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Biomedical subjects

H Frances

Publications and source records attributed to H Frances.

34 records · Page 2Linked to original sources
PubMed1986

Chronic beta-adrenergic stimulation increases in mice the sensitivity to methysergide and the number of cerebral high affinity serotonin binding sites (5-HT-1).

Reserpine administration in mice causes, among other effects an akinesia which can be reversed by the serotonin agonist-antagonist methysergide. The effect of methysergide is potentiated by clenbuterol, a beta-adrenergic agonist, which itself causes hypomotility. Potentiation is weak after a single injection of clenbuterol, but becomes much stronger after repeated administration for 12 days. This treatment also causes a 50% increase in the number of high affinity 5-HT-1 binding sites in the brain. This increase would explain the increased potency of methysergide against reserpine-induced akinesia. These results show that: a beta-adrenergic drug, clenbuterol modulates the serotoninergic system; this modulation takes its importance after chronic treatment only; this interrelation may be important in depressive illness since it is observed on a test used in the screening of antidepressant drugs.

Animals↗
PubMed1986

The calcium entry blockers: anti-manic drugs?

The reported property of calcium antagonists as antimanic drugs has been investigated in three models of hyperactivity in mice. The hyperactivity was induced by amphetamine, oxolinic acid or reserpine after inhibition of monoamine oxydase (MAO). Nicardipine (a dihydropyridine derivative) reduces the three hyperactivities, verapamil (a diphenylalkylamine derivative) reduces only oxolinic acid hyperactivity, and diltiazem (a benzothiazepine derivative) was active except in the MAOI-reserpine test. Levomepromazine used as a reference drug reduced the three hyperactivities. The three calcium entry-blockers reduce the different hyperactivities at doses which already decrease motor activity. And so, it seems that their action was not specific. On the contrary, levomepromazine antagonizes MAOI-reserpine induced hypermotility at a dose which is not sedative. These results do not strengthen the property of calcium antagonists as antimanic drugs.

Amphetamines↗
PubMed1985

Comparison of imipramine-imipraminium in mice. To elucidate central or peripheral origin of effects of imipramine.

Imipramine hydrochloride shows effects in a battery of tests used for the screening of antidepressant drugs. The central origin of these pharmacological effects of imipramine has not been clearly established. Imipramine methiodide is a quaternary derivative of imipramine which does not cross the blood-brain barrier easily. The effects of the two forms of imipramine have been compared: on an effect known to have a central origin; on two effects known to have a peripheral origin; on a battery of tests used for the screening of antidepressant drugs. It has been demonstrated that imipramine methiodide is as active as imipramine hydrochloride on two effects of peripheral origin, less active than imipramine hydrochloride on an effect considered to have a central origin and less active than imipramine hydrochloride or inactive on the tests which are used for the screening of antidepressant drugs. Consequently, the tests used for the screening of antidepressant drugs represent, primarily or exclusively, effects of central origin.

Animals↗
PubMed1985

Dissociation of head twitches and tremors during the study of interactions with 5-hydroxytryptophan in mice.

Intraperitoneal injection of 5-hydroxytryptophan and 5-methoxy-N,N-dimethyltryptamine is shown to provoke characteristic behaviors in mice that can be quantified. The two principal phenomena described here are head twitches and tremors. Tremors became more frequent when doses of the two substances studied were increased. Head twitches appeared at lower doses, but beyond a certain dose, they decreased and even disappeared. The effects on these movements of agents that modify serotonin function were then studied. The results pose problems of interpretation that are discussed.

Animals↗
PubMed1984

Stimulation of beta-adrenergic receptors and spontaneous motor activity in mice.

The effects of 3 beta-adrenergic agonists (clenbuterol, isoproterenol and salbutamol) on the spontaneous motor activity of mice were studied. The present research indicated that motor activity was significantly decreased 30 minutes after IP injection of either clenbuterol (0.06 mg/kg), isoproterenol (0.5 mg/kg) or salbutamol (2 mg/kg). Hypomotility induced by clenbuterol was also significantly antagonized by propranolol in doses ranging from 1 to 8 mg/kg and by penbutolol in doses from 0.03 to 0.5 mg/kg. However, practolol, which does not cross the blood brain barrier, did not antagonize the effect of clenbuterol. Therefore, it may be hypothesized that beta adrenergic agonists decrease motor activity by a central mechanism. It was also found that tachyphylaxis or resistance to treatment, observed in cardiovascular and bronchopulmonary systems with beta-adrenergic agonists, developed after 7 injections of clenbuterol (0.25 mg/kg IP, twice daily) in the behavioral model of spontaneous motor activity in mice.

