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Biomedical subjects

C Gramsch

Publications and source records attributed to C Gramsch.

At least 55 records · Page 3Linked to original sources
PubMed1982

The influence of selective adeno- and neurointermedio-hypophysectomy upon plasma and brain levels of beta-endorphin and their response to stress in rats.

Selective ablation of the anterior lobe (AL) of the pituitary led to a fall in basal plasma levels of beta-endorphin immunoreactivity (beta-EI) at 3 and 20 weeks post-surgery (p.s.). Further, the stress-evoked rise in circulating levels of beta-EI was abolished. This operation did, however, severely deplete the beta-EI content of the neurointermediate lobe (NIL). Removal of the NIL did not, in contrast, decrease the beta-EI content of the AL but depressed basal plasma levels of beta-EI at 3 weeks p.s. and attenuated, but did not abolish, the increase in these elicited by stress at both 3 and 20 weeks p.s. In rats not possessing a NIL, a secretion of beta-EI into plasma can thus occur. The possibility that NIL pools of beta-EI contribute to circulating levels of beta-EI is discussed. Removal of the AL depressed the beta-EI content of the hypothalamus and periventricular tissue at 3 and 20 weeks p.s. The Met-enkephalin-immunoreactivity (ME-I) content of the hypothalamus was, in contrast, unaffected. These animals still responded to stress at 20 weeks p.s. with a significant fall in hypothalamic levels of beta-EI. Extirpation of the NIL did not, in contrast, change brain levels of either beta-EI or ME-I. The presence of the AL, but not the NIL, is thus essential for the maintenance of usual levels of beta-EI and ME-I in the brain.

Animals↗
PubMed1982

Immunoreactive dynorphin in human brain and pituitary.

The distribution of immunoreactive dynorphin (ir-dyn) has been determined in various regions of human brain and pituitary by use of a highly specific radioimmunoassay. The concentrations of ir-dyn in the substantia nigra (24.5 pmol/g) and hypothalamus were among the highest in the 26 brain areas examined. Substantial amounts were also measurable in other extrapyramidal structures such as the caudate nucleus, pallidus and putamen. Lower concentrations of ir-dyn were detected in the amygdala, hippocampus, periaqueductal gray matter, colliculi, pons, medulla and area postrema, but only low amounts were found in the posterior lobe of the pituitary, while no ir-dyn was detectable in the anterior lobe. By gel permeation chromatography the brain immunoreactivity was shown to consist of 3-4 peaks of apparent molecular weights of about 12,000, 6000, 1800 and less than 1000. It was possible to demonstrate the high opioid potency of 2 of these peaks in the guinea-pig ileum longitudinal muscle bioassay after purification by immunoprecipitation. A comparison of the distribution pattern of ir-dyn revealed some parallels with enkephalin, whereas the distribution of ir-beta-endorphin is quite different.

Adult↗
PubMed1981

Stress-induced release of brain and pituitary beta-endorphin: major role of endorphins in generation of hyperthermia, not analgesia.

The present paper examines the conjectured causal relationship between the alterations in brain, pituitary and plasma levels of endorphins and the antinociception (analgesia) and hyperthermia elicited by acute stress. A 5-min foot-shock instigated a significant depression in the levels of beta-endorphin immunoreactivity (beta-EI) in both the hypothalamus and periventricular beta-endorphinergic fibre-containing tissue. A large elevation in plasma levels of beta-EI, consisting of about 70% beta-endorphin (beta-EP), and 30% beta-lipotropin (beta-LPH) was associated with a significant reduction in the beta-EI content of both the anterior (AL) and neurointermediate (NIL) lobes of the pituitary. No concomitant changes in the levels of Met-enkephalin immunoreactivity (M-EI) in discrete areas of brain and pituitary were detectable. Application of a high (10 mg/kg) but not a low (1 mg/kg) dose of naloxone, prior to foot-shock, slightly reduced the increase in tail-flick latency evoked by this stress. In contrast, both of these doses strongly and dose-dependently attenuated the accompanying rise in core temperature (Tc). Chronic (approximately 30 day) morphine treatment resulted in a 45% decrease in the NIL content of beta-EI and a clear depression in its basal plasma levels, although a substantial post-stress rise in plasma beta-EI was still found: stress-induced analgesia (SIA) was enhanced, but the concurrent stress-induced hyperthermia (SIH), reduced in morphinized animals. These data demonstrate that stress produces a generalized mobilization of both central and pituitary pools of beta-EI, and indicate that endorphins may play a more important role in the mediation of changes in Tc than in the generation of the concomitant increase in nociceptive threshold, upon activation by stress.

