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R F Weick

Publications and source records attributed to R F Weick.

At least 37 records · Page 2Linked to original sources

A reevaluation of the refractory period following the estrogen-induced luteinizing hormone surge in the rhesus monkey.

A refractory period of 6-8 days following the estrogen-induced luteinizing hormone (LH) surge in the rhesus monkey has been reported, the estrogen having been applied as injections of estradiol benzoate. This was reinvestigated using Silastic capsules filled with estradiol-17-beta. Mature intact female rhesus monkeys were given two successive exposures to estrogen, each of 48 h duration. In one experiment the second exposure started 4 days after the capsules were first implanted (2 days after removal), in the second experiment, 3 days after implantation (1 day after removal). LH surges were seen in response to both estrogen treatments in both experiments. The results suggests that a period of exposure to relatively low estrogen levels is required before a second LH surge can be elicited. This period of time can be as short as 24 h.

Animals↗

Hypothalamic and extrahypothalamic mediation of pulsatile discharges of luteinizing hormone in the ovariectomized rat.

Various hypothalamic lesions were placed in long term ovariectomized rats, and their effects on pulsatile discharges of LH were noted in order to determine which neural regions are involved in the control of this mode of LH secretion. Complete hypothalamic deafferentiation did not affect pulsatile patterns of LH secretion unless the anterior portion of the cut also lesioned the anterior portion of the arcuate nuclei, in which case pulsatile LH discharges were completely blocked. Pulsatile LH secretion was not blocked by bilateral electrolytic lesions placed in ventromedial, paraventricular, or suprachiasmatic nuclei or anterior or posterior portions of the arcuate nuclei, although the nuclei were not completely destroyed by the lesions. When bilateral electrolytic lesions of the anterior portions of the arcuate nuclei were combined with anterior hypothalamic deafferentation, however, pulsatile discharges of LH were completely blocked. These results suggest that two pathways can stimulate the pulsatile mode of LH secretion independently of each other. One of these pathways involves the arcuate nuclei and possibly nearby structures, while the other appears to include extrahypothalamic structures and to enter the hypothalamus anteriorly.

Afferent Pathways↗

Acute effects of adrenergic receptor blocking drugs and neuroleptic agents on pulsatile discharges of luteinizing hormone in the ovariectomized rat.

Blood samples were taken every 5 min for a 3-h period from ovariectomized (OVX) adult rats bearing chronic venous catheters. After 1 h of sampling, an experimental drug was injected through the sampling catheter. The neuroleptics, chlorpromazine and haloperidol, blocked pulsatile discharges of luteinizing hormone (LH) in some animals, for periods of 65-120 min, as did the alpha-adrenergic receptor blockers, phenoxybenzamine and phentolamine. Pimozide, a more specific dopaminergic blocking agent, had less effect, while neither the beta-adrenergic receptor blocker, propranolol, nor the control treatments had any influence on the pulsatile LH patterns. The temporal pattern of inhibition of pulsatile discharges of LH by these drugs is more rapid than the inhibition caused by estrogen treatment in the OVX rat. These results suggest the presence of alpha, but not beta, adrenergic elements in the pulsatile mode of LH release in the OVX rat. They do not support the presence of dopaminergic elements, but neither do they conclusively deny it.

Animals↗

Effects of estrogen and progesterone on pulsatile discharges of luteinizing hormone in the ovariectomized rat.

The effects of both acute and chronic systemic administration of estrogen and progesterone on pulsatile discharges of luteinizing hormone were observed in ovariectomized rats. Intravenous injection of 10 microgram of 17beta-estradiol resulted in a gradual decrease in plasma luteinizing hormone (LH) concentrations but did not completely block the pulsatile discharges. Subcutaneous implantation of Silastic capsules containing 17beta-estradiol caused similar decreases; plasma LH concentrations decreased for the first 6 h but periodic increases continued, with nearly complete suppression of such pulsatile discharges by 24 h. Such inhibition was maintained for the 14-day course of the experiments. Progesterone alone, whether administered by Silastic capsule or by daily subcutaneous injection in oil, was without apparent effect on either plasma LH concentrations or temporal patterns of the hormone. Further, progesterone combined with 17beta-estradiol was little, if any, more effective in this regard than estradiol alone. These results indicate that estrogen is an effective feedback signal inhibiting pulsatile release of LH in the rat and that progesterone alone has little, if any, influence in this regard.

Animals↗

Pulsatile discharges of luteinizing hormone in the ovariectomized rat during the 24-hour day.

Blood samples were taken every 5 min for a 2-h period commencing at 09.00 h or epsilon 13.00 h from long-term ovariectomized (OVX) rats under regular lighting conditions (lights on 05.00-19.00 h), and commencing at 09.30 h or 14.00 h from long-term OVX rats under reversed lighting conditions (lights on 18.00-08.00 h), the latter equivalent to starting sampling at 20.30 h or 01.00 h under regular lighting. Five rats were used in each group, and luteinizing hormone (LH) was measured in duplicate aliquots of each sample by radioimmunoassay. Pulsatile increases in plasma LH concentrations were observed in all 20 animals, and mean, peak, and nadir plasma LH concentrations for each group did not differ between sampling periods. Similarly, the time of day did not affect the frequency at which pulsatile discharges of LH occurred. These data suggest that pulsatile discharges of LH in long-term OVX rats occur throughout the 24-h day.

Animals↗

A comparison of the disappearance rates of luteinizing hormone from intact and ovariectomized rats.

Hypophysectomy was performed on intact female rats during the proestrous LH surge and on ovariectomized rats, and plasma concentrations of LH were measured every 5 min for approximately the next hour. The disappearance rate of LH from ovariectomized rats corresponded to an initial half-life of 23.1 +/- 2.9 min, which is within the range previously reported for this species. The disappearance of LH from intact rats, however, corresponded to an initial half-life of 13.7 +/- 0.7 min. In a second experiment, blood was taken from ovariectomized rats and from intact female rats during the LH surge. The sera were injected iv into hypophysectomized female rats (with ovaries intact) bearing chronic venous catheters, and plasma concentrations of LH were measured every 5 min for the next hour. LH from ovariectomized rats disappeared at a rate corresponding to an initial half-life of 22.7 +/- 2.2 min, while the half-life for LH from proestrous intact rats was 13.4 +/- 1.2 min. These results suggest a change in the circulating form of LH following ovariectomy, in that LH in the ovariectomized rat is cleared more slowly. Further, it appears that LH is removed from the circulation of the intact rat at a higher rate than has previously been reported.

Animals↗