Biomedical subjects

C A Blake

Publications and source records attributed to C A Blake.

At least 37 records · Page 2Linked to original sources

PubMed1993

Effects of injection of anti-luteinizing hormone (LH)-releasing hormone serum and anti-gonadotropin-releasing hormone-associated peptide serum into neonatal rats on LH and follicle-stimulating hormone cells.

Relatively little is known regarding the potential importance of LHRH and of gonadotropin-releasing hormone-associated peptide (GAP) on the postnatal development of gonadotrophs. We investigated the effects of administration of anti (A)-LHRH serum or A-GAP serum to neonatal rats on the development of LH and FSH immunoreactivity in anterior pituitary gland (APG) cells. Serum (sheep non-immune [NSS], sheep A-LHRH, sheep A-LHRH/GAP [which bound LHRH and GAP], rabbit non-immune [NRS], or rabbit A-GAP) was injected s.c. into neonatal female and male rats on Days 1 and 3 or Days 1, 3, 5, and 7 after birth. Pups were killed on Day 5 or 9, two days after the last injection. The percentages of APG cells immunoreactive for LH or FSH increased from Day 1 to Day 5 and did not change between Days 5 and 9 in female pups treated with NSS or NRS. There was a trend for the percentages of LH and FSH cells to increase from Day 1 to Days 5 and 9 in male pups treated with NSS or NRS, but the increases were not statistically significant. In both females and males, treatment with antisera that recognized LHRH reduced the percentage of FSH cells on Day 5 and the percentages of LH and FSH cells on Day 9. Treatment with A-GAP was without effect in both sexes. There were similar percentages of LH and FSH cells in females and a lower percentage of FSH than of LH cells in males in the Day 5 and 9 controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Estrogen alters the effects of neuropeptide-Y on luteinizing hormone and follicle-stimulating hormone release in female rats at the level of the anterior pituitary gland.

In recent years, several studies have shown that neuropeptide-Y (NPY) is involved in the control of LH secretion. We determined the effects of estrogen on NPY-induced LH and FSH release in the absence or presence of LH-releasing hormone (LHRH) at the level of the anterior pituitary gland (APG). Adult female rats were ovariectomized. Fifteen to 20 days later, they were given a blank or estrogen-filled capsule subdermally and killed 17-19 h later. APG cells were isolated and cultured for 3 days in medium containing 12.5% rat serum collected at death from the same rats used to make the respective APG cell pools. The cells were then challenged for 3 h with vehicle, NPY (10(-12)-10(-6) M), LHRH (10(-9)-10(-6) M), or combinations of NPY (10(-9)-10(-7) M) and LHRH (10(-9) M). LHRH stimulated LH and FSH release from nonestrogen and estrogen-primed cells. NPY at 6.7 x 10(-8)-10(-6) M increased (P < 0.05) LH release and at 10(-6) M increased (P < 0.05) FSH release from estrogen-primed cells, but was without effect on nonestrogen-primed cells. In contrast, NPY at 10(-9)-10(-7) M potentiated the action of LHRH (10(-9) M) to increase the release of LH and FSH from nonestrogen-primed cells, but was without potentiating effects in cultures of estrogen-primed cells. The results demonstrate that 1) NPY can release LH and FSH by a direct action on estrogen-primed APG cells; and 2) NPY can potentiate the action of LHRH to increase the release of LH and FSH by a direct action on nonestrogen-primed APG cells.

Animals↗

PubMed1992

Intraperitoneal injection of chloral hydrate causes intra-abdominal adhesions and unilateral testicular atrophy in golden Syrian hamsters.

