The Effects of Testicular Denervation on Spermatogenesis in the Sprague- Dawley Rat

Abstract

In the rat, regression of spermatogenesis during the chronic stages of spinal cord injury (SCI) occurs in the presence of normal function of the pituitary-testis hormone axis, thus suggesting that nonendocrine mechanisms might be involved. The current study examined whether disruption of neural input to the testis contributes to the cascade that leads to the regression of spermatogenesis. Four weeks after denervation of the superior spermatic nerve (SSN), testis weight was 25% lower (p < 0.01) than that of the contralateral sham-operated testis. Defects in spermatogenesis including phagocytosis of mature spermatids, vacuolization of spermatid nuclei, delayed spermiation and incomplete cellular associations were observed in >60% of the tubules. In the remaining 30–40% of tubules, the seminiferous epithelium was severely regressed. While cutting the inferior spermatic nerve (ISN) alone did not affect spermatogenesis significantly, it enhanced the effect of SSN denervation on both spermatogenesis and testis weight (p < 0.01). Spermatogenesis was totally regressed in the SSN/ISN-denervated testes. At this time, quantitatively normal spermatogonial proliferation was maintained in SSN- or ISN-denervated testes. Twelve weeks after surgery, regression of the seminiferous epithelium characterized by absence of proliferating spermatogonia, while undifferentiating spermatogonia were present, was observed in all SSN-denervated testes. At this time, regression of the seminiferous epithelia also occurred in >30% of the tubules in ISN-denervated testes. At both times, serum follicle-stimulating hormone, luteinizing hormone and testosterone levels were normal and >60% of normal testicular testosterone concentrations were maintained in the denervated testes. These results indicate that disruption of neural input to the testis is not a cause for the decrease in spermatogonial proliferation during the acute phase of SCI, but may contribute to the chronic effects of SCI on spermatogenesis.

Testicular Denervation in Prepuberty Rat Inhibits Seminiferous Tubule Development and Spermatogenesis

“…supply has chronic trophic effects on testicular development [12]. This was confirmed in our experiment by the fact that the weights and tubular areas of denervated testes were lower on PD90 than on PD60.…”

“…Thus, the testes are unable to adapt to the changes in air temperature that can inhibit the development of the seminiferous tubules [34]. The nervous supply has chronic trophic effects on testicular development [12]. This was confirmed in our experiment by the fact that the weights and tubular areas of denervated testes were lower on PD90 than on PD60.…”

“…Physical stimulation of this nerve does not have an obvious effect on the testosterone concentration or spermatic blood flow [3]. Rauchenwald et al [7] proved that the ISN is the dominant source of supply to the adult rat testis, but a more recent study showed that ISN transection alone did not affect spermatogenesis [12]. In addition, Frankel et al [2] reported that bilateral ablation of both the SSN and ISN in adult rats had no acute or chronic effects on testicular function.…”

Peptidergic Innervation of Blood Vessels and Interstitial Cells in the Testis of the Cat

“…Thus, testicular volume is significantly smaller in men with a complete spinal cord section including the T12 segment (Chapelle et al, 1988). Spermatogenesis regresses during the chronic stages of spinal cord injury in the rat, even in the presence of a normal pituitary-testis hormone axis, and severe defects of spermatogenesis occur after section of the rat SSN (Chow et al, 2000). On the other hand, an increase in catecholaminergic nerve fibers density has been detected in human testes with Sertoli cell only or with germ cell arrest syndromes (Mayerhofer et al, 1999).…”

Fertility and spermatogenesis are altered in α1b-adrenergic receptor knockout male mice

“…Adrenergic nerve varicosities were located mainly in proximity of the Leydig cells, lamina propria of seminiferous tubules, and perivascular wall (Prince 1992(Prince , 1996, suggesting that the norepinephrine released from sympathetic nerves has multiple sites of action in the control of testicular functions. Disruption of the neuronal input (Chow et al 2000), electrical stimulation of the spermatic nerves (Chiocchio et al 1999) as well as chemical sympathectomy with guanethidine (Rosa-e-Silva et al 1995) or 6-hydroxydopamine (Mayerhofer et al 1990) demonstrated that norepinephrine modulates luteinizing hormone (LH) receptors expression, testosterone output, spermatogenesis, and testicular blood flow. Interestingly, incubation of dispersed testicular cells with norepinephrine or epinephrine significantly enhanced the viability of spermatogenetic cells (Nagao 1989).…”