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Biomedical subjects

M Daoust

Publications and source records attributed to M Daoust.

25 records · Page 2Linked to original sources
PubMed1986

Dynamic characteristics of dopamine, norepinephrine and serotonin metabolism in axonal endings of the rat hypothalamus and striatum during hypoxia: a study using HPLC with electrochemical detection.

The metabolism of dopamine, norepinephrine and serotonin was studied in normoxic or hypobaric hypoxic rats, using HPLC with electrochemical detection. The changes in serotonin and its metabolite 5 hydroxy indolacetic acid (5 HIAA) levels in the hypoxic striatum and hypothalamus suggest an inhibition of 5 HIAA formation and a complex interaction between synthesis, release and uptake. Hypoxia caused a decrease of the striatal levels of homovanillic acid (HVA), dihydroxy 3-4 phenylacetic acid (DOPAC) [inhibition of tyrosine hydroxylase (TH) and monoamine oxidase (MAO)] and 3-methoxytyramine (3 MT) (inhibition of release). Striatal dopamine levels were increased, suggesting an increase in granular dopamine storage, with an impaired release. Hypothalamic levels of norepinephrine were decreased during hypoxia [(inhibition of TH, MAO, and dopamine beta-hydroxylase (DBH)].

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Survival time in hypoxic mice: differentiation between apomorphine-induced hypothermia and antihypoxic properties.

The effects of apomorphine on survival time of mice during lethal anoxic hypoxia were studied. Apomorphine induced hypothermia and an increase in survival time. Both these effects were mediated by cerebral dopamine receptors, however with different affinity for the neuroleptics haloperidol and sulpiride. These data suggest that apomorphine's antihypoxic effect is not only mediated by the classical effect of hypothermia but also by slowing of oxydative metabolism.

Animals↗
PubMed1985

Ability of calcium bis acetyl homotaurine, a GABA agonist, to prevent relapse in weaned alcoholics.

After they had been weaned off alcohol in hospital 85 severe alcoholics (above 200 g alcohol/day) were included in a double-blind study of calcium bis acetyl homotaurine (Ca AOTA, 25 mg/kg/day), a new gamma-aminobutyric acid agonist, versus placebo. Patients were treated as outpatients during the 3-month study. The only other treatment that patients received was meprobamate, 800 to 1200 mg/day, in the first month. The criterion for success was abstinence at 3 months (with normal gamma-glutamyl transpeptidase being one of the criteria). Of the 70 patients who completed the study, 33 received Ca AOTA and 37 placebo. 20 patients on Ca AOTA did not relapse, compared with 12 on placebo (p less than 0.02 by X2 test). Side-effects were noted by 7 patients on Ca AOTA and 2 on placebo. The results suggest that Ca AOTA may be useful in helping severe alcoholics who have been weaned off alcohol not to relapse.

Acamprosate↗
PubMedDate not supplied

GABA transmission, but not benzodiazepine receptor stimulation, modulates ethanol intake by rats.

Adult male Long Evans were selected as ethanol preferring rats (DR) during 28 days. After this period, they were daily IP injected during 14 days with one of the next drugs: diazepam 1 mg.kg-1, alprazolam 1 mg.kg-1 (benzodiazepines), progabide 25 mg. kg-1 (GABA A and B agonist), nipecotic acid 150 mg.kg-1 (GABA uptake inhibitor), muscimol 0.2 mg.kg-1 (GABA A agonist), AOAA 10 mg.kg-1 (GABA decarboxylase inhibitor), baclofen 3 mg.kg-1 (GABA B agonist), or NaCl 0.9% (1 ml/200 g). During treatment, rats were isolated, had free access to food, and free choice between ethanol (12%) and water whose respective consumption were daily noted. Among treatments, only AOAA and baclofen were able to decrease significantly ethanol intake, without modifying total liquid intake. The action of these different drugs on GABA transmission and on ethanol intake was discussed. It was concluded that GABA A and benzodiazepine receptors were not implicated in ethanol intake, but that modulation of voluntary ethanol intake could be associated with a modification of GABA metabolism and/or stimulation of GABA B receptors. An intervention of GABA B receptors on noradrenergic pathways was also evoked.

Alcohol Drinking↗
PubMedDate not supplied

[Alcohol and the serotonin system].

There is considerable evidence from animal and human studies that serotonin plays a role in the modulation of alcohol intake and/or alcohol dependence. Biochemical, behavioral and pharmacological studies both in animal and man had verified this hypothesis. Central and peripheral levels of serotonin and of its metabolite 5-hydroxyindoleacetic acid (5-HIAA) are modified by alcoholisation. Moreover, the use of pharmacological drugs modifying specifically serotonin transmission decreases ethanol intake. Our own studies suggest that a dysfunctioning of serotonin uptake system could be implicated in the individual risk of alcohol dependence. Even if other systems, e.g. amino acids, are involved in the regulation of alcohol behavior, all data are in favor of a modulation of alcohol intake by serotonin transmission.

Alcohol Drinking↗
PubMedDate not supplied

[Absence of the antihypertensive effect of chronic treatment with prazosin in the spontaneously hypertensive rat (SHR) and their offspring].

Seven consanguine monogamous SHR couples (G 1) were treated from their 5th to their 39th week of age with prazosin, 100 micrograms/kg/day i.p. Male rats were treated without interruption. Treatment was withheld in female rats from delivery to weaning. They were compared to seven similar SHR couples who were only daily i.p. injected with the same volume of solvent. Second (G 2) generation rats (untreated were studied. In G 1 female rats only, prazosin induced a transient decrease in systolic blood pressure (SBP), 6 hours after the injection, at 25 weeks of age. SBP, heart weight/body weight ratio and plasma renin activity remained unchanged at 39 weeks of age. Gestational parameters were not changed by the treatment, and no parameter was changed in G 2 rats. A previous study in the same conditions with another alpha 1-adrenoreceptor blocking agent, nicergoline, showed an inhibition of hypertension development in G 1 rats together with a preventive effect on untreated G 2 SHR (Moore et al., 1983). Thus prazosin failed to produce similar antihypertensive effects both in the treated rats and in their offspring and one can therefore conclude that nicergoline's effects were not only due to alpha 1-adrenoceptor blockade.

Aging↗