We investigated the reason for the high mortality we had observed in hypophysectomized-orchidectomized Golden Syrian hamsters that were anesthetized with intraperitoneal (i.p.) injections of chloral hydrate (CH). Intact male Golden Syrian hamsters were injected intraperitoneally with 0.1cc/100g BW of a 35% solution of CH, a 35% solution of sodium chloride, or double-distilled water. Equal numbers of hamsters in each group were injected on the right or left side of the abdomen. Within 10 days, 35% of the CH-injected hamsters were dead or had to be euthanized. Autopsy revealed severe peritonitis and adynamic ileus. CH-injected hamsters that survived gained weight at a rate similar to that of the controls. All surviving hamsters were killed 18 days after the injections. Among the surviving CH-injected hamsters, 84.6% had intra-abdominal adhesions, 61.5% had unilateral testicular atrophy, and 53.8% had a yellowish necrotic mass in the epididymal fat pad (EFP). All the lesions occurred on the side that was injected. The atrophied testes had been rendered cryptorchid due to involvement with intra-abdominal adhesions. In the water-treated controls, there were no abnormalities; whereas, in the saline controls, 75% had a mass in the EFP. Histology of the EFP mass was similar in hamsters injected with CH or hypertonic saline and suggested a diagnosis of fat necrosis. The results suggest that the mortality, the intra-abdominal adhesions, and the unilateral cryptorchidism were caused by a single i.p. injection of CH, but the fat necrosis in the EFP was probably caused by high concentrations of salt. The results further suggest that high concentrations of CH should not be injected intraperitoneally for anesthesia in chronic studies, particularly of the male reproductive system.

Adipose Tissue↗

PubMed1992

Gonadotropin-releasing hormone-induced accumulation of follicle-stimulating hormone beta-subunit messenger ribonucleic acid in adenohypophysial cells developing in an ectopic position.

We investigated the influence of LHRH on the accumulation of FSH beta messenger RNA (mRNA) in anterior pituitary glands removed from hamster pups less than 36 h old and transplanted beneath the renal capsules of adult male hamsters (hosts). Three experiments were performed in which some hosts were injected sc with LHRH (1 microgram/injection) and others were injected with vehicle. Injections were begun in the afternoon of the day of transplantation (day 1) and were given at 0800 and 1700 h for 6 days and at 0800 h on the eighth day. An additional experiment was performed in which adult male hamsters not bearing allografts were injected with the same regimen of LHRH or vehicle. The hamsters were decapitated on the eighth day of the study, 2 h after the last injection. The allografts, adenohypophyses of the hosts, adenohypophyses of hamsters without allografts, and adenohypophyses of normal adult male rats were removed and frozen on dry ice immediately. Additionally, adenohypophyses were collected from hamster pups less than 36 h old and 8 and 15 days of age. Total RNAs from some pooled specimens were electrophoresed on a formaldehyde-agarose gel. After transfer to Nytran, the RNAs were hybridized sequentially to complementary DNAs for rat FSH beta and hamster beta-actin. The rat FSH beta complementary DNA probe hybridized to a single RNA (approximately 1.7 Kb) in rat adenohypophyses. It predominantly hybridized to RNA of approximately 1.7 Kb from hamster adenohypophyses. Sometimes it hybridized to RNAs ranging in size from 0.5 Kb to 1.7 kb. The hybridization signals for all samples obtained from dot blot analyses were quantitated and normalized to the signals for beta-actin. The hybridization signals obtained from adenohypophyses of hamsters of different ages increased from 36 h of age to adulthood. The hybridization signal obtained from adenohypophyses of hamsters less than 36 h old (the same age as the donor hamsters) was similar to the hybridization signal obtained from allografts in vehicle-treated hamsters. The relative levels of FSH beta mRNA in allografts of LHRH-treated hosts were: 1) greater than the relative levels in adenohypophyses of hamsters less than 36 h old (P less than 0.05) and in allografts in vehicle-treated hamsters (P less than 0.05), 2) greater than the relative levels in adenohypophyses of 8-day-old hamsters (P less than 0.05), and 3) not different compared to the relative levels in adenohypophyses of 15-day-old hamsters and adult male hamsters.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Basal luteinizing hormone and follicle-stimulating hormone release rates as a function of time after castration in female and male rats.

