Differential effects of gonadal steroids on dopamine metabolism in mesolimbic and nigro-striatal pathways of male rat brain

Alderson, Lloyd M.; Baum, Michael J.

doi:10.1016/0006-8993(81)91300-7

Cited by 101 publications

(27 citation statements)

References 37 publications

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“…This time-dependent increase of dopamine release from castrated males may be related to the time-dependent increase in the synthesis of catecholamines within the striatum which show no changes at 10 days, but markedly increase and achieve maximal activity by 20 days post-castration (25). Interestingly, this castration-induced increase in catecholamine synthesis appears to be localized directly to nerve terminals of the CS (26). It should be noted that determinations of caudate-putamen dopamine concentrations have failed to indicate any difference between intact and castrated male rats (26,27).…”

Section: Discussionmentioning

confidence: 92%

Effects of Orchidectomy on Nigro‐Striatal Dopaminergic Function: Behavioral and Physiological Evidence

Dluzen

Ramírez

1989

J Neuroendocrinology

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In the present experiments, we examined the effect of castration upon two indices of nigro-striatal dopaminergic function in the male rat. In Experiment I, differences in spontaneous locomotor behavioral activity between intact and castrated male rats were examined. The total distance traveled, horizontal activity and mean revolutions of castrated male rats were significantly greater than that of intact males. No significant differences between intact and castrated males were obtained for vertical activity. In Experiment 11, the spontaneous in vifrodopamine release from the corpus striatum of intact and castrated rats as sampled during the light-phase (1500 h) and dark-phase (2400 h) of the photoperiod was examined. At both time periods, the spontaneous in vifrodopamine release of castrated males was significantly greater than that of intact males. Both intact and castrated males showed statistically significant increases in dopamine release at the 2400 h compared to the 1500 h time period. To examine if testicular hormones were responsible for these castration induced changes in dopamine release, in Experiment Ill we treated castrated male rats with testosterone propionate. Administration of testosterone propionate (0.1 mg/day x 5 days) significantly reduced in vifro dopamine release compared to untreated or castrated male rats receiving vehicle treatment. These results demonstrate that testicular hormones, most likely testosterone, have a markedly suppressive effect upon the nigro-striatal dopaminergic system as evidenced from changes in spontaneous behavioral activity and in vifro dopamine release.Within our laboratory, we have been interested in examining the modulatory effects of gonadal steroid hormones upon the nigrostriatal dopaminergic system of the female rat (1, 2). Our results, as well as those from other laboratories, have demonstrated that the corpus striatum (CS) is an important target site of the CNS for both estrogen and progesterone (3-6). The role of the male gonadal steroid hormone, testosterone, upon the nigro-striatal dopaminergic system has received relatively less attention. Indirect indices of dopaminergic activity as determined with amphetamine-stimulated behavioral measures have indicated that testosterone attenuates the effects of amphetamine on locomotor activity and stereotyped behavior (7-9) and the duration of specific amphetamine-stimulated behaviors in castrated male rats are prolonged compared to those of intact and castrated plus testosterone-treated male rats (10). In addition, castration reduces and testosterone reinstates yawning behavior in male rats (1 l), a behavior, which in part, appears to be under control of the dopaminergic system (12). These results suggest that, similar to that of the female, the nigro-striatal dopaminergic system of the male rat is also subject to the influences of gonadal steroids. More specifically, it would appear that testicular steroids exert a predominantly suppressive effect upon dopaminergic activity in the male rat.In this report...

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Section: Discussionmentioning

confidence: 92%

Effects of Orchidectomy on Nigro‐Striatal Dopaminergic Function: Behavioral and Physiological Evidence

Dluzen

Ramírez

1989

J Neuroendocrinology

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“…27] showing that DHT facilitates sexual behavior and penile reflexes in intact male rats, and restores copulation in cas trated male rats when given together with estradiol ben zoate suggesting that the two steroids act in concert to modulate penile erection and yawning. The mechanisms by which castration prevents and ste roid supplementation restores either penile erection and/ or yawning induced by apomorphine or by oxytocin might be related either to a reduced dopaminergic neurotrans mission that is reversed by testosterone or estradiol ben zoate + DHT [30][31][32][33] The above findings support the hypothesis that testos terone and its neural metabolites, estradiol benzoate and DHT, are all necessary for the expression of penile erec tion and yawning and that their concentrations must be within a specific range in order to allow these behavioral manifestations. Accordingly, completely different effects of the above steroids on apomorphine-and oxytocininduced penile erection and yawning are found in intact male rats.…”

Section: Discussionmentioning

confidence: 99%

Apomorphine- and Oxytocin-Induced Penile Erection and Yawning in Intact and Castrated Male Rats: Effect of Sexual Steroids