Animals↗
PubMed1980

Pro-opiocortin fragments in human and rat brain: beta-endorphin and alpha-MSH are the predominant peptides.

The 'pro-opiocortin' fragments, beta-lipotropin, beta-endorphin, ACTH and alpha-MSH, were estimated in discrete areas of rat and human brain and pituitaries by means of radioimmunoassay in combination with gelfiltration. These peptides exhibited parallel patterns of distribution, but with beta-endorphin and alpha-MSH predominant in the brain of rat and man, and, in contrast, their respective precursors. beta-LPH and ACTH predominant in the adenohypophysis of rat and man. These data may be indicative of important differences in post-translational processing of 'pro-opiocortin' between these contrasting tissues.

Adrenocorticotropic Hormone↗
PubMed1980

Extrahypothalamic corticotropin and alpha-melanotropin in human brain.

The distribution of corticotropin (ACTH) and alpha-melanotropin (alpha-MSH) in human brain was investigated by radioimmunoassay using an antiserum which recognized h-ACTH1-39 and alpha-MSH to an equal degree on a molar basis. Significant amounts of material, which migrated on calibrated Sephadex G-50 columns as synthetic h-ACTH1-39 and synthetic alpha-MSH, were detected in distinct brain areas. The highest concentrations of ACTH and alpha-MSH were found in the diencephalon (hypothalamus 4.2 and 12.5 pmol/g wet weight, respectively) and in midbrain (periaqueductal gray 0.5 and 1.7 pmol/g, respectively) and smaller quantities in the rhombencephalon and telencephalon. The ACTH concentration in human pituitary (adenohypophysis) was 10(4)-fold greater than that in the hypothalamus. alpha-MSH was confined to the midpart and/or stalk region of the pituitary.

Adrenocorticotropic Hormone↗
PubMed1980

'Proopiocortin fragments' in normal human adult pituitary. Distribution and ultrastructural characterization of immunoreactive cells.

The distribution and ultrastructure of cells immunoreactive towards antisera against synthetic fragments of proopiocortin were studied in human pituitaries by immunohistochemical methods. Anterior lobe cells exhibiting the ultrastructural characteristics of corticolipotropes, as well as all epithelial cells 'invading' the posterior lobe, display beta-endorphin/beta-lipotropin-ACTH immunoreactivities. At low dilution a beta-lipotropin antiserum, raised with highly purified antigen, stains also somatotropes. alpha-MSH antibodies bind to certain corticolipotropic cells in the pars distalis and to only a few of the cells 'invading' the pars nervosa. Met-enkephalin antisera react only with isolated cells in the anterior lobe. These results indicate a striking difference in the processing of the proopiocortin precursor molecule in different corticolipotropic cells of the human hypophysis. Furthermore, the hypothesis of a homology between cells 'invading' the human neurohypophysis and those of the intermediate lobe of lower vertebrates, is questioned.

Adrenocorticotropic Hormone↗
PubMed1980

Functional aspects of endorphins.

