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Biomedical subjects

S Taleisnik

Publications and source records attributed to S Taleisnik.

At least 55 records · Page 3Linked to original sources
PubMed1976

Inhibition of gonadotropin secretion induced by stimulation of thalamic nuclei.

The effect of electrochemical stimulation (anodic current, 100 micronA/30 sec) of thalamic nuclei was studied in nonanesthetized freely-behaving rats bearing chronic implanted electrodes and plastic cannulae inserted into the jugular vein for blood sampling. Stimulation of the anterior thalamic nuclei, the nucleus (n.) mediodorsalis thalami (MD) and the n. posteromedianus thalami at 2 p.m. on the day of proestrus prevented spontaneous ovulation and the release of LH which takes place on that day. No effect on ovulation or LH release was observed after stimulation of the n. lateralis thalami, the n. ventralis thalami or other thalamic nuclei or after passing a cathodic current through the n. MD. Stimulation of the n. MD resulted also in a significant decrease of the elevated serum LH levels found after an injection of progesterone into ovariectomyzed estrogen-primed rats. These results indicate that nuclei of the medial thalamic region are capable of inhibiting LH secretion. No stimulatory influence of LH release was observed after thalamic stimulation in ovariectomized estrogen-treated rats.

Animals↗
PubMed1976

Interaction between oestrogen and gonadotrophin- releasing hormone on the release and synthesis of luteinizing hormone and follicle-stimulating hormone from incubated pituitaries.

The release and synthesis of LH and FSH were studied in adenohypophyses from ovariectomized rats incubated for a period of 4 h in flasks containing 1 ml Eagle's medium. One hemipituitary was used as the experimental gland and the other half served as a control. Glands from ovariectomized untreated animals showed a spontaneous release of LH and FSH and the amount of hormones released (per mg gland) by both the hemipituitaries was not significantly different. Also the content of the hormones at the end of the incubation period was similar in both halves. Gonadotrophin-releasing hormone (Gn-RH) added to the incubation medium stimulated the release of LH and FSH. A dose--response relationship was obtained between doses of 0-51 and 8-00 ng/ml medium. Although lower doses were required to increase the release of LH, the amount of FSH released was higher when expressed as a percentage of gland content. Pituitary glands from ovariectomized rats treated with 5 mug oestradiol benzoate 24 h before being killed showed an increase in sensitivity to Gn-RH, but the response decreased when oestrogen was injected 2 h before death. Also the addition of oestradiol-17beta to the incubation medium inhibited LH and FSH release induced by Gn-RH. Gonadotrophin-releasing hormone increased the spontaneous synthesis of LH and FSH observed in the incubated pituitaries. This effect of Gn-RH was stimulated by the injection of oestrogen into the donor animals whereas administration of oestrogen into the medium enhanced the synthesis of LH and partially inhibited that of FSH. These results provide evidence for a dual effect of oestrogen on the release of LH and FSH induced by Gn-RH. They also show that synthesis of gonadotrophic hormones was favoured by oestrogen or by increased gonadotrophin release.

Animals↗
PubMed1971

Regulation of formation and proposed structure of the factor inhibiting the release of melanocyte-stimulating hormone.

Microsomal preparations from the stalk median eminence of female rats are shown to contain an enzymic activity that is responsible for the formation of MSH-release-inhibiting factor (MSH-R-IF). The amount of this activity remains constant throughout the estrous cycle. The corresponding mitochondrial preparations from the stalk median eminence contain another enzymic principle, estrous cycle-dependent, which competes with the enzyme present in the microsomal preparation for the same "substrate", and can thereby prevent the formation of MSH-R-IF. Several neurohypophyseal hormones, analogs, and peptide intermediates have been tested for their intrinsic MSH-R-IF activity and for their ability to be transformed into MSH-R-IF by incubation with microsomal preparations of stalk median eminence from male rats; it is concluded that the enzyme responsible for the formation of MSH-R-IF is an exopeptidase and that the release-inhibiting factor itself is a tripeptide. Oxytocin is converted by the incubation to (L)-prolyl-(L)-leucylglycinamide; nanogram amounts of this tripeptide inhibit the release of MSH from the pituitary both in vivo and in vitro.

Animals↗