PubMed Health⌕ Search

Biomedical subjects

J M van Ree

Publications and source records attributed to J M van Ree.

At least 163 records · Page 9Linked to original sources
PubMed1981

Gamma-melanotropin and brain function.

In view of the close structural similarity between the pro-opiocortin fragment, gamma-MSH, and ACTH/MSH-type peptides, the behavioural profile of gamma-MSH was explored. Attention was first focused on behavioural procedures in which ACTH/MSH-related neuropeptides have been found effective. It was found that gamma-MSH and ACTH-like neuropeptides had opposite effects on avoidance behaviour. In this respect the activity of gamma-MSH resembles that of opiate antagonists rather than that of beta-endorphin. Accordingly, ACTH(1-24) induced excessive grooming which is blocked by opiate antagonists and is attenuated by gamma-MSH. In addition, gamma-MSH injected into the periaqueductal grey matter of the brainstem of opiate-naive rats elicited symptoms reminiscent of those seen after opiate withdrawal. Gamma-MSH attenuated several effects of intracerebroventricularly administered beta-endorphin (e.g. antinociception, hypothermia, alpha-MSH release) and decreased the acquisition of heroin self-administration. Although gamma-MSH at rather high doses displaced naloxone from its specific binding sites in brain homogenates, it did not interfere with beta-endorphin-induced effects on in vitro muscle preparations (guinea-pig ileum; rat rectum). Interestingly, gamma-MSH induced relaxation of the rat rectum in vitro. It is postulated that gamma-MSH may attenuate beta-endorphin-induced effects by acting via gamma-MSH receptor sites (functional antagonism), although a pharmacological antagonism cannot be excluded as yet.

Adrenocorticotropic Hormone↗
PubMed1981

Influence of beta-lipotropin fragments on responsiveness of rats to electric footshock.

Subcutaneous administration of graded doses of neuropeptides related to lipotropin (beta LPH) changed responsiveness of rats to electric footshock. gamma-Endorphin and related peptides increased the susceptibility of rats, whereas beta-endorphin induced a reversed effect. The enhanced responsiveness induced by DT gamma E, persisted for more than 24 hr and appeared to be of a central origin. Structure-activity relationship studies revealed that the sequence LPH 65-69 may contain the active core in this respect. An increased sensitivity to electric shock within one test procedure was observed with DT gamma E and alpha-endorphin. Prior experience with the test procedure diminished or abolished this effect of alpha-endorphin. It is suggested that beta-endorphin and its fragments play a physiological role in adaptive behavioral changes induced by peripheral stimuli.

Amphetamine↗
PubMed1981

(Des-tyrosine1)-gamma-endorphin in schizophrenia: clinical, biochemical, and hormonal aspects.

The neuropeptide (des-tyrosine1)-gamma-endorphin (DT gamma E; beta-LPH 62-77) was given to 10 schizophrenic patients who had been free of neuroleptic medication for at least 3 weeks. DT gamma E was injected intramuscularly in a dose of 1 mg daily for 10 days following a double-blind placebo-controlled crossover design. In 4 of the 10 patients a pronounced antipsychotic effect was observed; in 3 a temporary or slight reduction of psychotic symptoms occurred; and in 3 no response was noted. DT gamma E led to decreased plasma levels of prolactin and in some patients to increased concentrations of homovanillic acid in cerebrospinal fluid (CSF). Neither plasma levels of growth hormone and cortisol nor CSF concentrations of 5-hydroxyindoleacetic acid were affected by DT gamma E. These data confirm that DT gamma E has antipsychotic properties in a number of schizophrenic patients and suggest an interaction between DT gamma E and central dopaminergic systems.

Adult↗
PubMed1981

Hypothalamic catecholamine levels in dogs with spontaneous hyperadrenocorticism.