Radioimmunoassay of methionine-enkephalin, leucine-enkephalin and beta-endorphin were used in order to study the distribution and release of endorphins. The distribution pattern of enkephalin immunoreactivity in brain, including human brain, is quite different from that of beta-endorphin immunoreactivity. Separation of beta-endorphin and beta-lipotropin by column chromatography revealed that the contribution of beta-lipotropin to beta-endorphin immunoreactivity in brain is very small. In the anterior lobe of the pituitary both beta-endorphin and beta-lipotropin were found, whereas in the intermediate/posterior lobe almost all immunoreactivity was due to beta-endorphin; considerable amounts of enkephalin were also detected. Raising the concentration of potassium ions stimulated the release of met- and leu-enkephalin from striatal slices and the release of beta-endorphin immunoreactive material(s) from hypothalamic slices; both phenomena were dependent upon the presence of calcium ions. Studies of the release of beta-endorphin from isolated rat pituitaries revealed characteristic differences between the anterior and intermediate/posterior lobes; e.g., lysine vasopressin and extracts from the median eminence were highly effective in releasing beta-endorphin from the anterior lobe without affecting the release from the intermediate/posterior lobe; on the other hand, dopamine inhibited beta-endorphin release from the intermediate/posterior lobe without affecting release from the anterior lobe. Increased beta-endorphin levels were found after various stress conditions in rat plasma, as well as after treatment with metyrapone and vasopressin. In normal human plasma significant amounts of beta-endorphin were detected; increased levels were found in Addison's, Nelson's and Cushing's disease. Chronic opiate treatment of rats for 10 days did not affect brain levels of enkephalin or the beta-endorphin content of the hypothalamus, pituitary and plasma. Precipitated withdrawal decreased beta-endorphin in the anterior lobe and hypothalamus and increased beta-endorphin levels in the plasma. Long-term morphine treatment (30 days) decreased enkephalin and beta-endorphin content in some brain areas and in the intermediate/posterior pituitary lobe but not in the anterior lobe.

Animals↗
PubMed1979

Regional distribution of methionine-enkephalin- and beta-endorphin-like immunoreactivity in human brain and pituitary.

Concentrations of methionine-enkephalin- (Met-enkephalin) and beta-endorphin-like immunoreactivities were determined in 33 areas of human brain and pituitary using highly sensitive radioimmunoassays in combination with affinity chromatography for the purification of beta-endorphin. It was found that they have quite different distribution patterns, suggesting the existence of both endorphins in independent systems in the central nervous system. Determination of Met-enkephalin and beta-endorphin immunoreactivities in chronic alcoholics and opiate-dependent subjects revealed no gross changes in comparison to the normal subjects.

Adult↗
PubMed1977

Changes in striatal dopamine metabolism during precipitated morphine withdrawal.

Precipitation of withdrawal in morphine tolerant/dependent rats by either naloxone or the partial agonist ZK 48491 caused a significant increase in the contration of striatal DA, which persisted for at least 1 h. During the same time the probenecid-induced accumulation of HVA and DOPAC was reduced in the striatum in relation to probenecid-treated tolerant/dependent controls. 20 min after precipitation of withdrawal by naloxone, the striatal concentration of 3-methoxytyramine was decreased by about 40%, while the activity of the DA metabolizing enzymes, MAO and COMT, remained unchanged. Naloxone-precipitated withdrawal was, further, found to delay the depletion of striatal DA caused by inhibition of synthesis 90 min after alpha-methyl-p-tyrosine treatment. All these results provide evidence for a decreased release of DA from the striatum during precipitated morphine withdrawal.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Central serotonergic mechanisms and development of morphine dependence.

The effects of different manipulations of brain serotonin (5-HT) content on the development of morphine dependence were investigated in rats, which were implanted with morphine pellets for 40 days. Serotonin content was decreased by (a) short or long term inhibition of tryptophan hydroxylase with para-chlorophenylalanine (PCPA), (b) by short or long term degeneration of 5-HT containing nerve terminals with 5,6-dihydroxytryptamine or (c) by degeneration of 5-HT containing nerve terminals by lesioning of midbrain raphe nuclei. With all methods used, the frequency of withdrawal jumping was significantly reduced, while other withdrawal signs remained more or less unchanged. Additional administration of 5-HTP to chronically PCPA treated rats did not reverse the PCPA effect. Since chronic reduction of 5-HT level during the whole time of morphine exposure changed withdrawal symptomatology in nearly the same way as did a decrease in 5-HT level during the time of withdrawal only, it is suggested that serotonergic mechanisms are not linked to the basic processes underlying dependence development but that they are only involved in the nervous pathways mediating the expression of some withdrawal signs.

5,6-Dihydroxytryptamine↗