We investigated the potential importance of the basal follicle-stimulating hormone (FSH) and luteinizing hormone (LH) release rates in causing the acute and chronic elevations in serum FSH and LH concentrations which occur after ovariectomy (OVX) and orchidectomy (ORCH) of rats. Diestrous day 1 female and male rats were decapitated or castrated and killed 2, 4 or 8 h or 1, 2, 7, 21 or 35 days later. In females, the weight of the anterior pituitary gland (APG) did not change. Serum FSH rose within 4 h and then progressively higher until 35 days after OVX. These increases were paralleled nearly perfectly with increases in APG FSH concentration which was first elevated at 1 day after OVX and in the basal FSH release rate (measured in vitro) which was first elevated at 4 h after OVX. Serum LH levels rose by 7 days after OVX and then more dramatically thereafter. These increases were associated with increased APG LH concentrations. The pronounced increases in serum LH levels between 7 and 35 days after OVX were associated with marked increases in the basal LH release rate. In males, APG weight was increased at 21 and 35 days after ORCH. Serum FSH levels were elevated at 1 day after ORCH and continued to rise until 21 days after ORCH. APG FSH concentration was decreased at 2 and 7 days and increased at 35 days after ORCH. The basal FSH release rate per milligram APG did not change significantly after ORCH. Serum LH levels were elevated at 8 h after ORCH. They rose further by 1 day and then further between 7 and 21 days after ORCH. APG LH concentration and the basal LH release rate per milligram APG were elevated at 21 and 35 days after ORCH. The results suggest that changes in basal FSH and LH release are (1) involved to a major extent in causing the post-OVX rise in serum FSH concentration during the first 5 weeks after OVX and in serum LH concentration between 7 and 35 days after OVX, (2) not involved in causing the post-ORCH rises in serum FSH and LH concentrations during the 1 week after ORCH, and (3) involved to some extent in causing the elevations in serum FSH and LH concentrations observed at 3 and 5 weeks after ORCH. The results also indicate that (1) increases in the basal gonadotropin release rates per milligram APG after castration may be coupled in some way with increased synthesis of gonadotropin, and (2) increases in the basal LH release rate per milligram APG can occur independently of an increase in the basal FSH release rate per milligram APG.

Animals↗

PubMed1990

Blockade of the selective increase in serum follicle-stimulating hormone concentration in immature female rats and its effects on ovarian follicular development.

We investigated whether administration of monosodium L-glutamate (MSG) to neonatal female rats would block the selective increase in serum follicle-stimulating hormone (FSH) concentration in immature rats in an attempt to provide a model in which to study the importance of the selective FSH rise on ovarian follicular development. In two separate experiments, s.c. injections of MSG (4 mg/g BW) on Days 1, 3, 5, 7 and 9 after birth blocked the selective increase in serum FSH concentration observed on Days 7 and 15 without blocking basal FSH secretion. Serum luteinizing hormone (LH) levels were unaffected in the first experiment and changed little in the second. MSG-treated rats had smaller ovaries on Days 15 and 23. The ovaries of MSG-treated rats on Day 15 showed decreased follicular growth as evidenced by a decrease in the number and percentage of follicles with diameters greater than 50 microns, in the number of follicles with greater than 1 layer of granulosa cells, and in the number of follicles beyond the primary stage of follicular development. These differences between MSG-treated rats and controls all but disappeared by Day 23. The results demonstrate that neonatal administration of MSG blocks the selective increase in serum FSH concentration in immature female rats and suggest that this selective increase in serum FSH levels plays a role in the normal acceleration of ovarian follicular development but is not needed for the development of preovulatory follicles by the sixth week after birth.

Animals↗

PubMed1990

Luteinizing hormone (LH)-releasing hormone: effects on maintenance of immunoreactive follicle-stimulating hormone and LH in adenohypophysial cells.

We investigated the importance of LHRH on the maintenance of FSH and LH immunoreactivity in gonadotrophs. Hypophysectomized orchidectomized hamsters (hosts) each received an allograft of a 7-week-old male hamster pituitary gland beneath their right renal capsule. Starting 6 days after transplantation, hosts were injected sc, twice daily with 1 micrograms LHRH or vehicle for 16 days. Twelve hosts in each group were killed by decapitation 16 h after the last injection. Allografts from six of the hamsters in each group and pituitary glands in situ from 10-week-old normal males were prepared for histological examination. Sections of tissue were stained for FSH or LH and with hematoxylin. Allografts from the remaining hamsters were homogenized to measure FSH and LH concentrations. In allografts from the vehicle-treated hosts, 22.8% of adenohypophysial cells stained for LH, while only 16.9% stained for FSH. In allografts from LHRH-treated hosts, 22.6% and 23.8% of the adenohypophyses cells stained for LH and FSH, respectively. Adenohypophyses that developed for the same length of time in situ had 24.8% and 24.1% of the cells staining for LH and FSH, respectively. Matching of some of the FSH and LH cells in serial flip-flopped sections of tissue from all hamsters revealed that many if not all gonadotrophs contained LH. LH- and FSH-containing cells in allografts were similar in size and shape, but were smaller and more circular in profile than those observed in situ. Treatment of hosts with LHRH did not alter gonadotroph size or shape, but it did reduce allograft LH concentration and elevate the serum FSH concentration compared to that in the vehicle-treated hamsters. These results suggest that in the hamster LHRH 1) plays a major role in maintaining FSH immunoreactivity in adenohypophysial tissue, 2) does not play a role in maintaining numbers of immunoreactive LH cells in adult adenohypophysial tissue, and 3) functions to maintain FSH synthesis at least in part in cells that contain LH.

