Search PubMed⌕ Search

Biomedical subjects

C Kordon

Publications and source records attributed to C Kordon.

At least 199 records · Page 11Linked to original sources

Delayed effects of in vivo LHRH immunoneutralization on gonadotropins and prolactin secretion in the female rat.

A single ip injection (0.2 ml) of a rabbit antiserum to LHRH was given at noon on proestrus (day 0) to 4-day cycling rats. A blockade of the preovulatory surge of LH and FSH was observed, as well as inhibition of ovulation; the prolactin (PRL) surge was unaffected. Four days later, palsma LH and FSH were still low and hypoprolactinemia appeared, while the estrous cycle was unaffected. Then, after a transient diestrous period, vaginal smears indicated a pattern of persistent estrus for at least 240 days starting from day 8 after treatment. Hypothalamic LHRH remained low throughout this period, with the exception of a transient rise around day 36; hypothalamic serotonin and dopamine were unchanged. A peak of FSH in serum appeared on day 28 and an elevation of serum LH on day 36; this latter rise was concomitant with the increase of hypothalmic LHRH and with ovarian luteinization. Except for this short period, the ovaries showed a picture of persistent estrus, with large, cystic follicles. During the whole experimental period, basal serum FSH levels were higher than those of LH. Pituitary FSH and LH contents remained in the range usually found during the normal estrous cycle. Starting from the 8th day after treatment, a marked hyperprolactinemia appeared. Serum estradiol and progesterone were assayed on days 10 and 40 after injection; no significant increase in either steroid was observed on day 10, but on day 40 the levels of estradiol increased to values similar to those of progestrus, while progesterone showed only a small, but significant, increase. Thus, a single injection of LHRH antiserum (AS) in a normal cycling rat provoked a long-term alteration in hypothalamic function. The results so far obtained suggest that the long-lasting hyperprolactinemia induced by this treatment, might be due to an abnormal ovarian secretion.

Animals↗

Participation of serotonin in the phasic release of LH. I. Evidence from pharmacological experiments.

Subcutaneous implantation of a silastic tubing containing crystalline estradiol in castrated female rats results in a circadian rhythm of LH release. Under such conditions, blockade of serotonin (5-HT) biosynthesis by p-chlorophenylalanine (PCPA) completely inhibits the afternoon elevation of plasma LH. Gonadotropin peaks remain inhibited as long as the concentration of the transmitter is effectively depleted. Intraperitoneal administration or intraventricular infusion of minute doses of the immediate precursor of the amine, 5-hydroxytryptophan (5-HTP), results in the reappearance of the next afternoon rise of plasma gonadotropin, whenever hypothalamic levels of 5-hydroxyindole acetic acid (5-HIAA), the main metabolite of 5-HT, are significantly increased over their value in PGPA-treated animals. The administration of methiothepin, a 5-HT receptor blocker, 9 hours of more prior to the next expected LH rise, similarly inhibits the cycle, whereas a dopamine receptor inhibitor has no effect under the same time conditions. We have concluded that serotoninergic neuron systems can have a positive, permissive effect on the transfer of neural information resulting in phasic gonadotropin release; this action of the amine is different from, but not contradictory to, the known inhibitory effect of 5-HT on the release of LHRH from the median eminence.

Animals↗

In vitro release of luteinizing hormone-releasing hormone (LHRH) from rat mediobasal hypothalamus: effects of potassium, calcium and dopamine.

A suitable preparation to study the effect of dopamine (DA) on in vitro LHRH secretion is presented. Enzymatic degradation of LHRH in the incubation medium is completely inhibited by bacitracin (2 X 10(-5) M). Ahigh potassium concentration (56mM) induces an increase in LHRH release from entire pieces of mediobasal hypothalamus (MBH), but not from a synaptosomal pellet; this release is inhibited when calcium is omitted. The depolarization-induced LHRH in the MBH. In contrast, DA (10(-6)M) is not effective in vitro on MBH from ovariectomized rats but induces a fast release of LHRH from MBH of normal male and estradiol-pretreated ovariectomized rats. The preparation presented here appears to be of great interest in investigating amine-steroid-LHRH interactions at the cellular level.

Animals↗

Distribution of LH-RH in subcellular fractions of the basomedial hypothalamus.

Subcellular fractionation of the mediobasal hypothalamus (MBH) and other brain structures was achieved by differential and sucrose gradient centrifugation. The fractions were monitored by measuring lactate dehydrogenase (LDH) activity (a marker for the soluble cytoplasmic fraction) and by electron microscopic examination. The luteinizing-hormone-releasing-hormone (LH-RH) content of the fractions was evaluated both by bioassay and radioimmunoassay. Significant amounts of LH-RH were found only in the MBH and in an anterobasal location corresponding to the organum vasculosum of the lamina terminalis. Within these areas, LH-RH activity was present in the first supernatant (homogenate with the exclusion of the nuclear pellet). Seventy percent of the LH-RH activity was recovered in the crude mitochondrial fraction. After further fractionation on a sucrose gradient, the distribution of LH-RH was parallel with that of LDH activity. Since LDH is predominantly located in the synaptosomal soluble fraction, it is concluded that the vast majority of LH-RH is contained within nerve endings. This finding is consistent with cyto-immunological data on the distribution of the neuropeptide in the rat hypothalamus.

Animals↗

Differential effects of hypothalamic deafferentation upon luteinizing hormone-releasing hormone in the median eminence and organum vasculosum of the lamina terminalis.

Complete deafferentation of the medial basal hypothalamus (MBH) was performed in male rats to ascertain the location of the cell bodies of nerve terminals containing luteinizing hormone-releasing hormone (LH-RH) in the external layer of the median eminence and the organum vasculosum of the lamina terminalis (OVLT). Radioimmunoassayable LH-RH in the MBH decreased to one-fourth of the control value 10 days after complete deafferentation, whereas, no change was observed in an area coextensive with the OVLT. Immunohistochemical staining of LH-RH appeared less intense within the median eminence of deafferented animals but was normal in the OVLT. These results suggest that the cell bodies of neurons producing LH-RH found in terminals in the OVLT lie outside the MBH. The possible explanations for the decreased LH-RH content in the median eminence are discussed.

Animals↗