Biomedical subjects

C Monier

Publications and source records attributed to C Monier.

At least 37 records · Page 2Linked to original sources

PubMed1994

Behavioral effect of beta-blocking drugs resulting from the stimulation or the blockade of serotonergic 5-HT1B receptors.

The present study was aimed at determining the relative potency of various beta-blocking drugs as agonists or antagonists at 5-HT1B receptors. The behavioral model used (increase in escape attempts of isolated mice) has been previously shown to be exclusively responsive to 5-HT1B agonists such as 1-3-(trifluoromethyl) phenylpiperazine (TFMPP). Beta-blocking drugs acted in three different ways: they were either inactive, or acted as agonists or as antagonists at 5-HT1B receptors. The specific beta-blocking drugs: atenolol and betaxolol (beta-1) and ICI 118,551 (beta-2) were inactive by themselves and in interaction with TFMPP. The mixed beta-1 beta-2 blocking drug 1-penbutolol, (but not d-penbutolol), inactive alone, behaved as an antagonist: it impaired in a dose-dependent way the effect of TFMPP. (+/-)Pindolol and (-)pindolol was inactive. None of the (-), (+), or (+/-)pindolol was able to impair TFMPP effect. The increase in escape attempts induced by (+/-)pindolol was antagonized with 1-penbutolol or after a specific desensitization. Cyanopindolol and S-tertatolol (but not R-tertatolol) acted as agonists. SDZ 21009 was inactive as agonist or antagonist. It may be concluded that all beta-blocking drugs are not equivalent regarding their effect at 5-HT1B receptors. L-penbutolol was the only drug acting as an antagonist.

Adrenergic beta-Antagonists↗

PubMed1993

Benzodiazepines reverse the anti-immobility effect of antidepressants in the forced swimming test in mice.

The present study provides evidence that, in mice subjected to the forced swimming test, the anti-immobility effect of the tricyclic antidepressants, desipramine and imipramine (16-32 mg/kg) was antagonized by the acute co-administration of a benzodiazepine, diazepam (0.25-2 mg/kg) and lorazepam (0.125 mg/kg). This effect cannot be accounted for by variations in plasma and/or brain levels of each compound since brain and plasma concentrations of desipramine and plasma levels of diazepam and desmethyldiazepam, measured immediately after the swimming test, were not significantly modified by the co-administration. Diazepam (2 mg/kg) also counteracted the reduction of time spent immobile induced by the MAO inhibitors, toloxatone (256 mg/kg) and selegiline (4 mg/kg) and the 5-HT1A receptor agonist, 8-OH-DPAT (1 mg/kg), but not by the psychostimulant, caffeine (32 mg/kg). The sedative neuroleptic, thioridazine (4 mg/kg) was also found to reverse the anti-immobility effect of desipramine whereas the non-benzodiazepine anxiolytics, alpidem (8 mg/kg) and buspirone (0.5 mg/kg) did not. These results indicate that the observed interactions were unlikely to be accounted for by a reduction of the stressful aspect of the situation whereas the participation of some motor or sedative component could not be totally ruled out.

Analysis of Variance↗

PubMed1993

Brain weight and noradrenaline content in mice selected for low (MGL) and high (MGH) blood magnesium.

Brain noradrenaline content was determined by high performance liquid chromatography in adult male mice from three different strains: 40 mice with genetically low (MGL) or high (MGH) blood magnesium levels, obtained by selective breeding and 20 outbred Swiss albino mice. Brain wet weight and noradrenaline levels were significantly higher in MGL than in MGH and Swiss mice. Few or no differences were found between MGH and Swiss mice. MGL and MGH animals had a similar mean body weight, were raised in identical conditions, and were fed with a normal diet, rich in magnesium. These results together with the higher urinary noradrenaline excretion previously observed in the MGL line, indicate that the mere selection for genetic traits inducing low blood magnesium levels entails an increased catecholamine production. This phenomenon most probably accounts for the higher sensitivity and/or reactivity of MGL animals to stress. The possible role of magnesium-controlling genetic factors in the regulation of brain growth is also suggested.

Animals↗

PubMed1992

Behavioral tolerance to one effect of the serotonergic agonist TFMPP.

1. In mice isolated for one week and observed in pairs with non-isolated mice under a reversed beaker, the serotonergic agonist: 1-3-(trifluoromethyl)phenylpiperazine (TFMPP) increased the number of escape attempts. 2. A partial tolerance to this effect has been observed in mice which were tested a first time after administration of TFMPP one week sooner. 3. An analysis of this form of tolerance was carried out by changing successively and separately each of the events concomitant of this tolerance. 4. The results show that this tolerance is not a pharmacocinetic or a pharmacodynamic one. Observation of the tolerance required the performance of the first test in a drug state. The more likely explanation is that this tolerance results from a conditioned opponent response.

Animals↗

PubMed1991

Tolerance to the behavioural effect of serotonergic (5-HT1B) agonists in the isolation-induced social behavioural deficit test.