Animals↗

PubMed1990

Luteinizing hormone (LH)-releasing hormone: chronic effects on LH and follicle-stimulating hormone cells and secretion in adult male rats.

We investigated whether chronic administration of LHRH to normal adult rats could increase the percentages of anterior pituitary gland (APG) cells that contain immunoreactive LH and/or FSH and gonadotropin secretion. Vehicle or 1 microgram LHRH was injected sc twice daily for 6 days, and rats were decapitated 16 h after the last injection. Treatment with LHRH caused nearly a doubling in the numerical density of LH and FSH cells and in the percentage of APG cells that contained LH or FSH. It also caused a shift in the gonadotroph population from LH and LH/FSH cells to LH/FSH cells. It did not change the mean size of gonadotrophs or APG weight. These changes at the light microscopic level were not accompanied by any apparent changes in LH cells at the ultrastructural level. However, they were accompanied by an approximate doubling of the basal serum LH and FSH concentrations, an increase in the APG FSH concentration, and an increase in the basal FSH release rate (measured in vitro). The results indicate that exogenous LHRH can be administered to increase numbers of gonadotrophs in the APG, synthesis of FSH in gonadotrophs, and basal serum LH and FSH concentrations.

Animals↗

PubMed1990

The response of splenic lymphocytes removed from hypophysectomized-orchidectomized hamsters to phytohemagglutinin correlates with somatic growth but not with circulating prolactin levels.

To examine the relationship between PRL and the mitogenic capacity of lymphocytes, we studied the relationships among circulating PRL levels, somatic growth, and the response of splenic lymphocytes to the mitogen phytohemagglutinin (PHA) in hamsters. In the first experiment, no differences were observed in the PHA responses of lymphocytes removed from intact or hypophysectomized-orchidectomized hamsters. No relationships were observed between circulating PRL levels and either the PHA responses or somatic growth. However, significant positive correlations were observed between the somatic growth of intact or hypophysectomized-orchidectomized hamsters and the PHA responses (r = 0.741; P less than 0.01 for intact hamsters; r = 0.642; P less than 0.01 for hypophysectomized-orchidectomized hamsters). In three subsequent experiments we tested the effects of placing muscle or hypophysial allografts in hypophysectomized-orchidectomized hamsters on somatic growth, the PHA responses, and circulating PRL levels. Neither type of allograft altered the somatic growth of hypophysectomized-orchidectomized hamsters. The hypophysial allografts did elevate serum PRL levels. In all experiments the responses of splenic lymphocytes to PHA showed a significant positive correlation with somatic growth, but not with serum PRL levels. These results minimize a role of PRL in this particular lymphocyte response. The results suggest that a strong correlation exists between mechanisms responsible for somatic growth in hypophysectomized-orchidectomized hamsters and the immune status, as determined by the response to PHA, of the animals. This relationship also may exist in intact hamsters.

Adrenal Glands↗

PubMed1989

Effects of corticotrophin-releasing hormone on corticotrophs in anterior pituitary gland allografts in hypophysectomized, orchidectomized hamsters.

