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Biomedical subjects

G T Campbell

Publications and source records attributed to G T Campbell.

At least 19 recordsLinked to original sources
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

Sequence and expression of hamster prolactin and growth hormone messenger RNAs.

Complementary DNAs encompassing the complete protein-encoding regions for PRL and GH of the Syrian Golden hamster were sequenced and used as probes to examine the expression of hamster PRL and GH messenger RNA (mRNA)s. The complementary DNA (cDNA) for hamster PRL encodes a 226 amino acid preprotein which, by analogy to rat and mouse PRLs, is predicted to be processed to yield a 197 amino acid secreted protein. The hamster GH cDNA codes for a 216 amino acid preprotein predicted to yield a 190 amino acid secreted protein. Both hamster proteins are highly homologous to the corresponding rat and mouse hormones. For the secreted proteins, hamster PRL has 82% amino acid identity with rat PRL and 72% identity with mouse PRL. The rodent GH sequences are more strongly conserved, with 97-98% sequence identity between hamster, rat, and mouse GHs. The hamster hormones contain the highly conserved cysteine residues (six in hamster PRL and four in hamster GH) present in other mammalian PRLs and GHs. Neither hamster PRL nor hamster GH contains cysteine residues corresponding to the unique pair of cysteines present in hamster placental lactogen-II. The hamster PRL and GH cDNAs each hybridized to pituitary mRNAs of approximately 1 kilobase. Expression of hamster PRL and GH mRNAs was compared between 2 days of the estrous cycle (proestrus and estrus) and early, mid, and late pregnancy (days 5, 10, and 15). PRL mRNA levels in cycling hamsters were approximately 50% of those in pregnant hamsters. No other significant differences in PRL or GH mRNA levels were observed, suggesting that differences in circulating PRL and GH protein levels during the estrous cycle and pregnancy in the hamster are the result largely of factors other than changes in mRNA levels.

Amino Acid Sequence↗
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

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

Development and retention of phenotypically specialized cells in pituitary allografts in the hamster (Mesocricetus auratus).

We used immunohistochemistry to identify cells present in pituitary allografts in the hamster. Hypophyses removed from neonatal hamsters or adenohypophyses removed from adult females were placed beneath renal capsules of hypophysectomized adult females. Serum PRL, LH, and GH concentrations were measured at two, five and eight weeks after placement of allografts. Allografts were removed after eight weeks and stained for cells containing PRL, LH, FSH, GH, or ACTH. Allografts did not release LH or GH. Those of adult adenohypophyseal tissue released significantly more PRL. The morphology of allografts of neonatal hypophyseal tissue resembled that of the adult adenohypophysis in situ. Lactotrophs, corticotrophs, somatotrophs and LH-cells were observed; very few FSH-cells were present. Allografts of adult adenohypophyseal tissue contained pituitary cells, numerous cavities, often enclosing lymphoid cells, and fibrous tissue. Atypical lactotrophs were the numerically dominant cells in these allografts; all other cells were present. The LH-cells outnumbered FSH-cells. These observations suggest that: (a) development of normal adenohypophyseal morphology can occur in an ectopic position; (b) intracellular hormones are present in cells in an ectopic site; (c) development and retention of intracellular FSH is more dependent on occupation of the normal position of the adenohypophysis than is retention of intracellular LH; and (d) release of PRL occurs from atypical cells in allografts of adult adenohypophyseal tissue.

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

Hamster placental lactogens: gestational profiles and high molecular weight forms.

