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Biomedical subjects

M Daoust

Publications and source records attributed to M Daoust.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1985

Isolation and striatal (3H) serotonin uptake: role in the voluntary intake of ethanol by rats.

Ethanol preferring rats were selected and showed a constant voluntary intake of a 12 percent ethanol solution during 14 days (about 5 g/kg body weight daily). Analysis of 3H serotonin uptake by striatal synaptosomes showed that steady state 3H serotonin synaptosomal levels were lower in alcohol preferring rats. Grouping these rats (5 per cage) reduced both voluntary intake of ethanol and synaptosomal 3H serotonin uptake. Furthermore, blocking the serotonin uptake by clomipramine 5 mg X kg-1 or 10 mg X kg-1 also reduces voluntary intake of ethanol. These data are in agreement with the hypothesis of a modulation of the voluntary intake of ethanol both by chemical and housing stimulation of striatal receptors for serotonin.

Alcohol Drinking↗
PubMed1985

Hemodynamic, behavioral and biochemical disturbances induced by an experimental cranio-cervical injury (whiplash) in rats.

Two days after an experimental whiplash performed on anesthetized Long-Evans female rats, without any direct blow to the head, we observed: (1) a hypotension (in supine position) (P less than 0.01), (2) a disturbance of the postural regulation of cerebral blood flow (P less than 0.01), (3) a disturbance of learning behavior characterized by decreased acquisition and retention (conditioned avoidance response and labyrinth tests), (4) an increase of the dopamine level (whole brain, cerebellum, thalamus + hypothalamus, corpus striatum and rest), (5) a decrease of the noradrenaline level in whole brain (P less than 0.05) and in the medulla oblongata but an increase in thalamus plus hypothalamus, hippocampus and corpus striatum, (6) an increased reactivity of the peripheral alpha and beta receptors, determined by analyzing the hemodynamic consequences of i.v. injection of norepinephrine or isoproterenol, (7) there was no modification of the brain content of water or of serotonin and (8) finally, the injured rats displayed a remarkably aggressive behavior, though this was not quantified. These results are in agreement with the hypothesis that a change in brain amines metabolism could explain the different functional effects of whiplash. We therefore believe that the postconcussion syndrome is not subjective and that the neck injury is primary in the determination of the syndrome.

Animals↗
PubMed1985

Oxotremorine-induced cholinergic syndrome: modifications by levodopa and/or oral cytidine diphosphocholine.

A peripheral and cerebral cholinergic syndrome was induced in mice by oxotremorine administration; pretreatment orally with cytidine diphosphocholine (CDP-choline) does not potentiate this syndrome and even antagonizes oxotremorine-induced salivation. Levodopa antagonizes the oxotremorine-induced cerebral symptoms (akinesia + tremor); however this antagonism disappears when mice are chronically pretreated orally with CDP-choline, confirming the action of CDP-choline on dopaminergic pathways. The proven efficacy of CDP-choline in Parkinsonism could then be mediated by a hypersensitivity of some cerebral dopamine receptors, and not by a direct stimulating effect of the striatal dopaminergic receptors.

Administration, Oral↗
PubMed1985

Use of RU 25960, a new calcium antagonist, in normobaric and hypobaric hypoxia.

RU 25960--3-[Bis(3,3-diphenylpropyl)-amino]-propan-1-ol hydrochloride--a vasodilator with calcium antagonist properties, was tested on learning in hypobaric hypoxic rats and survival time in normobaric hypoxic mice. It decreased learning in hypobaric hypoxia, but did not change survival time in mice. This suggests that the mechanisms underlying learning and survival are not the same, and that like other calcium antagonists, RU 25960 has no protective effect against the deleterious effects of hypoxia on the brain.

Aerospace Medicine↗
PubMed1984

A homotaurine derivative reduces the voluntary intake of ethanol by rats: are cerebral GABA receptors involved?

The effects of some derivatives of homotaurine (3 APS), the well known GABA agonist, were tested on the voluntary intake of ethanol by rats. Spontaneously ethanol drinking rats (DR) were selected and had a constant voluntary intake of ethanol by rats. Spontaneously ethanol drinking rats (DR) were selected and had a constant voluntary intake of a 12% ethanol solution (VIE) during 14 days (about 5 g/kg body weight daily). Calcium acetylhomotaurine (0.26 and 0.52 mmol/kg daily IP) significantly reduced VIE and this was inhibited by the GABA antagonist bicuculline (2 mg/kg IP). The conditioned aversion test to saccharin was negative. Bicuculline alone did not affect VIE. Other homotaurine (3-APS) derivatives: sodium acetyl homotaurine (Na AOTA), homotaurine (OTA), sodium acetyltaurine (Na A TA) and calcium chloride (CaCl2) did not affect VIE. These data suggest that the gabaergic system could be implicated in VIE. MERAM Lab. patent.

