Selective activation of D1 dopamine receptors exerts antidepressant-like activity in rats.

Background: Major depressive disorder is a common illness that severely decreases psychosocial functioning. Due to the major limitations of current treatments including response failure, it is crucial to develop better therapy strategies. Evidence suggests that dopamine dysregulation might play a major role in major depressive disorder physiopathology.

Brain plasticity and cognitive functions after ethanol consumption in C57BL/6J mice.

Acute or chronic administrations of high doses of ethanol in mice are known to produce severe cognitive deficits linked to hippocampal damage. However, we recently reported that chronic and moderate ethanol intake in C57BL/6J mice induced chromatin remodeling within the Bdnf promoters, leading to both enhanced brain-derived neurotrophic factor (BDNF) expression and hippocampal neurogenesis under free-choice protocol. We performed here a series of cellular and behavioral studies to analyze the consequences of these modifications.

Involvement of histamine receptors in the atypical antipsychotic profile of clozapine: a reassessment in vitro and in vivo.

Rationale: The basis of the unique clinical profile of the antipsychotic clozapine is not yet elucidated. Brain histamine receptors may play a role in schizophrenia and its treatment, but their involvement in the profile of clozapine remained unknown.

Objectives: We explored the properties of clozapine and its two metabolites, N-desmethylclozapine (NDMC) and clozapine N-oxide, at the four human histaminergic receptors.

[The histaminergic system: a target for innovative treatments of cognitive deficits].

The central effects of histamine are mediated by H(1), H(2) and H(3) receptors. The H(3) receptor inhibits histamine release in brain. Therefore, H(3) receptor inverse agonists, by suppressing this brake, enhance histamine neuron activity.

Activation of brain histaminergic neurotransmission: a mechanism for cognitive effects of memantine in Alzheimer's disease.

We previously reported that some N-methyl-D-aspartate (NMDA)-receptor antagonists enhanced histamine neuron activity in rodents. Here, we have investigated the effects of memantine, an NMDA-receptor antagonist used for the treatment of Alzheimer's disease, on histaminergic neurotransmission. In vitro, memantine antagonized native NMDA receptors with a micromolar potency but had no effect at recombinant human histamine receptors.

Effects of betahistine at histamine H3 receptors: mixed inverse agonism/agonism in vitro and partial inverse agonism in vivo.

We previously suggested that therapeutic effects of betahistine in vestibular disorders result from its antagonist properties at histamine H(3) receptors (H(3)Rs). However, H(3)Rs exhibit constitutive activity, and most H(3)R antagonists act as inverse agonists. Here, we have investigated the effects of betahistine at recombinant H(3)R isoforms.

Autoregulation of McA-RH7777 hepatoma cell proliferation by histamine H3 receptors.

Previous studies have suggested that histamine (HA) acts as an autocrine growth factor. We have explored the modulation of cell proliferation by HA using McA-RH7777 hepatoma cells. High L-histidine decarboxylase (HDC) expression and HA synthesis were found in McA-RH7777 cells.

Modulation of stress proteins by Cd2+ in a human T cell line.

We previously showed in a human T cell line (CEM-C12 cells) that Cd2+ induced gene expression of stress proteins, metallothionein-IIA and heat shock protein 70 in a time- and dose-dependent manner. In the present study, CEM-C12 cells were pretreated for 24 h with 1 microM Cd2+ and then challenged with toxic concentrations of this metal. We found that maximal expression of the metallothionein-IIA and heat shock protein 70 genes was increased and this maximal level occurred at higher Cd2+ toxic concentrations.

Human basophil degranulation triggered by very dilute antiserum against IgE.

When human polymorphonuclear basophils, a type of white blood cell with antibodies of the immunoglobulin E (IgE) type on its surface, are exposed to anti-IgE antibodies, they release histamine from their intracellular granules and change their staining properties. The latter can be demonstrated at dilutions of anti-IgE that range from 1 x 10(2) to 1 x 10(120); over that range, there are successive peaks of degranulation from 40 to 60% of the basophils, despite the calculated absence of any anti-IgE molecules at the highest dilutions. Since dilutions need to be accompanied by vigorous shaking for the effects to be observed, transmission of the biological information could be related to the molecular organization of water.

In vitro immunological degranulation of human basophils is modulated by lung histamine and Apis mellifica.

1. The effect of high dilutions of two homeopathic drugs Lung histamine (Lung his) and Apis mellifica (Apis mel) used for the treatment of allergic diseases has been assessed on in vitro human basophil degranulation. Experiments were conducted blind.

Effect of mouse peritoneal macrophages of orally administered very high dilutions of silica.

The activity of very high dilutions of silica, a substance cytotoxic for macrophages, was tested on the synthesis by mouse peritoneal macrophages of the inflammatory ether-lipid paf-acether and its precursor lyso paf-acether. C57Bl6 female mice received for 25 days either 1.66 X 10(-11) M silica (11 sil) or 1.

Effect of dietary (n--3) fatty acids on platelet function and lipid metabolism in rats.

Six groups of rats were fed diets containing 40% (by weight) lipids, mostly as saturated fatty acids (from 78 to 90%), with a basic amount of linoleic acid (18:2) (1.9%). In four groups, 5% of the saturated fats were substituted with an oil (vegetable: corn, rapeseed; or fish: cod liver, maxepa) and in one group 0.

Vitamin E prevents the platelet abnormalities induced by estrogen in rat.

Platelet lipid biosynthesis in relation to aggregation has been studied in female rats treated with ethynylestradiol and fed laboratory chow or a vitamin E-deficient diet. In both normal and vitamin E-deficient rats, administration of ethynylestradiol highly significantly (p less than .001) increased the biosynthesis of total lipids but mostly of lanosterol (+ dihydrolanosterol) by thirteen-fold in normal rats and by nine-fold in vitamin E-deficient rats.

Effects of dietary lipids on behaviour, lipid biosynthesis and lipid composition, in rat platelets.

Rats of either sex were fed for 18 and 34 weeks respectively diets containing 40% (by weight) lipids with polyunsaturated fatty acids representing 1.34% or 13.2% of total calories.

Influence of sex and dietary fats on platelet lipid biosynthesis in rat.

The platelet biosynthesis of total lipids, lipid fractions and fatty acids was determined by incorporation of [14C]acetate in normal and castrated rats of both sexes. Comparison was made between animals fed laboratory chow alone, and animals receiving, in addition, for 4 days by stomach tube a saturated (cream) or polyunsaturated (sunflower seed oil) fat. In male rats, the polyunsaturated fat increased slightly the total platelet lipid biosynthesis.

Biosynthesis of platelet lipids in relation to aggregation in women using oral contraceptives.

The platelet lipid biosynthesis in relation to platelet aggregation and lipemia was studied by 14C-acetate and mevalonate incorporation into platelets of seventeen women without medication and of eighteen women using a low estrogen oral contraceptive. The lipid biosynthesis was significantly increased by 59% (mevalonate) and 38% (acetate) in women on oral contraceptives. From mevalonate, lipid synthesis was increased mostly in the lanosterol-dihydrolanosterol fraction (p less than .

Oral contraceptive and Platelet lipid biosynthesis in female rats: dose-response relationship.

Female rats were treated with different doses of an oral contraceptive (ethinyl estradiol + lynestrenol) and lipid biosynthesis was studied in blood platelets by acetate incorporation into different fractions separated by thin layer chromatography. A marked increase in lipid biosynthesis was observed, especially in the sterol fractions (cholesterol and lanosterol-dihydrolanosterol). It was dose-dependent, observed after a lag-phase, maximal in 3 days and normalized in 8 days.