We previously reported the purification of a lactogenic protein, hamster placental lactogen (haPL; now designated haPL-II) from late pregnant hamster placentas. In this study the lactogenic factors in maternal serum during the second half of pregnancy were measured using RIAs for haPL-II and haPRL and a RRA for total lactogenic activity. haPL-II was first detectable on day 10 of pregnancy and reached a maximal concentration [12.3 +/- 0.8 microgram/ml (mean +/- SEM); n = 6] on day 16 (term). PRL concentrations were relatively low during the second half of gestation. Significant amounts of lactogenic activity that could not be ascribed to haPL-II or haPRL were detected throughout this period, with maximal concentrations on days 10-12. Gel filtration chromatography of day 10 serum gave an apparent mol wt of 35,000 for this lactogenic factor. A lactogenic factor with a similar mol wt (37,000) was detected in an extract of day 10 placenta. This lactogenic factor was designated haPL-I. The most prominent forms of haPL-II in day 16 serum were several disulfide-bonded forms with mol wt greater than 200,000. Smaller quantities of lower mol wt forms, including monomeric haPL-II, were present, but circulated as noncovalently bound complexes with mol wt greater than 100,000. Complete conversion to monomeric haPL-II was found only after treatment with both sodium dodecyl sulfate and 2-mercaptoethanol. The high mol wt forms of haPL-II in maternal serum were composed of two different monomeric species of haPL-II.

Animals↗
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↗
PubMed1986

Ontogenesis of corticotropes and lactotropes in situ in the pituitary gland of the hamster. An immunohistochemical study.

The development of corticotropes and lactotropes was investigated in the golden Syrian hamster using an anti-porcine ACTH antiserum and a homologous anti-hamster PRL antiserum. Oval corticotropes were first visible in the ventral region of the pars distalis at 13 days of gestation. By the end of gestation, corticotropes were found throughout the pars distalis and in the pars intermedia. Corticotropes in the pars distalis of postnatal hamsters were either round or irregularly-shaped, often appearing in clusters. Throughout development, corticotropes often appeared to be surrounding other cells. Scarce, very small lactotropes were first observed in the pars distalis of hamsters on the first postnatal day. The number of these cells, which were either round or polyhedral, increased dramatically between 4 and 20 days of postnatal life. These observations indicate that the sequence of appearance of corticotropes and lactotropes in the hamster is similar to that in other species and that lactotropes are confined to the pars distalis of postnatal hamsters.

Adrenocorticotropic Hormone↗
PubMed1979

Luteinizing hormone-releasing hormone (LH-RH) neurons in cultures of fetal rat hypothalamus.

Hypothalamic fragments from 21-day-old fetal rats were cultured in Maximow double-coverslip assemblies for 1 to 2 months. Neurons containing LH-RH were demonstrated immunohistochemically using an antiserum to LH-RH (Dermody; 1:500--1:4,000). LH-RH was demonstrable only in neuronal perikarya (8--13 micrometer) and in small (less than 1 micrometer) round structures nearby, primarily in explants of the median eminence-arcuate nucleus region. Reactive neurons were not found in explants of the preoptic area and could not be demonstrated in fetal hypothalami at the time of explantation. The presence of mature-looking LH-RH containing neurons in these cultures suggests that this tissue culture system can be used for the study of hypothalamic development.

Animals↗
PubMed1979

Immunohistochemical visualizations of prolactin, growth hormone, and a substance resembling placental lactogen in the in situ and ectopic pituitary in the hamster.

The effects of transplanting neonatal adenohypophyseal tissue into the hamster cheek pouch on the presence of intracellular materials related to PRL in the allografts were examined using immunohistochemistry. In situ pituitary and placental tissue were used as control. Cells with antirat PRL-reactive sites were scarce in the grafts, and radioimmunoassayable serum PRL was not detectable in hypophysectomized hosts with grafts. Antirat GH- and antihuman placental lactogen (hPL)-reactive sites were visualized in the grafts and in situ pituitary tissue. Intracellular material in hamster placental tissue was visualized with anti-hPL only. Results of various immunohistochemical procedures using in situ pituitary tissue and antirat GH and anti-hPL antisera indicated that three cell types could exist: 1) a cell type visualized with only antirat GH, 2) a cell type visualized with only anti-hPL, and 3) a cell type, the most frequently observed, visualized with both antisera. The physiological significance of this intracellular product, which resembles hPL and perhaps hamster PL immunologically, in hamster adenohypophyseal cells is unknown. Additionally, our data indicate that the ectopic site for pituitary transplantation in the hamster may influence the cell types present in the grafts.

Animals↗