Melis

Mauri²,

Argiolas³

1994

Neuroendocrinology

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The effect of apomorphine (80 µg/kg s.c.) and oxytocin (30 ng i.c.v.) on penile erection and yawning was studied in intact and castrated male rats. In castrated rats both apomorphine and oxytocin responses were abolished. In these animals, testosterone (100 µg/kg s.c. once a day for 3 days), restored penile erection while estradiol benzoate (10 µg/kg s.c. once a day for 3 days) restored yawning induced by both compounds. 5-Dihydrotestosterone (DHT) or progesterone (each at a dose of 100 µg/kg s.c. once a day for 3 days) were ineffective. Given together, estradiol benzoate and DHT partially restored apomorphine- and oxytocin-induced yawning and penile erection, whereas estradiol benzoate and progesterone restored only yawning. Estradiol benzoate-induced recovery of yawning was prevented by the antiestrogen tamoxifen (1 mg/kg s.c. once a day for 3 days). In intact rats, progesterone increased and estradiol benzoate decreased apomorphine- and oxytocin-induced yawning without modifying penile erection, although oxytocin-induced yawning was prevented much less by estradiol benzoate than that induced by apomorphine. Testosterone or DHT were ineffective on both responses. Estradiol benzoate inhibition of apomorphine- and oxytocin-induced yawning was prevented by tamoxifen, which per se failed to modify apomorphine and oxytocin responses, as well as by testosterone or progesterone. The present results suggest that apomorphine-and oxytocin-induced penile erection and yawning are endocrine-dependent and differentially modulated by sexual steroids, suggesting that the mechanisms controlling the two behaviors are different even though they are often associated.

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“…Administration of AS can produce EEG activity similar to that of psychostimulants (Itil, 1976;Itil, Cora, Akpinar, Herrmann, and Patterson, 1974;Stenn, Kaliber, Vogel, and Broverman, 1972). Androgens can act on the dopamine reward system in a manner similar to cocaine or other stimulants (Alderson, and Baum, 1981;Goudsmit, Feenstra, and Swaab, 1990;Jalilian-Tehrani, Karakiulakis, LeBlond, Powell, and Thomas, 1982;Mitchell and Stewart, 1989;Kaskin and Kleber, 1989;Vermes, Varszegi, Toth, and Telegdy, 1979). Notably, the mesolimbic dopamine system is often considered the final common pathway for many dependence-producing drugs (Koob and LeMoal, 1997;Koob, 1992;Wise and Bozarth, 1987;Robinson and Berridge, 1993).…”

Section: Are Actions Of 3α-diol At Dopaminergic Neurons Essential Formentioning

confidence: 99%

Some rewarding effects of androgens may be mediated by actions of its 5α-reduced metabolite 3α-androstanediol

Frye

2007

Pharmacology Biochemistry and Behavior

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The abuse of anabolic androgenic steroids (AS) is a growing problem; however, the effects and mechanisms underlying their addictive effects are not well understood. Research findings regarding androgen abuse in people and hedonic effects of androgens in laboratory rats are reviewed. Androgens, like other steroids, can have traditional actions via cognate intracellular steroid receptors, as well as other substrates. Our recent results indicate that testosterone (T) metabolites may have actions in part via γ-aminobutyric acid (GABA) A /benzodiazepine receptor complexes (GBRs) and/ or dopaminergic neurons in the nucleus accumbens, to mediate T's positive hedonic states. This may provide the basis for positive reinforcing effects of androgen seeking and use behavior. Following a comprehensive review of the background literature, our findings are presented that have explored the extent to which metabolites of T mediate euphorogenic effects of androgens by acting in the nucleus accumbens. Then results regarding whether GBRs are necessary substrates for androgens' positive hedonic effects are discussed. Lastly, research that addresses if dopaminergic neurons in the nucleus accumbens are necessary for these effects of androgens are discussed. This review provides a comprehensive examination of the hedonic properties and abuse/addiction potential of androgens and the putative mechanisms underlying these effects.

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Differential effects of gonadal steroids on dopamine metabolism in mesolimbic and nigro-striatal pathways of male rat brain

Cited by 101 publications

References 37 publications

Effects of Orchidectomy on Nigro‐Striatal Dopaminergic Function: Behavioral and Physiological Evidence

Effects of Orchidectomy on Nigro‐Striatal Dopaminergic Function: Behavioral and Physiological Evidence

Apomorphine- and Oxytocin-Induced Penile Erection and Yawning in Intact and Castrated Male Rats: Effect of Sexual Steroids

Some rewarding effects of androgens may be mediated by actions of its 5α-reduced metabolite 3α-androstanediol

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