Acamprosate↗
PubMed1984

The effects of chronic treatment with captopril in spontaneously hypertensive rats (SHR) and their offspring.

Ten consanguine monogamous SHR couples (G1) were treated from their 5th to their 37th week of age with captopril, 50 mg/kg/day i.p. Male rats were treated without interruption. Treatment was withheld in female rats from delivery to weaning. They were compared to ten similar SHR couples which were only daily i.p. injected with the same volume of solvent. Second (G2) generation rats (untreated) were studied. In G1 rats, systolic blood pressure (SBP) and heart weight/body weight (HW/BW) ratio were decreased, while heart rate (HR) was not changed. Plasma renin activity remained unchanged at 37 weeks of age though the treatment was effective. Parental treatment did not reduce SBP and HW/BW ratio in G2 rats. This indicates that reduction of hypertension in SHR is not enough to prevent hypertension development in the offspring of the treated rats.

Animals↗
PubMed1983

The effects of nicergoline on spontaneously hypertensive rats and their offspring.

Six consanguine monogamous SHR couples (G1) were treated from 5 weeks of age on with an alpha blocker, nicergoline, 0.1 mg/kg/day i.p.. Male rats were treated without interruption; treatment was withheld in female rats from delivery to weaning. They were compare to six similar SHR couples who were only daily i.p. injected with the same volume of solvent in the same conditions as controls, as well as with naive (untreated) rats. Second (G2) and third (G3) generation rats (untreated) were studied. In G1 rats, systolic blood pressure (SBP), heart rate, heart weight/body weight ratio and bulbar noradrenaline content were decreased (compared to control or naive rats), while plasma renin activity (PRA) and hypothalamic noradrenaline content were not changed. In G2 rats, SBP and PRA were decreased, all other parameters being unchanged. No parameter was changed in G3 rats. This appears to be the first report of a preventive effect of antenatal treatment on the development of hypertension in SHR.

Animals↗
PubMed1983

Effects of parenteral treatment by nicergoline on the development of hypertension of S.H.R.

Six consanguine monogamous SHR couples (G 1) were treated from 5 weeks of age on with an alpha blocker, nicergoline, 100 mcg. kg-1 day-1 i.p. Male rats were treated without interruption; treatment was withheld in female rats from delivery to weaning. They were compared with six similar SHR couples who were only daily i.p. injected with the same volume of solvent in the same conditions, as controls. Second (G 2) and third (G 3) generation rats (untreated) were studied. In G 1 rats, systolic blood pressure (SBP) was decreased, and no change was found in heart rate (H R), heart weight to body weight ratio (HW/BW), hypothalamic and bulbar noradrenaline content (HNA,BNA). In G 2 rats, SBP, BNA and plasma renin activity were significantly decreased, all other parameters being unchanged. No parameter change was observed in G 3 rats. We think that such long acting effects after antenatal treatment could only be due to an action on the origin of the SHR hypertension.

Animals↗
PubMed1983

Modification by sulpiride, pimozide, or domperidone of apomorphine's effects on learning in hypoxic rats.

The study of apomorphine's interaction with three dopaminergic antagonists (domperidone, sulpiride and pimozide) is an attempt to characterize the dopaminergic receptors involved in the dopaminergic agonist-induced protection against hypobaric hypoxia. Apomorphine (1 mg X kg-1 but not 0.01 mg X kg-1) reduced total performance (avoidance + escape responses); this effect was antagonised by domperidone and pimozide--not by sulpiride--and appeared to have a peripheral origin. Apomorphine (0.01 and 1 mg X kg-1) increased the avoidance performance during hypoxia. This antihypoxic protection was not suppressed by domperidone, confirming its central origin, but was antagonised both by sulpiride and pimozide. The receptors involved in the anti-hypoxic protective effect appear therefore to be cerebral D4 receptors, according to the classification of Seeman.

Animals↗
PubMed1982

Piribedil-induced anti-hypoxic protection in rats.