Adrenergic beta-Agonists↗
PubMed1984

Disappearance of the decrease in biting behavior induced by clenbuterol, a beta-adrenergic agonist, after chronic administration.

The beta-adrenergic agonist clenbuterol decreased interest in food in starved mice, 30 minutes after administration. This effect disappeared after repeated treatment with clenbuterol (0.25 mg/kg, twice daily). Three chronic injections were sufficient to prevent the effect of an acute dose of clenbuterol (0.125 mg/kg) up to 45 hours after treatment.

Aggression↗
PubMed1983

Attempt at pharmacological differentiation of central beta-adrenergic receptors.

The beta-adrenergic stimulants isoprenaline, salbutamol and clenbuterol decreased motor activity, reduced the interest of fasting mice in food pellets ('Tantale' test), and antagonized high-dose apomorphine hypothermia. Clenbuterol was 16--60 times more potent than the other two agonists in all tests, apparently because of better crossing into the C.N.S. The beta-adrenergic blockers, d,l-propranolol and l-penbutolol, completely antagonized the effects of salbutamol and clenbuterol in tests of motor activity and apomorphine hypothermia, penbutolol being 30--60 times more active than propranolol, perhaps due to its greater lipid solubility. The Tantale test allows unambiguous differentiation between penbutolol and propranolol. While the first completely blocked the effects of clenbuterol and salbutamol, the second was effective only within a narrow dose range. Finally, the dose-effect relationships of the 3 agonists were parallel in the Tantale test, while they were divergent in the other two. This suggests that different classes of beta-adrenergic receptors may be involved in the various test.

Adrenergic beta-Agonists↗
PubMed1981

Effect of chronic lithium treatment on isolation-induced behavioral and biochemical effects in mice.

The following effects were induced in mice by a prolonged of isolation (6-7 weeks from weaning): (1) reduction in motor activity; (2) reduction in the effect of oxotremorine on rectal temperature; (3) increase in the response to salbutamol, a beta-adrenergic stimulant. Chronic lithium treatment (2 mg/ml in the drinking water during the last 3-4 weeks of isolation) prevented these phenomena. The number and affinity of beta-adrenergic receptors in the whole mouse brain (excluding the cerebellum) was unmodified by either isolation or by lithium. It is suggested that lithium blocks isolation-induced hypersensitivity, especially of the beta-adrenergic system; this mechanism may be involved in the therapeutic action of lithium.

Animals↗
PubMed1981

Beta-adrenergic stimulation and antidepressant activity.

The results presented here, together with the literature data, support the noradrenergic hypothesis of depressive states, and especially the involvement of beta-adrenergic receptors: --In animals, beta stimulants have the same spectrum of activity as other antidepressants. --These effects of both classical antidepressants and beta-adrenergic stimulants are antagonized by beta blockers. --Chronic administration of antidepressants results in a decrease of beta receptors. --Salbutamol, a beta-adrenergic stimulant had, in depressed patients, a clear and rapid antidepressant effect.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Influence of social isolation and 6-OHDA lesion on the effects of quinelorane.

The sensitivity of the response to the preferential dopaminergic D3 (DAD3) receptor agonist, quinelorane, was compared in mice housed socially and in mice isolated for 4 weeks. Quinelorane (1, 5, 10, 50 and 100 microg/kg) was administered intraperitoneally. Motor activity was measured for 60 min posttreatment. Rectal temperature was measured prior to and 1 h following the administration of quinelorane (10, 50 and 100 microg/kg i.p.). Quinelorane significantly and dose-dependently decreased locomotor activity in social and in isolated mice. The locomotor activity of isolated mice was significantly lower than that of social mice, but isolation had no effect on quinelorane-induced hypomotility. Quinelorane decreased dose-dependently rectal temperature in isolated and social mice, but isolation had no effect on quinelorane-induced decrease in rectal temperature. The lesions of dopaminergic terminals with intracerebroventricular administration of 6-OHDA decreased the dopamine (DA) level by 93% in the nucleus accumbens and by 91% in the corpus striatum; these lesions impaired neither the hypolocomotion nor the hypothermia induced by quinelorane. Thus, it may be concluded that social isolation has no influence on the quinelorane-induced decreases in rectal temperature and in locomotor activity and that the DA receptors involved in these effects of quinelorane are located postsynaptically.

Animals↗