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Biomedical subjects

Y Koch

Publications and source records attributed to Y Koch.

At least 55 records · Page 3Linked to original sources

Release of thyrotropin releasing hormone into hypophysial portal blood is high relative to other neuropeptides and may be related to prolactin secretion.

The amount of immunoreactive TRH released into hypophysial portal blood of female rats was about 2 orders of magnitude greater than gonadotropin releasing hormone and somatostatin. The turnover of TRH, as high as 80% of the total hypothalamic content per hour, was also much greater than that of any other known peptide. TRH release increased during the expected proestrous surge of prolactin and also in some animals during suckling.

Animals↗

Variations in the number of pituitary LHRH receptors correlated with altered responsiveness.

Isolated pituitary cells from metestrous, ovariectomized (OVX), and ovariectomized-estradiol treated (OVX-EB) rats were employed to study the gonadotrophin response to luteinizing hormone-releasing hormone (LHRH) challenge and to quantitate LHRH receptors, using a labeled LHRH analog. Ovariectomy (3-4 weeks post castration) resulted in a reduction of LHRH receptor concentration from 34.4 +/- 2.1 in metestrous females to 14.3 +/- 0.9 fmoles/10(6) cells. Concomitantly, the luteinizing hormone (LH) response to a near-maximal dose of LHRH (5 ng/ml) decreased from a 3-fold stimulation in intact females to 1.13-fold stimulation in cells from OVX rats. Replacement therapy with EB (50 ug/rat for 2 days) to OVX rats restored LH response and LHRH binding sites (a 2.5-fold stimulation in LH secretion and 32.0 +/- 2.1 fmoles/10(6) cells, respectively). The LH response to LHRH stimulation was not altered after one day of EB treatment although the number of LHRH binding sites was increased. The changes in the number of LHRH binding sites were not accompanied by any alterations in the affinity of the LHRH analog (K3 approximately equal to 0.5 X 10(-9)M). It is concluded that variations in LHRH receptor number reflect the degree of pituitary sensitivity to LHRH and it may suggest that LHRH and estradiol modulation of gonadotropin release is mediated by these receptors.

Animals↗

Histidyl-proline diketopiperazine: its biological role as a regulatory peptide.

Histidyl-proline diketopiperazine [cyclo(His-Pro)] is a metabolite of thyrotropin releasing hormone (TRH). This review summarizes the literature concerning cyclo (His-Pro) and, in addition, some studies dealing with TRH and other peptide that are considered of interest. The enzymes concerned with the metabolism of TRH are discussed. Distribution studies of peptides by immunological methods show that, while TRH is concentrated in synaptosomes, cyclo (His-Pro) is not, suggesting that cyclo (His-Pro) is not a classical neurotransmitter. Rat brain contains approximately three times as much cyclo (His-Pro) as TRH, mainly localized in the pituitary and hypothalamus. While the TRH is found in a free form, the cyclo (His-Pro) is bound to a carrier of molecular weight approximately 70,000. While specific membrane receptors for TRH have been detected in pituitary cells, no such receptors for cyclo (His-Pro) have yet been found in brain or pituitary; however, there is a specific binding of cyclo (His-Pro) to adrenal cortex membranes. Both TRH and cyclo (His-Pro) have effects in the central nervous system or pituitary. These include effects on prolactin release, thermoregulation, CNS depression, stereotypic behavior and cyclic nucleotide levels. Possible mechanisms and interrelations of these effects are discussed.

Animals↗

Luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in human and bovine milk.

Two hypothalamic peptide hormones, luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH), have been isolated from human milk and bovine colostrum. Acidified methanolic extracts, prepared from human milk, bovine colostrum and rat hypothalami, as well as synthetic LHRH and TRH markers were subjected to high-pressure liquid chromatography (HPLC). The eluates were tested for the presence of LHRH and TRH by specific radioimmunoassays. It was found that milk extracts contain significant amounts of LHRH (3.9 - 11.8 ng/ml) and TRH (0.16 - 0.34 ng/ml), which comigrate with the corresponding marker hormones and with those of hypothalamic origin. The HPLC-purified LHRH from both human and bovine milk was bioactive in a dose-response manner similar to synthetic LHRH.

Animals↗

A novel method for localization of gonadotropin releasing hormone receptors.

Two 125I-labeled analogs of GnRH, [acidobenzoyl-D-Lys6]GnRH (I) and [D-Lys6]GnRH (II) were used for the localization of GnRH receptors in pituitary cells. The analogs exhibited high binding affinity to pituitary membrane preparations and after photoactivation (analog I) or cross-linking with glutaraldehyde (analog II), these analogs are bound covalently to pituitary cells. The distribution of the labeled hormones by light and electron microscopic autoradiography indicated that after exposure of pituitary cells to 125I-labeled hormones at 4 C (90 min), most of the labeled hormones were associated with the cell surface membrane, while at 37 degrees C (30 min) most of the cell-bound labeled hormones were internalized.

Animals↗

Bisexual behavior in male rats treated neonatally with antibodies to luteinizing hormone-releasing hormone.

