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M Ruberg

Publications and source records attributed to M Ruberg.

104 records · Page 6Linked to original sources
PubMed1981

[PRF activity of VIP in vitro (author's transl)].

The effect of VIP on prolactin secretion from incubated rat hemipituitaries was characterized. Under these conditions, the secretion of GH, LH, FSH, ACTH was not affected, indicating that the effect of VIP is hormone specific. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations, whereas another partial analogue, glucagon, was ineffective. Furthermore, VIP does not act through pituitary DA receptors since alpha-flupentixol, a potent dopaminergic antagonist, does not block the stimulation of prolactin secretion by VIP. In addition, stimulation by VIP and TRH was additive. Naloxone and met-enkephalin were ineffective on the VIP effect on prolactin release. In contrast, SRIF seems to inhibit the VIP stimulation of prolactin release. Our data suggest that VIP, which was found in the hypothalamo-hypophyseal blood at concentrations of the same order of magnitude as that found to stimulate PRL in vitro, could be a physiological PRF.

Animals↗
PubMed1980

Stimulation of in vitro prolactin release by vasoactive intestinal peptide.

VIP stimulated prolactin secretion from incubated rat hemipituitaries. Under the same conditions, the secretion of GH, LH, FSH was not affected. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations whereas another partial analogue, glucagon, was ineffective. The effect of VIP was not blocked by alpha-flupentixol, a potent dopaminergic antagonist, at concentrations which antagonized the dopamine inhibition of prolactin secretion. Stimulation by VIP and TRH was additive. Neither Met-enkephalin nor naloxone interfered with the response to VIP. It thus seems that specific VIP receptors are present on pituitary prolactin cells. VIP, present in the mediobasal hypothalamus and detected in the hypothalamo-hypophyseal portal blood therefore is a good candidate as a physiological PRF.

Animals↗
PubMed1980

[Effect of neuropeptides on prolactin secretion by the adenohypophysis (author's transl)].

In order to identify prolactin regulating factors, the effect of various neuropeptides on prolactin secretion by the adenohypophysis has been tested. 1 degree Histidyl-proline-diketopiperazine (DKP), a major degradation product of TRH in hypothalamus and pituitary, inhibited prolactin secretion from incubated hemipituitaries (Fig. 1) with an apparent affinity of 0.5 nM. Histidyl-prolineamide and histidyl-proline, other degradation products of TRH, had no effect. TSH secretion was not affected under the same conditions. 2 degrees Vasoactive intestinal peptide (VIP) stimulated prolactin secretion in vitro in a dose dependent manner. The secretion of other adenohypophyseal hormones was not affected. This effect is not mediated by a dopaminergic mechanism, since it was not blocked by neuroleptics (Table I). 3 degrees Morphinomimetic peptides had no effect on prolactin secretion in vitro, but blocked the dopamine inhibition of prolactin secretion. The effect of metenkephalin and beta-endorphin was dose dependent and was blocked by naloxone (Fig. 2 and 3). Thse results indicate that specific receptors to various neuropeptides seem to be present on prolactin cells.

Animals↗
PubMed1979

Independent inhibition of prolactin secretion by dopamine and gamma-aminobutyric acid in vitro.

gamma-Aminobutyric acid (GABA) inhibits PRL release from incubated hemipituitaries in a dose-dependent manner. The maximum inhibition obtained with GABA is less than that obtained with dopamine. Its affinity is 100 times lower. The effect is blocked by picrotoxin but not by a dopamine inhibitor; alpha-flupentixol but not picrotoxin antagonizes dopamine inhibition. This indicates that dopamine and GABA inhibit PRL release through independent receptors. The hypothalamic extract contains sufficient GABA to inhibit PRL release in our in vitro conditions. Picrotoxin, however, does not significantly inhibit the nondopaminergic PRL-inhibiting activity of mediobasal hypothalamic extracts. Another nondopaminergic PRL-inhibiting factor, therefore, seems to be present in the hypothalamus.

Animals↗
PubMed1979

[Mental disorders and prolactin secretion].

Recent reports suggest that selective endocrine disturbances are often associated with mental disease, and that hormonal responses to treatments with antipsychotic drugs can be related to their clinical efficiency. The importance of central monoamine neuron systems for both hormonal control and mental disease probably accounts for these correlations. Measurement of prolactin, a hormone primarily regulated by hypothalamic dopaminergic neurons, provides a useful tool which can help to define the symptomatology of schizophrenic or depressed patients, to calibrate drug therapy and to obtain advance warning of therapeutical side effects. The hormone can also be used as an excellent index for screening dopamine agonist or antagonist properties of new drugs.

Dopamine↗
PubMedDate not supplied

Neuropharmacologic aspects of apoptosis: significance for neurodegenerative diseases.

The cause of neuronal death in Parkinson's, Alzheimer's, and other neurodegenerative diseases is not known, except in some hereditary forms of these disorders in which a mutated gene has been identified. Even in these cases, the molecular mechanisms that underlie the loss of specific populations of neurons have not been determined, although it is highly probable that apoptosis is involved. Some of the biochemical events that occur during apoptosis have been elucidated. We focus in this review on the role played by the proapoptotic caspases, the antiapoptotic proteins of the Bcl-2 family, and the apoptosis associated signal transducers such as ceramide, calcium, and reactive nitrogen or oxygen species. The role of the mitochondria and the possible implication of cell cycle regulators will also be addressed. Of particular interest are the endogenous inhibitory mechanisms and the pharmacologic agents that can be used to block apoptosis signaling cascades, because they offer models for the development of therapeutic strategies designed to prevent the evolution of pathologic neurodegeneration.

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