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Stress et Spermatogénèse

Stress and spermatogenesis

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Le stress, dont le point de départ est cérébral, peut agir sur la spermatogénèse par les voies hormonale ou nerveuse. La voie hormonale aboutit à une baisse de production de LHRH, à une chute des récepteurs à LH des cellules de Leydig et à une diminution de l’activité enzymatique 17α hydroxylase. Ainsi, en cas de stress important et prolongé, la sécrétion de testostérone diminue et la spermatogénèse peut en être affectée. La question de l’influence des stress de faible intensité reste posée.

La voie nerveuse comporte des fibres effectrices à catécholamines qui innervent les différentes parties du testicule. La destruction expérimentale de ces voies entraîne une régression de l’épithélium séminal. En outre, la destruction expérimentale du néocortex antérieur, chez le rat, provoque des altérations de la spermatogénèse. Les étages les plus élevés de la sphère nerveuse pourraient donc participer au contrôle de l’épithélium germinal.

On peut cependant faire l’hypothèse que c’est lorsque la production spermatique est basse qu’un stress momentané peut, en aggravant la situation, devenir nocif. Ainsi, l’impact du stress ou des facteurs psychiques sur la spermatogénèse pourrait n’être que relatif.

Abstract

Stress, which originates in the brain, can influence spermatogenesis hormonally or via the nervous system. The hormonal route commences with the central secretion of Corticotrophin-Releasing Factor, leading to a fall in LHRH production, a decrease in Leydig cell LH receptors and a decrease in 17 a hydroxylase activity. Thus, in the case of major, prolonged stress, testosterone secretion falls, which in turn affects spermatogenesis. However, given that the testosterone threshold required for normal seminiferous epithelium function is significantly less than the mean circulating level of this hormone, the importance of low intensity stress remains unknown.

The nervous route involves catecholaminergic fibres which, in the testis, innervate the Highmore corpus, the vessels, the area adjacent to the Leydig cells, and the basement membrane of seminiferous tubules. The experimental destruction of these fibres leads a regression of the seminiferous epithelium. Moreover, the experimental ablation of the rat anterior neocortex leads to changes in spermatogenesis. Therefore, given that the endocrine system does not seem to be involved in these changes, these results indicate that the highest level of the nervous system may participate in the controlling the germinal epithelium which, all things considered, would tend to support psychosomatic influences.

However, given that the number of spermatozoa varies significantly between ejaculate and independantly of the level of testosterone secretion necessary for normal spermatogenesis, it may be hypothesized that it is only when sperm production is low that temporary stress, in aggravating the situation, becomes deleterious to spermatogenesis. Since, under normal conditions, such periods are short, the role of the influence of stress on spermatogenesis can only be relative. Nevertheless, if variations occur during permanently low sperm production, the likelihood of negative effects is increased. Consequently, the impact of stress or psychological factors on spermatogenesis might well depend upon particular circumstances.

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Correspondence to Maurice Auroux.

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Auroux, M. Stress et Spermatogénèse. Androl. 5, 55–61 (1995) doi:10.1007/BF03034304

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Mots clés

  • spermatogenèse
  • stress
  • testostérone
  • système nerveux

Key-Words

  • spermatogenesis
  • stress
  • testosterone
  • nervous system