For investigating the possibility that the neuropeptide luteinizing hormone-releasing hormone (LHRH) is involved in the process of sexual differentiation, male rat pups were injected on Days 1 and 3 of life with specific antibodies to LHRH (AB-LHRH); control rats were treated with normal rabbit serum (NRS). At maturity, males treated with AB-LHRH were as fertile as controls, and their amount and intromission latencies and the postejaculatory interval were extended only slightly. However, they showed high levels of lordotic behavior, including ear wiggling, when castrated and primed with estrogen or with estrogen plus progesterone. Testosterone propionate, administered neonatally together with AB-LHRH, did not reverse these effects. There was no evidence that neonatal treatment with antiserum to LHRH affected testosterone levels, as measured by radioimmunoassay. Males treated with AB-LHRH and castrated as adults did not respond to estrogen priming by releasing a surge of luteinizing hormone, a result indicating that they did not possess the female type of gonadotropin regulation. These findings indicate that neutralization of endogenous LHRH during neonatal life selectively blocks defeminization of behavior without affecting the process of masculinization.

Animals↗

Ontogeny of the sensitizing effect of oestradiol and luteinizing hormone releasing hormone on the anterior pituitary gland of the female rat.

The ontogeny of the facilitatory effect of oestradiol and luteinizing hormone releasing hormone (LH-RH) on the responsiveness of the anterior pituitary gland to LH-RH has been studied in vitro using pituitary glands from female rats age 15, 17, 20, 31, 35 and 38 days. The facilitatory effect of oestradiol was already well established by day 15, while the facilitatory effect of LH-RH (priming effect) developed only after day 17. Although it increased the overall response of the gland to LH-RH, oestradiol did not selectively enhance the priming effect of LH-RH. Both the effect of oestradiol and LH-RH reached a peak on day 25, 7 days before vaginal opening in this colony, and, as assessed by measuring pituitary LH contents, were not dependent upon the synthesis of LH. These data show that different mechanisms may be involved in the facilitation of pituitary responsiveness by oestradiol and LH-RH, but that both mechanisms appear to depend more upon an increase in the sensitivity of the receptor/release apparatus rather than in the gonadotrophin content of the gonadotrophs.

Animals↗

Chemical and enzymatic changes in the cell walls of Candida albicans and Saccharomyces cerevisiae by scanning electron microscopy.

Candida albicans and Saccharomyces cerevisiae cells were examined by scanning scanning electron microscopy before and after extraction of the mannans of the cell wall. The surfaces of control cells were smooth; after mannan extraction they were rough and showed erosions which were particularly striking within the area of the scars. Helicase digested irregular holes through the cell wall within 20 min; these increased in size during an additional 40 min of digestion. These holes were not localized in or on the bud scars, which remained intact even after the long digestion period. The results were used to construct a model for yeast cell wall structure.

Candida albicans↗

Demonstration of prolactin-releasing activity in the pigeon.

The capacity of the pigeon pituitary gland to release prolactin was investigated in vivo, to evaluate its hypothalamic regulation and to establish the dominant hypothalamic factor for prolactin secretion. After 3 days of systemic administration of some physiological and pharmacological agents, followed by 2 consecutive days of local intradermal injections of prolactin into their crop sacs, the crop mucosa was scraped, dried and weighed. The substances tested were: oestradiol and tamoxifen (antioestrogen), thyrotophin-releasing hormone (TRH) and anti-TRH serum, perphenazine (releases prolactin in mammals) and bromocriptine (suppresses prolactin in mammals). Prolactin and anti-prolactin serum were tested as controls. While prolactin markedly proliferated and anti-prolactin serum significantly inhibited the mucosal weight, oestradiol, TRH and perphenazine dramatically depressed proliferation of the mucosa, suggesting that prolactin secretion was inhibited. Tamoxifen, anti-TRH serum and bromocriptine significantly increased the proliferation of the crop mucosa, indicating an increase in the endogenous release of prolactin. Since the effect of these substances on prolactin release in the pigeon is the opposite from their well-established effects in mammals, these results suggest, in a specific and homologous model, that the dominating regulator for prolactin in the pigeon is contrary to that in the mammal, namely prolactin-releasing factor, and that TRH may play a significant role in the physiological regulation of prolactin secretion.

Animals↗

Immunization against gonadotrophin-releasing hormone: histopathological and hormonal changes in the female rat.

Immunization of female rats against gonadotrophin-releasing hormone (GnRH) resulted in cessation of the oestrus cycles, undetectable serum gonadotrophin levels and a reduction of pituitary gonadotrophin stores and of hypothalamic content of GnRH. Immunization abolished the post-ovariectomy rise in serum levels and in pituitary content of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) without affecting prolactin levels. This suggests that GnRH is involved in the regulation of synthesis as well as the secretion of LH and FSH. Histopathological changes were found in the pituitary, ovaries and uterus of the immunized rats. A marked reduction in the number of gonadotrophs as well as a small decrease in the size of other cells was observed in the pituitaries of rats having high anti-GnRH titres. Rats immunized 5 weeks before castration showed a marked reduction in the number and in the size of castration cells. The ovaries exhibited various degrees of atrophy which were correlated with the anti-GnRH titres. Rats with high anti-GnRH titres revealed extensive atrophy of stromal cells with disappearance of large follicles and corpora lutea; ovaries of rats with low titres of antibodies exhibited small corpora lutea and larger follicles, some of which were cystic. Uteri of rats having high titres of anti-GnRH were severely atrophied with cystic glandular dilation. Uteri of rats with low anti-GnRH titres showed squamous-cell metaplasia and fibrosis of the endometrial stroma.

Animals↗