We investigated the effects of corticotrophin-releasing hormone (CRH) on the percentage of anterior pituitary gland (APG) cells which are corticotrophs as well as the size and shape of corticotrophs. Pituitary glands were removed from 7-week-old male hamsters and placed beneath the renal capsules of hamsters that had been hypophysectomized and orchidectomized 3 weeks previously. Beginning 6 days after each host had received a single allograft, each was injected subcutaneously twice daily with 4 micrograms CRH or vehicle for 16 days. Six hosts in each group were decapitated 16 h after the last injection. Sections of anterior pituitary tissue were stained for ACTH and with hematoxylin. The percentage of corticotrophs among APG cells was greater in allografts exposed to exogenous CRH (approximately 20%) than in allografts exposed to vehicle (approximately 15%). Exposure to exogenous CRH increased the cross-sectional area of corticotroph cells in allografts to values greater than those measured for corticotrophs in allografts exposed to vehicle, without altering the shape of cells. Results of subsequent studies suggested that hamsters with allografts injected with vehicle do not release ACTH and that exogenous CRH causes an abrupt release of ACTH from allografts. These results indicate that CRH releases ACTH from ectopic corticotrophs and that administration of CRH can increase corticotroph size and the percentage of APG cells that are corticotrophs.

Adrenocorticotropic Hormone↗

PubMed1989

Basal gonadotropin hormone release rates during the period of selective follicle-stimulating hormone release in the juvenile female rat.

There are situations in which adult female rats release increased amounts of follicle-stimulating hormone (FSH) independent of increased luteinizing hormone (LH) release. This results from, at least in part, a selective increase in the basal FSH release rate. We investigated whether an increase in the basal FSH release rate is contributory to the rise in serum FSH levels which occurs independent of a rise in serum LH levels in the immature female rat. Rats had high serum FSH concentrations on days 7 and 15 after birth, low serum FSH levels on day 23, and low serum LH levels on all three days. In contrast, anterior pituitary gland (APG) FSH and LH concentrations and contents increased from day 7 to day 15 and the contents increased further from day 15 to day 23. Similarly, basal FSH and LH release rates per mg APG or per APG, as assessed by measurement of FSH and LH released into culture medium containing APG(s) from different aged rats, increased from day 7 to day 15 but did not increase further between days 15 and 23. The results indicate that unlike situations observed to date in adult female rats, a mechanism(s) other than an increase in the basal FSH release rate is involved in selective FSH release in the immature female rat.

Aging↗

PubMed1989

Luteinizing hormone (LH)-releasing hormone: effects of induction of LH, follicle-stimulating hormone, and prolactin cell differentiation.

We investigated the influence of LHRH on the differentiation of gonadotrophs and lactotrophs in fetal pituitary glands transplanted beneath the renal capsules of adult hypophysectomized-orchidectomized hamsters (hosts). Hypophyses were removed from hamster fetuses at a gestational age of 14 days. Some of these were immediately fixed in Bouin's solution, and others were transplanted into the hosts. The hosts were injected sc twice daily with 1 microgram LHRH or vehicle for 16 days. Six hosts in each group were killed by decapitation 16 h after the last injection. Six 14-day-old normal male hamsters (age-matched to correspond to the age of the allografts at the time of the hosts' decapitation) also were decapitated. Sections of hypophyses in situ from fetal hamsters, from 14-day-old controls, and from allografts in each group were stained for LH, FSH, or PRL and with hematoxylin. No PRL-containing cells and very few LH or FSH cells (less than 0.025% of the adenohypophysial cell population) were observed in fetal pituitary glands. In allografts from the vehicle-treated hosts, 21.1% of adenohypophysial cells contained LH, but only 1.8% contained FSH. In allografts from LHRH-treated hosts, 28.0% and 22.9% of the adenohypophysial cells contained LH and FSH, respectively. Adenohypophyses that developed for the same length of time in situ had smaller percentages of adenohypophysial cells containing LH (23.8%) and FSH (15.5%) than the LHRH-treated group. LH-containing cells in allografts in the vehicle-treated hamsters, but not in the LHRH-treated animals, were reduced in size compared to those measured in situ. The number of lactotrophs in all allografted tissue was markedly reduced compared to that of lactotrophs in situ, and injection of LHRH into hamsters with allografts did not alter the percentage of adenohypophysial cells that were lactotrophs. These results suggest that in the hamster LHRH 1) plays an important role in stimulating the formation of immunoreactive FSH in the pituitary gland, 2) can increase the number of gonadotrophs that develop during the neonatal period, and 3) plays a role in controlling the size of gonadotrophs during development. The results also suggest that the development of lactotroph cell number requires close proximity to the hypothalamus and/or exposure to a neonatal environment. We found no evidence to support the view that LHRH, LH, or FSH stimulates immunoreactive lactotroph differentiation.

Animals↗

PubMed1988

Effects of growth hormone-releasing hormone on somatotrophs in anterior pituitary gland allografts in hypophysectomized, orchidectomized hamsters.