The action of the dopaminergic agonist, piribedil, on a conditioned avoidance response was studied in normoxic or hypobaric hypoxic rats. This agonist has no effects in normoxia, but induced an anti-hypoxic protection (improvement of learning in hypoxia), antagonised by low doses of pimozide. The mechanism of the anti-hypoxic property seems to be mediated by the stimulation of the postsynaptic dopaminergic receptors, but does not exclude the role of noradrenergic pathways, as shown by the stabilisation of norepinephrine levels during hypoxia after treatment with piribedil.

Air Pressure↗
PubMed1981

Modifications of the dopaminergic receptors sensitivity and learning of normoxic or hypobaric hypoxic rats.

In the present work we attempted to show whether a modification of the sensitivity of the dopaminergic receptors could act on the learning process in hypobaric hypoxia. Acute treatment with 1 mg/kg-1/day-1 pimozide increases the hypoxia-induced deleterious effect on a conditioned avoidance test whilst chronic administration of pimozide improves behavioral performances in hypoxic rats. Chronic treatment with apomorphine does not modify the learning both in normoxic and hypoxic rats in comparison with control rats, while acute treatment induces an anti-hypoxic protection and a fall in total responses (avoidance + escape). A pimozide-induced hypersensitivity (by chronic treatment) or a direct apomorphine-induced stimulation (by acute treatment) of post-synaptic dopaminergic receptors oppose the deleterious effects of hypobaric hypoxia.

Animals↗
PubMedDate not supplied

Attenuation by antidepressant drugs of alcohol intake in rats.

Ethanol preferring rats were selected and showed a constant voluntary intake of a 12% ethanol solution during 14 days (about 5 g/kg body weight daily). These alcohol preferring rats were daily IP injected during two weeks with different antidepressant drugs, according to their specificity of action: nomifensine (5 and 10 mg/kg) and maprotiline (2.5 and 5 mg/kg) (dopamine uptake inhibitors), desipramine and metapramine (5 and 10 mg/kg) (noradrenaline uptake inhibitors) clomipramine and doxepin (5 and 10 mg/kg) (serotonin uptake inhibitors). Only desipramine, 5 and 10 mg/kg, metapramine, 10 mg/kg, clomipramine, 5 and 10 mg/kg and doxepin, 10 mg/kg, were able to reduce significantly the ethanol intake. These drugs specifically inhibit noradrenaline or serotonin uptake. These data lead us to think that norepinephrine and/or serotonin, but not dopamine, are involved in the voluntary intake of alcohol.

Alcohol Drinking↗
PubMedDate not supplied

Striatal dopamine does not appear involved in the voluntary intake of ethanol by rats.

Ethanol preferring and non preferring rats were selected. Ethanol preferring rats showed a constant voluntary intake of a 12% ethanol solution during 14 days (about 5 g/kg body weight daily) while the non preferring rats drank less than 1 g/kg body weight daily. Preferring rats were daily IP injected with 5 or 10 mg/kg of nomifensine, an inhibitor of dopamine uptake. Their intake of ethanol solution remained constant during the 14 days of treatment. Dopamine uptake into striatal synaptosomes was identical in ethanol preferring and non preferring rats. These data, as others, led us to suppose that striatal dopamine is not involved in the voluntary intake of ethanol by rats.

Alcohol Drinking↗
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

Regulation of rat neuronal nitric oxide synthase activity by chronic alcoholization.

Rat neuronal nitric oxide (NO) synthase (nNOS) activity was measured in frontal cortex, hippocampus, striatum and cerebellum using the assay of [3H]citrulline, following chronic alcoholization. The Km and Vmax values were significantly increased in the frontal cortex and in the striatum, and were not affected in the cerebellum and hippocampus.

Alcoholism↗
PubMedDate not supplied

Interference between central dopaminergic stimulation, and adrenal secretion in normoxic or hypobaric hypoxic rats.

Previous data have established that postsynaptic stimulation of central dopaminergic receptors was mainly involved in the protective action of apomorphine against the comportmental consequences of hypobaric hypoxia in rats: disturbances in a conditioned avoidance response. We confirm this notion showing that domperidone (a peripheral dopaminergic blocking agent) does not antagonize the protective effect of apomorphine. Furthermore, we establish that the action of apomorphine is at least partially mediated by adrenal glands since it is no longer seen in adrenalectomized rats. In normal rats, apomorphine enhances the corticosterone increase which is observed during hypobaric hypoxia and decreases the hypoxia-induced elevation of the adrenaline level. It is therefore concluded that the anti-hypoxic activity of apomorphine is probably mediated by a centrally mediated dopaminergic modification of the adrenal response to hypobaric hypoxia.

Adrenal Glands↗