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Biomedical subjects

C A Blake

Publications and source records attributed to C A Blake.

At least 73 records · Page 4Linked to original sources
PubMed1981

Further studies on the effectiveness with which exogenous luteinizing hormone and follicle-stimulating hormone stimulate the release of endogenous follicle-stimulating hormone during the rat oestrous cycle.

The effects of exogenous rat LH or FSH on the release of endogenous FSH in the cyclic rat have been investigated. Rats were administered phenobarbitone to block the spontaneous increases in gonadotrophins in plasma during pro-oestrus and oestrus and then cannulated through the jugular vein or cannulated and hypophysectomized during the late morning or early afternoon of pro-oestrus. Comparison of patterns of plasma FSH in hypophysectomized and intact rats after i.v. injection of 0.5 micrograms FSH at 17.00 h suggested that exogenous FSH stimulated the release of endogenous FSH in less than 5 h. Intravenous LH (2 micrograms at 16.00 and at 18.00 h) raised the level of FSH in plasma between 2 and 6 h after the first injection of LH. Both gonadotrophins stimulated FSH release by the pituitary gland during the morning of oestrus. Comparison of patterns of plasma FSH in hypophysectomized and intact rats after i.v. injection of 0.25 or 0.05 micrograms FSH at 14.00 h suggested that the latency between FSH injection and stimulation of some FSH release by the pituitary gland is as short as 2 h. Intravenous LH (3, 4 or 9 micrograms) at 14.00 h did not increase the level of FSH in plasma within 2 h and was only minimally effective in raising the level within 4 h. Intravenous LH (2 micrograms at 16.00 and at 18.00 h) on the afternoon of dioestrus day 2 was nearly as effective in increasing the levels of FSH in plasma as it was when administered to pro-oestrous rats. This procedure did not raise the plasma levels of FSH in rats used on dioestrus day 1. The results suggest that in the phenobarbitone-blocked, pro-oestrous rat (1) a small increase (less than that observed spontaneously) in plasma rat FSH during pro-oestrus is effective in stimulating FSH release by the pituitary gland, (2) an increase in plasma rat FSH can exert positive feedback on its own secretion within 2 h and (3) a large increase in plasma rat LH is not very effective in increasing the plasma level of FSH over a period of 4 h. The results also suggest that the spontaneous increase in plasma levels of FSH and, to a lesser extent, of LH is involved in causing the selective phase of FSH release which occurs during late pro-oestrus and the morning of oestrus, and that LH and FSH act differently, but not necessarily by way of a different mechanism, to stimulate release of FSH by the pituitary gland.

Animals↗
PubMed1981

Plasma prolactin and progesterone responses to mating are altered in ages rats.

The effects of varying amounts of copulatory stimulation on patterns of plasma concentrations of prolactin and progesterone were evaluated in 3- and 12-month-old female rats. The 12-month-old group included rats which still exhibited oestrous cycles and rats in persistent vaginal oestrus (PVO). The extent of copulatory stimulation was defined by the number of intromissions received during mating: less than or equal to 5, 15 or greater than 50. Blood samples were drawn over the 8 days after mating through a cannula inserted into the right external jugular vein. Plasma from the samples was assayed for prolactin and progesterone. In aged but still cyclic rats, pregnancy rates were positively correlated with the number of intromissions received during mating. Only one rat in PVO became pregnant. All animals which became pregnant and rats in PVO which, after mating, exhibited a disruption of the pattern of PVO, showed the nocturnal surge of plasma prolactin characteristic of pregnant and pseudopregnant rats. While these surges persisted until day 8 after mating in pregnant animals, they were absent by this time in the rats in PVO. Prolactin surges were present in some but not all of the aged rats which did not become pregnant. Progesterone concentrations were raised in all pregnant animals except the one pregnant rat in PVO and, while not related to the number of intromissions, concentrations were higher 8 days after mating in young compared with those in aged pregnant rats. Plasma progesterone was low in rats in PVO regardless of disruption of the pattern of PVO. We have concluded that the failure of limited copulatory stimulation to induce pregnancy in older rats results, at least in part, from its failure to initiate nocturnal prolactin surges. Nevertheless, our data suggest that matings which are not experimentally limited should provide ample stimulation to establish such surges. Although reduced plasma concentrations of prolactin and progesterone at pro-oestrus and reduced plasma progesterone through part of gestation may contribute to decreasing fertility in aged rats, other unidentified factors appear to be involved in mediating the capacity of extensive copulatory stimulation to induce pregnancy in these animals.

Aging↗
PubMed1981

Effects of oestradiol, hypothalamic extracts and luteinizing hormone releasing hormone on rat anterior pituitary gland gonadotrophin release in vitro before and after the preovulatory luteinizing hormone surge at pro-oestrus.