We investigated the influences of growth hormone-releasing hormone (GHRH) on the percentage, size, and shape of somatotrophs in ectopic anterior pituitary tissue. Entire pituitary glands removed from 7-week-old male hamsters were placed beneath the renal capsules of 12-week-old hamsters that had been hypophysectomized and castrated 3 weeks previously. Beginning 6 days after each host had received a single allograft, each was injected subcutaneously twice daily with 4 micrograms GHRH in 100 microliter of vehicle or 100 microliter of vehicle for 16 days. Six hosts in each group were killed by decapitation on day 17, 16 h after the last injection. Nine normal male hamsters were also decapitated and their pituitary glands were removed. Sections of anterior pituitary tissue were stained for GH and with hematoxylin. The percentage of anterior pituitary cells that stained for growth hormone was similar in the 3 groups. In contrast, somatotrophs in grafts had a smaller mean cross-sectional area than those observed in glands in situ. This effect was reversed by GHRH. Analysis of the shape of somatotrophs in both groups of grafts disclosed that they were less circular in cross-section than those in glands in situ. The results suggest that GHRH may not play a role in maintaining the percentage of somatotrophs among anterior pituitary cells, but that it does play a role in maintaining their size.

Animals↗

PubMed1987

An immunohistochemical study of adenohypophyseal cells containing follicle-stimulating hormone and luteinizing hormone during the phase of selective follicle-stimulating hormone release in postnatal female rats.

Serum concentration of follicle-stimulating hormone (FSH) in the juvenile female rat increases independently from that of luteinizing hormone (LH). The objective of this study was to determine whether this increase in serum FSH is accompanied by a proliferation of FSH-cells greater than the proliferation of LH-cells. Thus, we measured circulating FSH and LH in female rats on days 3, 10, 13, 17, and 20, calculated the percentages of adenohypophyseal cells that contained FSH or LH on days 3, 10, and 20, and determined whether cells containing only FSH existed on day 10. Serum FSH concentrations on days 10 and 13 were significantly greater than those on days 3, 17, or 20. No differences existed in serum LH concentrations. Cells containing FSH or LH were distributed throughout the entire adenohypophyses of 3, 10, and 20-day-old females. Clusters of these cells were observed in the ventral regions of adenohypophyses of 3-day-old females. The percentages of adenohypophyseal cells containing FSH increased significantly from approximately 9% in 3-day-old rats to approximately 17% in 10-day-old rats and then decreased to approximately 14% in 20-day-old animals. At all ages the percentages of adenohypophyseal cells containing FSH were similar to the percentages of cells containing LH. At 10 days of age, all cells containing FSH also contained LH and all cells containing LH also contained FSH. These data suggest that the increase in serum FSH in the juvenile female rat is associated with an increase in the percentage of adenohypophyseal cells containing FSH and that at this time all cells containing FSH also contain LH.

Aging↗

PubMed1987

Effects of hypothalamic neurohormones on prolactin release from pituitary allografts in the hamster.

Recent reports indicate that luteinizing hormone-releasing hormone (LHRH) releases prolactin (PRL) under some circumstances. We examined the chronic effects of LHRH, growth hormone-releasing hormone (GHRH), and corticotrophin-releasing hormone (CRH) on the release of PRL, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) by pituitary allografts in hypophysectomized, orchidectomized hamsters. Entire pituitary glands removed from 7-week-old-male Golden Syrian hamsters were placed under the renal capsule of hypophysectomized, orchidectomized 12-week-old hamsters. Beginning 6 days postgrafting, hamsters were injected subcutaneously twice daily with 1 microgram LHRH, 4 micrograms GHRH, or 4 micrograms CRH in 100 microliter of vehicle for 16 days. Six hosts from each of the four groups were decapitated on Day 17, 16 hr after the last injection. Prolactin, LH, and FSH were measured in serum collected from the trunk blood. Treatment with LHRH significantly elevated serum PRL levels above those measured in the other three groups, which were all similar to one another. Serum LH levels in hosts treated with vehicle were elevated above those measured in the other three groups. Serum FSH levels in hosts treated with LHRH were greater than FSH levels in any of the other three groups. These results indicate that chronic treatment with LHRH can stimulate PRL and FSH release by ectopic pituitary cells in the hamster.

