Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date, the possible functional interaction between the dopaminergic and the somatostatinergic system during the development of the brain is unknown. This study examines whether blockage of brain dopamine receptors during fetal life might influence postnatal somatostatin (SS) receptor development. Pregnant Sprague-Dawley rats were injected intraperitoneally with either haloperidol (2.5 mg/kg/day), which blocks dopaminergic receptors, or saline. The injections were given for 16 days, commencing on the 4th or 5th day after conception (as counted from the appearance of spermatozoa in daily vaginal smear). The administration of haloperidol during gestation did not affect the levels of somatostatin-like immunoreactivity (SLI) in the two brain areas at any of the times studied. However, this treatment resulted in a decrease in the total number of receptors for 125I-Tyr11-SS in frontoparietal cortex and hippocampal plasma membranes in the 14-day-old offspring but not at 21, 35, or 60 days after birth. No significant differences in the apparent SS binding affinity values were seen after fetal exposure to haloperidol. These results suggest that the development of SS receptors in rat frontoparietal cortex and hippocampus can be transitorily delayed by fetal blockage of dopamine receptors.
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PMID:Effect of prenatal dopamine receptor blocking on somatostatin receptor binding in the developing rat brain. 809 41

This study investigated the regulation of growth hormone (GH) release in stallions and tested the hypothesis that the somatotrophic axis influences testicular function. Basal plasma GH concentrations, effects of an experimental decrease of GH release on testicular function and an opioidergic regulation of GH release were investigated in Shetland stallions (n=6). No seasonal variations in plasma GH concentrations were found over a 12-month period. Treatment with the somatostatin analogue octreotid (100mg twice daily over 10 days) caused a decrease in semen motility from 38.7+/-8.4% progressively motile spermatozoa before treatment to 18.3+/-5.4% on day 3 after end of treatment (P<0.05). Values returned to 35.0+/-8.5% on day 5 after treatment. On the last day of octreotid treatment, a hCG stimulation test was performed (3000IU hCG i.v.). The hCG-induced testosterone release was significantly higher in saline treated than in octreotid pretreated animals (P<0.05). Neither plasma GH concentrations nor volume and density of ejaculates, total sperm count, or semen morphology were different between saline and octreotid treatments. Injection of the opioid antagonist naloxone (0.5mg/kg) significantly increased GH release in June (from 1.1+/-0.3ng/ml before to 3.7+/-2.2), while a minor and not significant increase occurred in January. In conclusion, our results indicate a non-seasonal basal GH release with a fine-modulation by season-dependent opioidergic mechanisms in the male horse. A transient decrease in semen motility and hCG-induced testosterone release following ocreotid treatment indicate a role of GH in the regulation of testicular function in stallions.
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PMID:Somatostatin treatment affects testicular function in stallions. 1262 May 89

Normal testicular function is dependent upon hormones acting through endocrine and paracrine pathways both in vivo and in vitro. Sertoli cells provide factors necessary for the successful progression of spermatogonia into spermatozoa. Sertoli cells have receptors for follicle stimulating hormone (FSH) and testosterone which are the main hormonal regulators of spermatogenesis. Hormones such as testosterone, FSH and luteinizing hormone (LH) are known to influence the germ cell fate. Their removal induces germ cell apoptosis. Proteins of the Bcl-2 family provide one signaling pathway which appears to be essential for male germ cell homeostasis. In addition to paracrine signals, germ cells also depend upon signals derived from Sertoli by direct membrane contact. Somatostatin is a regulatory peptide playing a role in the regulation of the proliferation of the male gametes. Activin A, follistatin and FSH play a role in germ cell maturation during the period when gonocytes resume mitosis to form the spermatogonial stem cells and differentiating germ cell populations. In vitro cultures systems have provided evidence that spermatogonia in advance stage of differentiation have specific regulatory mechanisms that control their fate. This review article provides an overview of the literature concerning the hormonal pathways regulating spermatogenesis.
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PMID:Hormonal regulation of spermatogenesis and spermiogenesis. 1840 Apr 89