Changes at the anterior pituitary and/or hypothalamic levels which result in selective FSH release during late pro-oestrus in the cyclic rat were investigated. The possible involvement of decreasing serum concentrations of oestrogen during pro-oestrus in such changes was studied. Rats were decapitated at 12.00 h on pro-oestrus, before the onset of the LH surge and first phase of FSH release, or at 24.00 h on pro-oestrus, shortly after the onset of the second or selective phase of FSH release. Other rats were given oestrogen (OE2) at 14.00 h and killed at 24.00 h pro-oestrus. Paired hemi-anterior pituitary glands were incubated with vehicle or OE2 with or without synthetic LH-releasing hormone (LH-RH) or hypothalamic acid extracts prepared from rats killed at 12.00 or 24.00 h on pro-oestrus. At 24.00 h pro-oestrus, serum FSH concentration was high while serum LH concentration was low regardless of whether rats were given OE2. Glands collected and incubated at 24.00 h released more FSH and less LH than did glands collected and incubated at 12.00 h pro-oestrus. Administration of OE2 in vivo and/or in vitro did not affect these responses. The increments in LH and FSH release attributed to LH-RH or hypothalamic extracts in the glands incubated at 24.00 h were not different from those of the glands incubated at 12.00 h. Also, the hypothalamic extracts prepared from rats killed at 24.00 h were no more effective than the extracts prepared from rats killed at 12.00 h in releasing LH or FSH from glands incubated at 12.00 or 24.00 h pro-oestrus. Administration of OE2 in vivo caused a small suppression of LH-RH-induced FSH release. We suggest that a change occurs at the level of the anterior pituitary gland during the period of the LH surge and first phase of FSH release to increase basal FSH secretion selectively and cause, at least in part, the second phase of increased serum FSH. This change is not mediated by a decrease in serum oestrogen concentration. We failed to observe any evidence that LH-RH causes preferential FSH release during late pro-oestrus or that a hypothalamic peptide with a preferential FSh releasing ability is involved in FSH release at this time.

Animals↗
PubMed1981

Effects of hypothalamic arcuate nucleus lesions on pulsatile luteinizing hormone concentration in ovariectomized rats.

We investigated the effects of hypothalamic arcuate nuclei destruction on the postovariectomy rise in plasma luteinizing hormone (LH) concentration and the pulsatile LH release mechanism in ovariectomized rats. Rats were injected with 1, 2, or 4 mg/g body wt of L-monosodium glutamate (MSG) on Days 1, 3, 5, 7, and 9 of life to lesion the arcuate nuclei. They were then ovariectomized as adults and used 2 or 4-8 weeks later. Serial blood sampling at 10-min intervals and measurement of plasma LH concentration revealed elevated plasma LH levels which fluctuated in a pulsatile fashion in all control and 1 and 2 mg/g/MSG-treated rats. In 4 mg/g MSG-treated rats, plasma LH levels were lower than in controls of both time periods after ovariectomy due to a decrease in the amplitude and/or frequency of LH pulses. Phenobarbital was administered to all 4- to 8-week ovariectomized rats to block endogenous pulsatile LH release. In phenobarbital-blocked rats, three sequential iv injections of LH releasing hormone (LHRH) caused substantial elevations in plasma LH concentrations even in the 4 mg/g MSG-treated animals which had low plasma LH concentrations during control bleedings prior to the injection of phenobarbital. The results indicate that the postovariectomy rise in plasma LH concentration and the associated pulsatile LH release mechanism are functional in rats with extensive arcuate nucleus lesions. The diminution in the rise in plasma LH levels and the decreased amplitude and/or frequency of LH pulses in the MSG-treated rats is likely due to a diminution in hypothalamic LHRH release.

Animals↗
PubMed1980

Plasma LH patterns after LHRH infusion in long-term, unanesthetized ovariectomized rats. Evidence for neural control of the pulsatile LH phenomenon.

Experiments were conducted in vivo to investigate further if the control of the pulsatile plasma LH phenomenon in ovariectomized (OVX) rats is located in the brain or in the adenohypophysis. Luteinizing hormone releasing hormone (LHRH) was infused at a constant rate (2--100 ng/h) through an indwelling venous cannula in unanesthetized, unrestrained OVX rats. Blood samples were collected at 5-min intervals through a second venous cannula prior to and during LHRH infusion for subsequent radioimmunoassay of plasma LH. LHRH infusion at 12.5, 50 and 100 ng/h did not interfere with the magnitude or the periodicity of LH pulses in plasma but the range within which plasma LH fluctuated was elevated. Phenobarbital (75 mg/kg BW; i.p.) blocked the pulsatile plasma LH and maintained the plasma LH nearly constant at reduced levels. Pulse i.v. injections of LHRH but not constant rate i.v. infusions restored pulsatile LH patterns in phenobarbital-treated OVX rats. The results are consistent with the view that pulsatile LHRH release is responsible for the pulsatile nature of plasma LH in OVX rats. The results do not support the concepts of a short-loop feedback of LH or an ultra-short-loop feedback of LHRH on LH secretion at least on an acute basis.

