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SUMMARY
Intact control and sham-operated rats, when given sodium pentobarbitone at 13.30 h on the day of pro-oestrus, mated (controls, 10/12; shamoperated, 13/15) that night and underwent copulation-induced ovulation. However, after removal of the olfactory bulbs only 13 out of 23 pentobarbitone-blocked rats mated. Of the mated animals only six ovulated as compared with ten in the unoperated group and ten in the sham-operated group. The incidence of ovulation in all non-mated animals was low. In addition, the bulbectomized, mated animals which ovulated shed significantly fewer ova than did intact controls and sham-operated rats (6·8 as compared with 11·3 and 13·4, respectively). The incidence of mating in bulbectomized animals was also lower than in sham-operated animals when pentobarbitone was not given (8/16 and 8/11, respectively). Ovulation was essentially complete in all groups except in bulbectomized, mated rats which shed significantly fewer ova. It is suggested that olfactory inputs are important in mediating copulation-induced ovulation in the pentobarbitone-blocked rat and that copulation in the absence of olfactory inputs interferes in some way with the normal sequence of secretion of ovulatory hormone(s) in the non-blocked rat.
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ABSTRACT
Pentobarbitone-blocked pro-oestrous rats were subjected to either limited mating (maximum of 30 mounts), all-night cohabitation with males or stimulation of the vagina and cervix with a glass rod (2 or 5 min) to determine which type of stimulus was most effective in inducing ovulation. All-night cohabitation was the most successful procedure and resulted in 100% ovulation in those rats which mated. Treatment with either phenoxybenzamine, propranolol or pimozide did not interfere with this copulation-induced ovulation whereas methysergide treatment completely blocked copulation-induced ovulation. Administration of atropine resulted in a loss of mating behaviour and these animals therefore did not ovulate. Further experiments provided evidence that administration of atropine also blocked ovulation in response to vaginal stimulation with a glass rod. Pretreatment with methysergide or atropine had no effect upon the percentage of pentobarbitone-blocked, pro-oestrous rats ovulating in response to administration of LH releasing hormone (LHRH). However, those rats given atropine shed significantly fewer ova per rat following LHRH or LH infusion when compared with controls. These results suggest that the synaptic mechanisms responsible for mediating copulation-induced ovulation are different from those mediating steroid-induced ovulation, and that ovarian cholinergic receptors may play a role in ovulation.
J. Endocr. (1984) 100, 361–365
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ABSTRACT
Pure antiandrogens, like flutamide, antagonize androgen action both peripherally and centrally at the hypothalamic–pituitary axis, which leads to an increase in LH and testosterone secretion. A new non–steroidal antiandrogen ICI 176,334 ((2RS)4′-cyano-3-(4-fluorophenylsulphonyl)-2-hydroxy-2-methyl-3′-trifluoromethyl)propion-anilide) has now been discovered which causes regression of the accessory sex organs but does not increase serum concentrations of LH and androgens. ICI 176,334 binds to rat prostate androgen receptors with an affinity around fourfold that of hydroxyflutamide. When administered s.c. concurrently with testosterone propionate (200μg/kg) for 7 days to immature castrated rats, ICI 176,334 (10mg/kg) significantly (P<0.001) inhibited growth of the seminal vesicles and ventral prostate gland. Oral administration of ICI 176,334 at doses of 1, 5 and 25mg/kg for 14 days to adult rats caused a dose–related reduction in accessory sex organ weights but had no effect on the testes. None of these doses caused a significant increase in serum LH and testosterone. Flutamide was around fourfold less potent and significantly increased serum LH and testosterone at the higher doses. ICI 176,334 was well tolerated. ICI 176,334 should, therefore, prove useful for the treatment of androgen–responsive benign and malignant diseases.
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Abstract
Antisera were generated to the synthetic peptides SREWEDS and KELTAE which correspond to residues 315–321 and 332–337 of human chromogranin A (CgA) respectively. KELTAE represents the C-terminal hexapeptide of WE-14, and SREWEDS (residue 316 human CgA Lys/Arg substitution) represents the C-terminal heptapeptide of the Intervening Peptide, located between pancreastatin and WE-14. The antisera were employed to study the occurrence of WE-14 and CgA-derived peptides in human and bovine gastro-entero-pancreatic (GEP) tissues and in a range of human GEP neuroendocrine tumours. Immunocytochemical analyses of normal human and bovine tissues demonstrated that each antiserum immunostained endocrine cells throughout the GEP tract. Variable intensities of immunostaining were detected in neoplastic tissues. Quantitatively, the highest levels of SREWEDS and KELTAE immunoreactivity were detected in pancreatic extracts, with lower levels in gastrointestinal tissues. Elevated levels of each immunoreactant were detected in neoplastic tissues. Chromatographic analysis resolved several SREWEDS-related peptides and a major KELTAE-related peptide that co-eluted with synthetic human WE-14. The present study has demonstrated that CgA is processed to generate distinct peptide products in normal and neoplastic tissues of the GEP system. A single molecular species co-eluting with synthetic human WE-14 was predominant and consistently detected in all the tissues studied.
Journal of Endocrinology (1996) 151, 409–420
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Abstract
Medullary thyroid carcinoma (MTC) is an APUDoma (APUD refers to amine precursor uptake and decarboxylation) arising from the parafollicular cells. Diarrhoea has been reported in some 30% of patients, variously attributed to excess production of calcitonin (CT), serotonin (5-HT), vasoactive intestinal peptide (VIP) or other factors.
The regulatory factors in MTC were examined employing immunocytochemistry and RIA to tumours and their extracts. The patients were followed up for more than 15 years. CT and calcitonin gene-related peptide were universally expressed in all the tumours. The neuroendocrine markers chromogranin A (and its fragments pancreastatin and WE-14), neurone-specific enolase, protein gene product 9·5 and carcino-embryonic antigen were found in the majority of MTCs and might be useful as immunocytochemical markers. 5-HT, substance P, neurokinin A, glucagon and VIP could not be detected, excluding them as candidates in the diarrhoea of MTC.
Journal of Endocrinology (1997) 152, 275–281
