponent bedding. Neurotransmitter levels were assessed using HPLC. Results showed that AAS males displayed significantly more mounts toward sexually receptive, vaginally obstructed females (OBS) and displayed significantly more threats towards ovariectomized females. SS males mounted OBS females significantly less and were not aggressive toward females. The role of olfactory cues in a neutral setting did not affect aggression regardless of treatment. AAS significantly increased brainstem DOPAC and NE. SS decreased 5HIAA, DA, DOPAC, and NE in brainstem. 5HIAA was significantly increased in the prefrontal cortex of all experimental groups. We conclude that AAS and SS differentially affect behavior towards females as well as neurotransmitter levels.
Adolescents and androgens, receptors and rewards
Hormones and Behavior, 2008
Adolescence is associated with increases in pleasure-seeking behaviors, which, in turn, are shaped by the pubertal activation of the hypothalamo-pituitary-gonadal axis. In animal models of naturally rewarding behaviors, such as sex, testicular androgens contribute to the development and expression of the behavior in males. To effect behavioral maturation, the brain undergoes significant remodeling during adolescence, and many of the changes are likewise sensitive to androgens, presumably acting through androgen receptors (AR). Given the delicate interaction of gonadal hormones and brain development, it is no surprise that disruption of hormone levels during this sensitive period significantly alters adolescent and adult behaviors. In male hamsters, exposure to testosterone during adolescence is required for normal expression of adult sexual behavior. Males deprived of androgens during puberty display sustained deficits in mating. Conversely, androgens alone are not sufficient to induce mating in prepubertal males, even though brain AR are present before puberty. In this context, wide-spread use of anabolic-androgenic steroids (AAS) during adolescence is a significant concern. AAS abuse has the potential to alter both the timing and the levels of androgens in adolescent males. In hamsters, adolescent AAS exposure increases aggression, and causes lasting changes in neurotransmitter systems. In addition, AAS are themselves reinforcing, as demonstrated by self-administration of testosterone and other AAS. However, recent evidence suggests that the reinforcing effects of androgens may not require classical AR. Therefore, further examination of interactions between androgens and rewarding behaviors in the adolescent brain is required for a better understanding of AAS abuse.
Behavioral effects of pubertal anabolic androgenic steroid exposure in male rats with low serotonin
2007
The goal of this study was to assess the interactive effects of chronic anabolic androgenic steroid (AAS) exposure and brain serotonin (5-hydroxytryptamine, 5-HT) depletion on behavior of pubertal male rats. Serotonin was depleted beginning on postnatal day 26 with parachlorophenylalanine (PCPA 100 mg/kg, every other day); controls received saline. At puberty (P40), half the PCPA-treated rats and half the saline-treated rats began treatment with testosterone (T, 5 mg/kg, 5 days/week). Behavioral measures included locomotion, irritability, copulation, partner preference, and aggression. Animals were tested for aggression in their home cage, both with and without physical provocation (mild tail pinch). Brain levels of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were determined using HPLC. PCPA significantly and substantially depleted 5-HT and 5-HIAA in all brain regions examined. Chronic T treatment significantly decreased 5-HT and 5-HIAA in certain brain areas, but to a much lesser extent than PCPA. Chronic exposure to PCPA alone significantly decreased locomotor activity and increased irritability but had no effect on sexual behavior, partner preference, or aggression. T alone had no effect on locomotion, irritability, or sexual behavior but increased partner preference and aggression. The most striking effect of combining T + PCPA was a significant increase in attack frequency as well as a significant decrease in the latency to attack, particularly following physical provocation. Based on these data, it can be speculated that pubertal AAS users with low central 5-HT may be especially prone to exhibit aggressive behavior.
Anabolic-androgenic steroid exposure during adolescence and aggressive behavior in golden hamsters
1997
Anabolic androgenic steroid (AAS) abuse by adolescents represents a significant health care risk due to the potential for long-term negative physical and psychological sequelae, including increased aggressive behavior. The current experiments examined the effects of AAS use in young male adolescent hamsters (Mesocricetus auratus) and their consequences on aggressive behavior. It was hypothesized that AAS administration during adolescence predisposes hamsters to heightened levels of aggressive behavior (i.e., offensive aggression). To test this hypothesis, adolescent male hamsters were administered high doses of synthetic AAS to mimic a 'heavy use' self-administration regimen used by athletes. Immediately following the exposure to AAS, hamsters were tested for aggressive behavior using a resident-intruder model. Animals treated with high doses of AAS during their adolescent development showed heightened measures of offensive aggression (i.e., decreased latency to bite and increased total number of attacks and bites) during the test period, while measures of total activity (total contact time) between the animals remained unchanged. AAStreated males did not differ in body weight from controls, suggesting that the increased aggression was not due to increased body mass. The results of this study show that exposure to AAS during adolescence facilitates aggressive response patterns, but does not alter body weight.