Animals↗
PubMed1980

Monosodium glutamate disruption of behavioral and endocrine function in the female rat.

Experiments were conducted to determine the effects of neonatal administration of L-monosodium glutamate (MSG) on behavioral and endocrine function in the female rat. Administration of MSG (4 mg/kg body weight) at days 1, 3, 5, 7 and 9 in neonates results in a delay of vaginal opening (VO) and the absence of ovulation at the time of VO. However, some rats were observed to ovulate after VO if they were subjected to sequential laparotomies. MSG-treated rats also fail to exhibit compensatory ovarian hypertrophy. Ovariectomized MSG-treated rats injected with estradiol benzoate (EB) followed by a progesterone injected 2 days later did not exhibit sexual beahvior to male rats, while all the control rats displayed lordosis. Chronic treatment with EB for 12 days, followed by a progesterone injection on the 12th day, resulted in a marked improvement of the sexual receptivity of the MSG-treated rats. The body weight of the MSG-treated animals was lower than that of the controls during development although the MSG animals looked obese. Food intake is normal in the MSG-treated rats, but when expressed as intake/100 g body weight, the MSG-treated rats appeared slightly hyperphagic, MSG-treated rats respond with increased food intake after ovariectomy and EB treatment suppresses the increased food intake. Thus, the control of food intake by estrogen does not seem to be affected by the MSG treatment; in fact, these animals seem to be more sensitive than control rats to the anorectic effects of EB. Neonatal MSG treatment appears to affect the neural control for the tonic secretion of gonadotropins by destroying arcuate nuclei. This undoubtedly reduces the reproductive capacity of the animals by impeding the growth and secretions of their ovaries. The findings that chronic estrogen followed by progesterone treatment can reinstate sexual receptivity in MSG-treated animals suggests that the arcuate nuclei are not needed for the expression of sexual behavior and that estrogens might remedy the fertility problems of MSG-treated animals.

Animals↗
PubMed1980

Hypothalamic-pituitary interactions during the periovulatory secretion of follicle-stimulating hormone in the rat.

We investigated the importance of anterior afferents to the medial basal hypothalamus (MBH) on the increases in plasma FSH during the periovulatory period in the 4-day cyclic rat. We served the anterior connections to the MBH either at 1200 h on proestrus (before the time of onset of the normal spontaneous LH surge in plasma and the associated first phase of FSH release) or near the end of the LH surge and first phase of FSH release at 2000 h on proestrus (before the onset of the second or selective phase of FSH release). Analyses of FSH and LH in blood collected through indwelling atrial catheters or from the trunk after decapitation showed that anterior deafferentation of the MBH at 1200 h on proestrus blocked the proestrous LH surge, the elevations in plasma FSH during proestrus and estrus, and ovulation. In contrast, when brain surgery was delayed until 2000 h on proestrus, the second phase of FSH release and ovulation occurred. In rats with retrochiasmatic transections made at 1200 h, a constant rate iv infusion of LHRH from 1500-1800 h on proestrus restored the LH surge, both phases of increased plasma FSH, and ovulation. The results suggest that 1) the prevolutory LH surge and the first phase of FSH release are dependent on rostral afferents to the MBH which result in hypothalamic LHRH release and 2) the role of rostral afferents to the MBH in the second phase of FSH release is solely to result in hypothalamic LHRH release during proestrus.

Animals↗
PubMed1980

Effects of long-term adrenalectomy on periovulatory increases in serum gonadotrophins and ovulation in rats.

The effects of chronic adrenalectomy on the oestrous cycle, periovulatory gonadotrophin surges in sera and ovulation in the rat were assessed. Rats which were exposed to a 14 h light : 10 h darkness lighting schedule for at least 3 weeks and those which showed at least two consecutive 4 day oestrous cycles were divided into three groups. One group (controls) was left untreated. The rest were adrenalectomized (ADX) or sham-adrenalectomized (Sham) during oestrus and then placed in a different animal room with the same lighting schedule but with the onset and end of the photoperiod delayed by 4 h. These operations did not interrupt the length of the oestrous cycles. Rats were decapitated for collection of trunk blood on the fifth pro-oestrous or oestrous day after the operation. Both Sham and ADX rats synchronized to the new lighting schedule in terms of the temporal patterns of their periovulatory surges in serum LH and FSH and the timing of ovulation. Neither adrenalectomy nor the sham-operation altered the magnitude of the pro-oestrous or oestrous increases in serum LH or FSH when compared with those in control rats. Body, uterine and ovarian weights as well as the number of ova shed were similar in the ADX and Sham groups. The results indicate that adrenal secretions are not necessary for rats to synchronize the timing of the periovulatory surges in serum LH and FSH or ovulation to a 14 h light : 10 h darkness schedule and the periovulatory surges of LH and FSH are unaltered in chronically adrenalectomized rats.

Adrenal Glands↗