Hypothalamic norepinephrine (NE) and dopamine content was studied in dogs with spontaneous and iatrogenic hypercortisolism and in untreated normal dogs. The concentration of NE in the hypothalamus was subnormal in 4 of 8 dogs with pituitary-dependent hyperadrenocorticism (PDH), whereas long-term administration of corticotropin or cortisone acetate did not result in low hypothalamic NE content. In dogs with hyperadrenocorticism due to adrenocortical tumor subnormal as well as normal and high hypothalamic NE levels were found. Hypothalamic as well as striatal dopamine content did not differ among groups of dogs with PDH, adrenocortical tumor, corticotropin treatment, cortisone treatment and in untreated normal dogs. The subnormal hypothalamic NE levels in dogs with PDH may be involved in the hypersecretion of ACTH found in this disease. The normal hypothalamic dopamine levels in dogs with PDH are not consistent with a dopaminergic-depletion as the cause of PDH.

Adrenal Gland Neoplasms↗
PubMed1981

Disposition of morphine in rat brain: relationship to biological activity.

The levels of morphine in plasma and brain subcortex of rats were determined by gas-liquid chromatography and radioimmunoassay at various time intervals after a single i.v. injection of graded doses of morphine (0.44, 1.04 and 2.25 mg/kg). The disappearance curve of morphine plasma levels appeared to be composed of at least two exponential terms: a rapid disappearance during the 1st hr, which was dependent on the unit dose of morphine injected and a slower disappearance rate after the 1st hr. The highest morphine levels in the brain were measured already 5 min after its injection and these levels only slightly decreased over the next 2 hr. Thereafter a more rapid disappearance of brain morphine was observed. The brain/plasma ratio gradually increased from 0.18 at 5 min after injection to about 1.0 at 60 and 120 min and decreased to approximately 0.4 at 4 hr after injection. This may suggest that morphine is retained in the brain during the 1st hr after injection and that it might be removed from the brain between 2 and 4 hr, possibly by an active process. The relationship between brain morphine levels and the degree of antinociception as assessed with the hot plate procedure appeared to be rather complicated. Shortly after morphine injection, but also at 60 and 120 min after injection, the antinociceptive effect was much lower than might be expected from the levels of morphine in the brain. Several possible explanations for this phenomenon are discussed. A high dose of naltrexone, which completely blocked the antinociceptive effect of morphine, did not affect brain and plasma levels of morphine. Rifampicin, which attenuates development of morphine tolerance, increased brain levels of morphine but did not change plasma levels. Pretreatment with the tripeptide prolyl-leucyl-glycinamide, which facilitates development of morphine tolerance, decreased brain morphine levels and increased plasma levels at 3 hr after morphine injection. This suggests that tolerance development and the rate with which morphine is removed from the brain may have at least some common underlying mechanisms.

Animals↗
PubMed1979

Improvement of schizophrenic patients treated with [des-Tyr1]-gamma-endorphin (DTgammaE).

It was postulated from animal experiments that gamma-endorphin and, in particular, the nonopiate-like peptide [des-Tyr1]-gamma-endorphin (DTgammaE, beta-lipotropin [beta-LPH]62-77) have neurolepic-like activity. To test this, 14 patients with long-lasting, relapsing schizophrenic or schizoaffective psychosis resistant to conventional neuroleptics were treated with DTgammaE. An open design was used first for six patients (study 1) and a double-blind, crossover design for the other eight (study 2). In study 1, all neuroleptic medication was discontinued and 1 mg of DTgammaE zinc phosphate was given daily intramuscularly for about seven days. In study 2, six patients were maintained with neuroleptic therapy and two patients were drug free; all eight received daily intramuscular injections of 1 mg of nonlasting DTgammaE in saline and solution for eight days. There was transient or semipermanent improvement in both studies in which the psychotic symptoms diminished or even disappeared. In study 2, there was a slight but significant improvement with the first treatment. Improvement continued and by day 4, the psychotic symptoms had almost disappeared. No toxic side effects were noted. These effects of DTgammaE may be a consequence of the normalization of beta-endorphin homeostasis in the brain.

Adult↗