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mise à jour du 6 mars 2003
Neuroendocrinology
1994;59:349-354
lexique
Apomorphine and oxytocin induced penile erection and yawning in intact and castrated male rats : effect of sexual steroids
Maria Rosaria Melis, Alessandro Mauri, AntonioArgiolas
Department of Neuroscience, University of Cagliari, Italy
 
Tous les travaux de MR Melis & A Argiolas 
Tous les travaux de M Eguibar & G Holmgren

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Dopaminergic agonists, such as apomorphine and oxytocin, are among the most potent inducers of both penile erection and yawning in laboratory animals. Several lines of experimental evidence suggest that a hypothalamic dopamine-oxytocin link plays a key role in the expression of such symptomatology and in male copulatory behavior. Interestingly, sexual steroids exert several effects on both central dopaminergic and oxytocinergic systems by acting either at the genomic or membrane level.
 
In particular, estrogens decrease the activity of the majority of hypothalamic dopaminergic neurons, including the incerto-hypothalamic dopaminergic neurons which are thought to play a key role in the expression of the above responses. Estradiol benzoate and progesterone alter the number and/or the affinity of dopaminergic receptors; estradiol benzoate prevents apomorphineinduced yawning, and castration abolishes apomorphine-induced penile erection.
 
Furthermore, estradiol benzoate influences oxytocin-immunoreactive brain systems, and induces the expression of oxytocin receptors in several brain nuclei, especially in the ventromedial nucleus of the hypothalamus, an effect that resembles the induction of oxytocin receptors in the pregnant uterus. Progesterone further enhances estradiol benzoate-induced oxytocin receptors, and is required after estrogen priming for the expression of several effects of oxytocin. Oxytocin receptors are also increased in the ventromedial nucleus of castrated male rats by testosterone, which probably induces this effect after its conversion to estradiol benzoate by brain aromatase. However, progesterone was much less effective in male rats than in female rats. The above results prompted us to study the effect of sexual steroids on apomorphine- and oxytocin-induced penile erection and yawning in intact and castrated male rats.
[...]
 
Discussion
The present results show that apomorphine- and oxytocin-induced penile erection and yawning are endocrine depenilent in male rats. Indeed, castration dramatically decreases both apomorphine- and oxytocin-induced penile erection and yawning. This might be due to the disappearance of testicular testosterone that causes the depletion of brain testosterone and its neural metabolites estradiol benzoate and DHT. However, this explanation is complicated by the finding that testosterone supplementation in castrated rats restores penile erection, but not yawning.
 
The ability of testosterone to restore penile erection selectively is in agreement with the hypothesis that testosterone has a permissive role in the expression of penile erection and sexual behavior, but not yawning. In contrast, the selective restoration of apomorphine- or oxytocin-induced yawning by estradiol benzoate suggests a facilitatory role of this testosterone metabolite in the expression of yawning, but not of penile erection. Estradiol benzoate, however, has been found to be as effective as testosterone in maintaining the copulatory behavior of castrated animals. While the ineffectiveness of progesterone in restoring apomorphine and oxytocin responses in castrated rats was expected because: the brain concentration of this hormone in male rats is related to its adrenal synthesis, and the brain of castrateo male rats contain very low levels of progesterone receptors, the inability of DHT to restore penile erection was surprising. This finding suggests that this testosterone metabolite is not involved in the expression of penile erection or yawning in the rat. However, against this hypothesis a partial recovery of both penile erection and yawning is induced by supplementation with both DHT and estradiol benzoate. This is in agreement with early studies showing that DHT facilitates sexual behavior and penile reflexes in intact male rats, and restores copulation in castrated male rats when given together with estradiol benzoate suggesting that the two steroids act in concert to modulate penile erection and yawning.
 
The mechanisms by which castration prevents and steroid supplementation restores either penile erection and/ or yawning induced by apomorphine or by oxytocin might be related either to a reduced dopaminergic neurotransmission that is reversed by testosterone or estradiol benzoate + DHT, or to a decrease in hypothalamic oxytocin-binding sites reversed by testosterone as well as estradiol benzoate supplementation without altering neuronal immunoreactive oxytocinergic pathways, or both.
 
The above findings support the hypothesis that testosterone and its neural metabolites, estradiol benzoate and DHT, are all necessary for the expression of penile erection 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 oxytocin induced penile erection and yawning are found in intact male rats.
 
Indeed, in intact animals estradiol benzoate prevents and progesterone potentiates yawning, and testosterone does not modify penile erection or yawning. While testosterone ineffectiveness might reflect an already existing maximal permissive role of the steroid on the above responses in the presence of normal levels of circulating testosterone estradiol benzoate prevention of apomorphine-induced yawning may be caused by a decrease in sensitivity and/or in the number of central dopaminergic receptors or by the inhibition of the neuronal targets of dopamine, i.e. oxytocinergic neurons mediating these behavioral responses.
 
However, the latter hypothesis is unlikely because oxytocin-induced yawning is affected much less by estradiol benzoate than that induced by apomorphine, suggesting that:
  1. in intact rats the activity of oxytocinergic neurons mediating penile erection and yawning is not modified significantly by estradiol benzoate, unlike some magnocellular oxytocinergic neurons
  2. that estradiol benzoate-induced oxytocin receptors are not involved in the expression of these behavioral responses.
On the contrary, the potentiating effect of progesterone on apomorphine and oxytocin-induced yawning in intact rats might be due either to an increase in dopaminergic receptors and/or their affinity for the agonist, or to an increased oxytocinergic transmission. The opposite effects and the reciprocal antagonism of estradiol benzoate and progesterone on yawning in intact rats are not surprising, since the opposite effects of the two steroids have been observed in several experimental conditions. Since estradiol benzoate effects are also prevented by the specific nuclear estrogen receptor antagonist tamoxifen, this might be related to opposite functional genomic effects of the two steroids. However, other explanations, such as competition of the two steroids for the same nuclear receptor or combined genomic and non-genomic, ie. membrane effects of the two steroids, cannot be ruled out. In view of the structural similarity between progesterone and testosterone, similar mechanisms might explain the prevention by testosterone of estradiol benzoate inhibition of apomorphine- and oxytocin-induced yawning.
 
In contrast, the failure of DHT to prevent estradiol benzoate effects suggests that this testosterone metabolite does not interfere with estradiol benzoate action either at the genomic level or with estradiol benzoate receptor binding.
 
Taken together, the ability of estradiol benzoate and progesterone to modify apomorphine- and oxytocin-induced yawning but not penile erection in intact rats, and the differential effect of testosterone and estradiol benzoate in restoring penile erection and yawning, respectively. suggest that the two behavioral responses, although often seen in the same experimental conditions, are mediated by neuronal pathways differentially influenced by sexual hormones. The identification of the exact brain sites where sexual hormones act to modify the above responses will help in identifying the neural pathways mediating the expression of penile erection and yawnig.

« It is ironic that testosterone "the male sex hormone," is more closely associated with the yawning rate than with the mounting or intromitting rates » Charles Phoenix
 
 
Sexual steroids exert several effects on both central dopaminergic and oxytocinergic systems by acting either at the genomic or membrane level  
Aging, dominance history, and social behavior in Java-monkey. Veenema HC, Spruijt BM, et al
yawns-canines
credit photo : "Asif A. Ghazanfar and Aristides Arrenberg"
Max Planck Institute for Biological Cybernetics
Tuebingen; Germany.
merci à eux