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C L Bethea

Publications and source records attributed to C L Bethea.

81 records · Page 5Linked to original sources
PubMed1982

Beta-endorphin concentrations in serum, hypothalamus and central gray of hypophysectomized and mediobasal hypothalamus lesioned rats.

The serum and brain concentrations of beta-endorphin immunoreactivity have been studied in intact, mediobasal hypothalamus (MBH) lesioned and hypophysectomized male rats. After hypophysectomy there is a major reduction (90%) of beta-endorphin concentration in the serum but only a partial reduction (20%) in the mediobasal hypothalamus. However, MBH lesions enhance beta-endorphin serum values in previously hypophysectomized rats. Long-term MBH lesions alone lead to an almost complete disappearance of beta-endorphin in the central gray matter with a slight decrease in the serum. These data clearly show that: (1) the pituitary is the major source of beta-endorphin in the serum; (2) the hypothalamus is the major source of beta-endorphin in the central gray matter; and (3) there is clear influence of the pituitary on hypothalamic beta-endorphin.

Animals↗
PubMed1982

Pharmacological evidence that serotonergic stimulation of prolactin secretion is mediated via the dorsal raphe nucleus.

Administration of the serotonin-releasing drug DL-p-chloroamphetamine (PCA) to rats caused a dose-dependent increase in plasma prolactin levels. The effect was maximal 2 h after administration. The effect of PCA was prevented by prior administration of the serotonin synthesis inhibitor p-chlorophenylalanine-methyl ester (PCPA). PCPA pretreatment did not prevent the increase in plasma prolactin levels after administration of the serotonin agonist quipazine which is consistent with a postsynaptic receptor interaction of quipazine. To determine which serotonergic neurons are involved, the prolactin responses to PCA were determined in rats sustaining lesions of the dorsal or median raphe nuclei. The lesions were produced in desmethylimipramine-pretreated rats by local injections of 5,7-dihydroxytryptamine (5,7-DHT) 2 weeks prior to the PCA challenge. In rats with dorsal raphe lesions, the effect of PCA on prolactin secretion was significantly attenuated. In contrast, median raphe lesions did not prevent the effect of PCA on plasma prolactin levels. In summary, these data support the hypothesis that release of serotonin increases prolactin secretion. In addition, these data suggest that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway which can mediate increases in prolactin secretion.

Animals↗
PubMed1981

Human prolactin secreting adenoma cells maintained on extracellular matrix.

In vitro maintenance of human prolactin secreting adenoma cells on a extracellular matrix (ECM) produced by bovine corneal endothelial cells is associated with the adoption of morphological properties that are not expressed when the cells are seeded on plastic. Cells seeded on ECM were firmly attached and highly flattened, whereas cells seeded on plastic formed aggregates which were loosely attached or floated in the medium. Moreover, prolactin production from cells on ECM is frequently stable for several weeks. Both tumor cells and normal cells are more likely to resemble their in vivo counterparts when maintained on extracellular matrix than on plastic, and therefore, cells cultured on ECM may provide a better system for oncogenic and endocrine studies.

Adenoma↗
PubMed1979

Age-related changes in reproductive hormones and in Leydig cell responsivity in the male Fischer 344 rat.

Age-related changes in testicular responsiveness to pituitary hormone stimulation were measured in Fischer rats. Suspensions of dispersed Leydig cells were prepared from the testes of groups which were 5, 12 and 29 months old. The suspended cells were challenged with 250, 750 and 2000ng Monkey-LH (LER 1909-2) for two hours and the medium subsequently assayed for testosterone. Concentrations of the hormone were determined per million cells in suspension. Besides measurement of testosterone production by each age group, pituitary and plasma LH, FSH and prolactin, and plasma testosterone were also assayed by radioimmuno-technique. Total testis weight increased in the oldest animals as the result of a high incidence of gonadal pathology. If tumorous tissue was excluded, however, testis weight fell for this group. Also, significant decreases in Leydig cell number were apparent in 12 and 29-month-old rats. Basal testosterone production, on a per million cell basis, however, was not significantly differnet in young and middle-aged rats, nor was the change in the amount of steroid produced by LH stimulation of the isolated Leydig cells. Seminal vesicle weight, prostate weight and serum testosterone decreased with age. Similarly, pituitary LH and FSH concentration decreased, but pituitary prolactin increased. Histological changes and pituitary hypertrophy reflected this increase in prolactin concentration. It is proposed that decreased testicular function in old age may not totally be the result of a decrement in Leydig cell steroid producing capacity, but that it may also occur due to Leydig cell loss, possibly as the result of age associated changes in the brain and pituitary.

Aging↗
PubMedDate not supplied

Neurochemical, endocrine and immunological responses to stress in young and old Fischer 344 male rats.

Two experiments were performed. In the first, a 20 min conditioned emotional response (CER) paradigm was used to compare the neurochemical, endocrine and immunological responses to stress of 7- and 22-month-old Fischer 344 (F344) male rats. In the second, corticosterone levels 20 min following ether stress, and regional brain type I and II corticosterone receptor densities were examined using 7- and 17.5-month-old F344 male rats. Dopamine (DA) metabolism in old nonstressed rats was significantly reduced in the medial frontal cortex, neostriatum, nucleus accumbens and hypothalamus, but not in the amygdala. The CER procedure, nevertheless, increased medial frontal cortical, nucleus accumbens and amygdaloid DA turnover in both the young and old rats. The young and old nonstressed rats did not evidence differences in norepinephrine (NE) and serotonin (5-HT) concentrations. However, stress resulted in a decrease in medial frontal cortical 5-hydroxyindoleacetic acid (5-HIAA) and hypothalamic 5-HT levels in old but not in young animals. These observations suggest age-related differences in the response of central NE and 5-HT systems to stress. Ether and the CER procedure led to exaggerated corticosterone responses in the old rats (17.5 and 22 month, respectively). Hippocampal type I but not type II corticosterone receptors were decreased by 47% in the 17.5-month-old rats. Thus, age-related changes in hippocampal corticosterone receptor types do not occur in unison, and the exacerbated corticosterone response to stress precedes the reported down-regulation of hippocampal type II corticosterone receptors in aged rats. Age-related changes were not observed in the concentrations of corticosterone receptors in other brain regions, or in the prolactin response to stress. The old rats, however, evidenced a reduction in the availability of the renin substrate, angiotensinogen, and in stress-induced renin secretion. Immune function was impaired in the old nonstressed rats, and further compromised by exposure to the CER procedure. In comparison to the young control rats, the old nonstressed rats showed an increased percentage of splenic large granular lymphocytes, reduced splenic natural killer cytotoxicity, and impaired Con-A-stimulated splenic T lymphocyte proliferation. Reductions in T splenic cell proliferation and natural killer cytotoxicity were observed in the young rats subjected to the CER paradigm, but not to the same extent as in the old rats. These observations indicate that aging male F344 rats evidence major alterations in basal central monoamine, endocrine and immune functions, and an increased sensitivity of these systems to stress.

Aging↗