Testosterone Programs Adult Social Behavior before and during, But Not after, Adolescence
Endocrinology, 2009
Whereas the adolescent brain is a major target for gonadal hormones, our understanding of hormonal influences on adolescent neural and behavioral development remains limited. These experiments investigated how variations in the timing of testosterone (T) exposure, relative to adolescence, alters the strength of steroid-sensitive neural circuits underlying social behavior in male Syrian hamsters. Experiment 1 simulated early, on-time, and late pubertal development by gonadectomizing males on postnatal d 10 and treating with SILASTIC brand T implants for 19 d before, during, or after adolescence. T treatment before or during, but not after, adolescence facilitated mating behavior in adulthood. In addition, preadolescent T treatments most effectively increased mating behavior overall, indicating that the timing of exposure to pubertal hormones contributes to individual differences in adult behavior. Experiment 2 examined the effects of preadolescent T treatment on behavior and brain regional volumes within the mating neural circuit of juvenile males (i.e. still preadolescent). Although preadolescent T treatment did not induce reproductive behavior in juvenile males, it did increase volumes of the bed nucleus of the stria terminalis, sexually dimorphic nucleus, posterodorsal medial amygdala, and posteroventral medial amygdala to adult-typical size. In contrast, juvenile anterodorsal medial amygdala and ventromedial hypothalamus volumes were not changed by preadolescent T treatment yet differed significantly in volume from adult controls, suggesting that further maturation of these brain regions during adolescence is required for the expression of male reproductive behavior. Thus, adolescent maturation of social behavior may involve both steroid-independent and -dependent processes, and adolescence marks the end of a postnatal period of sensitivity to steroid-dependent organization of the brain.
Steroid regulation of sexual behavior
Journal of Steroid Biochemistry, 1976
Experimental data on rats and rabbits are reviewed, in support of the idea that estrogen is involved in the control both of male and female sexual behavior in these species. Female sexual behavior is stimulated by estrogen alone or estrogen in combination with progesterone. It can, however, also be induced by aromatizable, but not by non-aromatizable, androgens. Masculine sexual behavior is stimulated by aromatizable androgens or by non-aromatizable androgens combined with estrogen. The stimulatory effect of androgen on masculine sexual behavior is blocked by some aromatization blockers. This blocking effect can be reversed by estrogen. It is suggested that under normal conditions estrogens and androgens interact in producing sexual behavior.
Exposure to an Anabolic Steroid Changes Female Mice's Sexual Responses According to Sex Partner
The Journal of Sexual Medicine, 2007
Introduction. Anabolic androgenic steroids (AAS) affect human female sexual behaviors. Animal models have been useful in uncovering the neural mechanisms governing changes in female sexual response upon AAS exposure. Aim. We quantify the sexual response of AAS-exposed gonadally intact female mice when paired with gonadally intact female or male pairs. Methods. C57Bl/6 female mice were systemically exposed to the AAS 17a-methyltestosterone (7.5 mg/kg) for 17 days via a subcutaneous osmotic implant. On days 15-17, these females were allowed to mate with males or proestrus female partners in familiar and unfamiliar testing arenas for 10 minutes. Main Outcome Measures. The following behavioral responses were registered: parameters related to mounting behavior such as the frequency of mounts, attempts to mount, and the latency to the first mount, anogenital investigation, fights and escapes, rejections, pelvic thrusts, and lordotic responses. Results. We found that males displayed a significant decrease in the frequency of mounts to AAS-exposed females, when compared with mating encounters with control females. We found no difference in the lordosis strength when control females were mounted by either a male or AAS-exposed females. However, females under androgen exposure attempted to mount control females, but not males, and their behavior was accompanied by significant increases in the number of fights, escapes, and rejections to the male. There were no differences between AAS-exposed females and males when the frequency of mounts and pelvic thrusts toward control females were compared. The lordotic quotient of control females was similar for either partner. Conclusions. Aside from showing a male-like pattern, AAS-exposed females displayed a higher frequency of anogenital investigations toward control females than males, and their latency to the first mount was as fast as that of males. Taken together, we conclude that the sex partner greatly influences the sexual response of AAS-exposed female mice. Barreto-Estrada JL, Parrilla-Carrero J, and Jorge JC. Exposure to an anabolic steroid changes female mice's sexual responses according to sex partner.
Brain Research, 2006
Illicit use of anabolic androgenic steroids (AAS) has become a prevalent health concern not only among male professional athletes, but, disturbingly, among a growing number of women and adolescent girls. Despite the increasing use of AAS among women and adolescents, few studies have focused on the effects of these steroids in females, and female adolescent subjects are particularly underrepresented. Among the hallmarks of AAS abuse are changes in reproductive behaviors. Here, we discuss work from our laboratories on the actions of AAS on the onset of puberty and sexual behaviors in female rodents, AAS interactions and sex-and age-specific effects of these steroids on neural transmission mediated by γ-aminobutyric acid receptors within forebrain neuroendocrine control regions that may underlie AAS-induced changes in these behaviors.