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The effect of right- and left-sided intra-amygdaloid injection of kainic acid on the hypothalamo-hypophyseal-testicular axis was studied in rats. Both right- and left-sided injection of the neurotoxin into the amygdala resulted in a significant decrease in basal testosterone secretion in vitro of both testes and in serum testosterone concentration. In addition, left-sided administration of kainic acid significantly suppressed serum luteinizing hormone level, while right-sided intervention did not alter this parameter. The results of the present study provide further evidence on the involvement of the amygdala in the control of testicular steroidogenesis. Furthermore, the observations suggest functional asymmetry of the amygdala concerning the mechanism of suppressed testosterone secretion.

We recently reported that immature porcine Leydig cells express both somatostatin (SRIF) and SRIF receptor type-2 (sst-2) transcripts. The present study was therefore undertaken to assess whether SRIF might exert autocrine actions on these cells through sst2A receptor, one of the two sst2 isoforms known to exert important neuroendocrine and endocrine functions. Using a polyclonal antibody directed towards the C-terminal tail of the sst2A receptor subtype, receptor immunoreactivity was detected in a subpopulation of Leydig cells and spermatogonia. To address the physiological correlates of this expression we then studied the possible involvement of sst2 receptor in the regulation of testosterone secretion. Functional assays showed that the sst2 agonist octreotide inhibited both basal and hCG-stimulated testosterone secretion by testosterone pretreated Leydig cells. To assess whether sst2 receptor expression might be regulated by testosterone, we performed a semi-quantitative RT-PCR analysis of sst2 mRNA expression in Leydig cells cultured in the presence or in the absence of the androgen. A significant increase in sst2 receptor transcripts was observed in testosterone-treated cells. Taken together, these data suggest that SRIF can inhibit testosterone secretion through the sst2A receptor. The mechanism of the local inhibitory actions of SRIF is probably autocrine since immature porcine Leydig cells express SRIF itself and it might involve testosterone-induced increase of sst2 receptor expression in immature Leydig cells.

The possible involvement of the insular cortex in the neural control of the hypophyseal-testicular axis was studied in male rats. Right- but not left-sided lesion of the insular cortex resulted in a significant decrease in basal testosterone secretion in vitro and serum testosterone concentration. Both right- and left-sided lesions of the insular cortex induced significant increase in serum luteinizing hormone (LH) concentration. Unilateral lesion of the insular cortex on either sides had no effect on serum follicle stimulating hormone (FSH) level. The results indicate that the insular cortex is involved in the control of testosterone and LH secretion. The data further suggest that the right insular cortex plays a predominant role in the control of male endocrine reproductive processes.

The effect of intratesticular administration of serotonin (5-HT), ketanserin (5-HT2 receptor antagonist), and 5,7-dihydroxytryptamine (5,7-DHT) (the neurotoxin that destroys serotoninergic neural elements) on steroidogenesis was studied in immature and adult rats. In adults, bilateral intratesticular injection of 5-HT resulted in a significant decrease in basal but not in hCG-stimulated testosterone secretion and in serum testosterone concentration, whereas ketanserin induced a significant rise in steroidogenesis 1 h post-treatment. There was no effect 1 day after administration of 5-HT or ketanserin, and 7 days after the injection of 5,7-DHT. In immature rats 1 day after bilateral testicular administration of ketanserin, basal testosterone secretion in vitro was significantly suppressed. In immature hemicastrates, local injection of 5-HT resulted (1 day post-treatment) in a significant rise in steroidogenesis while administration of 5,7-DHT decreased testosterone secretion 7 days after the injection of the neurotoxin. The results indicate that in adult rats 5-HT exerts a suppressive, whereas in immature rats, a stimulatory action on steroidogenesis occurs. Data also suggest that, in both age groups, the effect of 5-HT is mediated through 5-HT2 receptors. The observation that in immatures administration of the neurotoxin resulted in an effect similar to that found following the treatment with the receptor antagonist suggests that, in this age group, 5-HT derived from local neural elements might also be involved in the control of 5-HT on Leydig cell steroidogenesis.

Previous studies indicated that in immature rats testicular administration of oxytocin stimulates testicular steroidogenesis. In the present study, testicular treatment with oxytocin (50 ng) was combined with pharmacological or surgical denervation of the testis in hemigonadectomized immature rats. For denervation 5,6-dihydroxytryptamine (160 micrograms/testis), a substance that destroys serotoninergic neuronal elements, was injected intratesticularly or vasectomy was performed, which also includes transection of the inferior testicular nerve. In 9-day-old animals both vasectomy and pretreatment of the testis with 5,6-dihydroxytryptamine prevented the oxytocin-induced rise in serum testosterone concentration. In addition, intratesticular injection of oxytocin combined with vasectomy resulted in a significant increase in in vitro basal testosterone secretion of the testis. A similar effect was not observed in the 5,6-dihydroxytryptamine-pretreated group receiving oxytocin. The results indicate that testicular innervation is involved in the control of local peptide effects, and data further suggest a differential role of these neural elements in intratesticular regulatory processes.