Animals↗

PubMed1985

Monosodium glutamate and pituitary gland luteinizing hormone (LH) release in response to LH-releasing hormone: an in vitro study.

We studied whether an increase in the basal LH release rate and/or the anterior pituitary gland (APG) LH response to LHRH is involved in maintaining normal or near-normal serum LH levels in monosodium L-glutamate (MSG)-treated rats which have small APGs for their body weight. Female rats were injected with MSG (4 mg/g BW) or saline on days 1, 3, 5, 7, and 9 after birth (day of birth = 0). At 8-9 weeks of age, saline-treated and MSG-treated rats were ovariectomized, and 7 days later, they were decapitated. Trunk blood was collected from 18 controls and 19 MSG-treated rats, and serum LH concentrations were measured by RIA. APGs were bisected and each hemi-APG was placed in culture medium for a 30-min preincubation period, followed by two 30-min incubation periods during which water or 10 or 30 ng LHRH were added to the medium. Despite the fact that the APGs of the MSG-treated rats were half the size of those of the saline-treated rats, the serum LH levels in the 2 groups were not different. Basal LH release rates (the response to water) and LHRH-induced LH release per mg APG were increased in MSG-treated rats. Calculation of the basal LH release rates and LHRH-induced LH release on the basis of the entire weights of the APGs showed no differences between the MSG-treated rats and the controls. In 6 additional control and 6 additional MSG-treated rats, the APG LH concentration was measured and was not different between the 2 groups. The results suggest that increases in both the basal LH release rate per mg APG and the amount of LH released per mg APG in response to LHRH are of importance in the maintenance of normal or near-normal serum LH concentrations in MSG-treated rats with small APGs.

Animals↗

PubMed1985

Monosodium L-glutamate administration: effects on gonadotrophin secretion, gonadotrophs and mammotrophs in prepubertal female rats.

We have studied gonadotrophin secretion and immunocytochemically stained gonadotrophs and mammotrophs in 35-day-old female rats which had been treated with monosodium glutamate (MSG) as neonates. We also compared our morphometric data in the saline-treated controls with those we have previously obtained in normal adult female rats. The size of the anterior pituitary glands was reduced but the serum levels, the pituitary gland concentrations and contents, and the in-vitro basal release rates of LH and FSH were not significantly altered by MSG treatment. The size of the LH and FSH cells was reduced by MSG administration, but the volume and numerical densities of LH and FSH cells, and the percentage of LH and FSH cells in the pars distalis were not affected. The results suggest that in spite of the smaller size of LH and FSH cells and of the anterior pituitary glands in the MSG-treated rats, the cells contain normal amounts of hormone and the basal LH and FSH secretion rates of the glands are not significantly depressed, contributing to the maintenance of normal serum gonadotrophin concentrations. The volume density of prolactin cells was not increased by MSG treatment. The volume density of gonadotrophs and the percentage of cells which are gonadotrophs in anterior pituitary glands of prepubertal female rats were greater than those in adult female rats, but the reverse was true for the volume density of prolactin cells, suggesting a reciprocal relationship between the relative numbers of gonadotrophs and mammotrophs in prepubertal and adult female rats.

Animals↗

PubMed1984

A decrease in thymus-mediated immune responses as a result of treatment of neonatal rats with glutamate.

We investigated whether administration of monosodium 1-glutamate (MSG) to neonatal rats would disrupt immune responses in intact and orchidectomized adult male rats. Neonatal male rats were treated with saline or MSG which causes severe endocrine abnormalities. Half of each group of animals were orchidectomized as adults and killed one week later along with intact rats. MSG treatment resulted in suppressed serum LH levels in intact rats. Thymus weight and spleen cellularity in intact animals were not affected by MSG treatment, but thymus weight increased within one week after orchidectomy in both saline- and MSG-treated groups. In intact rats, lymphocyte stimulation by the T cell specific mitogens (concanavalin A or phytohemagglutinin) or the B cell specific mitogen (lipopolysaccharide) was unaffected by prior treatment with MSG. However, MSG treatment blocked the decrease attributable to orchidectomy in concanavalin A and phytohemagglutinin stimulation of lymphocyte blastogenesis. The results suggest that administration of MSG to neonatal male rats can alter some immune responses in the adult animal.

Animals↗