In mice, isolation-induced social behavioural deficits are attenuated by stimulants of 5-HT1B receptors, such as TFMPP or CGS 120 66B. Repeated treatment with RU 24969 (5 mg/kg, daily, for 3 days) reduced the effect of TFMPP and that of other 5-HT1B agonists (CGS 120 66B, m-CPP, RU 24969). Similarly, repeated treatment with CGS 120 66B (8 mg/kg, twice a day for 3 days) abolished the effect of a test-dose of the same drug. Desensitization of the 5-HT1B receptors involved in this effect is suggested to have occurred. Such a desensitization may be therapeutically relevant, since acute administration of benzodiazepines and chronic administration of antidepressants both reversed the effect of TFMPP.

Animals↗

PubMed1991

Isolation increases a behavioral response to the selective 5-HT 1B agonist CGS 120 66B.

The effect of two serotonergic drugs, CGS 120 66B acting specifically and TFMPP acting preferentially onto 5-HT1B receptors, was compared in preisolated and in pregrouped mice. Two mice put under an inverted beaker attempt to escape. The number of escape attempts of mice preisolated for 7 days was half that of pregrouped mice. In preisolated mice, TFMPP and CGS 120 66B increased the number of escape attempts up to, respectively, 200% and 300% of that of preisolated control mice. In pregrouped mice, CGS 120 66B was nearly inactive and TFMPP exerts a smaller effect. These results suggest that isolation increases the apparent responsiveness to 5-HT1B stimulants.

Animals↗

PubMed1990

Increase in the isolation-induced social behavioural deficit by agonists at 5-HT1A receptors.

The effect of 5-HT1A agonists was studied in the isolation-induced social behavioural deficit test. The drugs 8-OH-DPAT (0.125 mg/kg), buspirone (16 mg/kg) and ipsapirone (8 mg/kg) further increased the deficit. Unlike 8-OH-DPAT, the other two drugs may act non-specifically since they reduced spontaneous motor activity at 16 mg/kg, as measured in an activity meter. In addition, 8-OH-DPAT (0.25 mg/kg), buspirone (8 mg/kg) and ipsapirone (8 mg/kg) decreased exploratory activity in the open-field test. Since the smallest active doses were very close in the behavioural deficit and in the open-field tests, it is suggested that a common phenomenon, increased emotionality or reactivity, sustained both these reductions in activity. The increase in the behavioural deficit induced by 8-OH-DPAT, was likely to have resulted from stimulation of 5-HT1A receptors, since it was impaired by pretreatment with penbutolol, a beta-adrenergic-blocking drug, also known to bind to 5-HT1 receptors. Since it was previously shown that the behavioural deficit was reduced by agonists at 5-HT1B receptors, it is proposed that the behavioural inhibition, resulting from an isolation-induced increase in reactivity is bi-directionally modulated by serotonergic drugs, where 5-HT1A agonists increase and 5-HT1B agonists decrease this inhibition.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

Benzodiazepines impair a behavioral effect induced by stimulation of 5-HT1B receptors.

Seven days of isolation induce in mice a social behavioral deficit (decrease in escape attempts) reversed by TFMPP acting through activation of 5-HT1B receptors. The present experiments were performed to investigate the interaction between tranquillizing drugs and one aspect of the serotonergic functioning through the TFMPP-induced increase in escape attempts. The benzodiazepines diazepam, alprazolam, triazolam and chlordiazepoxide impaired significantly TFMPP-induced increase in escape attempts at behaviorally inactive doses. Buspirone opposed TFMPP effect, but the active doses 4 and 16 mg/kg alone decreased the number of escape attempts. ICS 205-930 in a large dose range (0.001-1 mg/kg) modified neither the number of escape attempts nor the increase induced by TFMPP. Chronic (11 days) treatment with buspirone (16 mg/kg) or ICS 205-930 (1 mg/kg) modified neither the number of escape attempts of isolated mice nor the increase induced by TFMPP. These results suggest that tranquillizing drugs of the benzodiazepines group, but not of other groups, interact with the 5-HT1B receptors; they add to the knowledge of relations between benzodiazepines and serotonin by specifying the involvement of 5-HT1B receptors.

Animals↗

PubMed1989

Opioid involvement in TRH-induced antinociception in the rat following intracerebral administration.

Thyrotropin-releasing hormone (TRH) has an antinociceptive action in the rat. Antinociception was observed using a thermal stimulus (tail-flick test) after TRH administration into lateral ventricle, nucleus raphe magnus, nucleus reticularis paragigantocellularis and amygdaloid nuclei. This effect was short-lived since it was completely abolished 60 min after intracerebroventricular administration. TRH may interact with the opioid systems as its antinociceptive effect was blocked by pretreatment with naloxone.

Analgesics↗

PubMed1983

[Anorexia nervosa. A clinical and psychometric study].

Psychiatric symptoms and psychometric variables were assessed in thirty three female inpatients with anorexia nervosa. Our sample was a relatively "severe" group. All of the patients were still in treatment at the time of the study and had fulfilled the strict diagnostic criteria clearly defined by Crisp, Bruch, Russell, Dally and Gomez. Since the initial descriptions of anorexia nervosa were made, there has been a great confusion about whether it is a homogeneous illness or not. Our findings bear consistently with the clinical observation that there are distinct diagnostic sub-groups within the anorexia nervosa syndrome. Objective psychological measures lend support to the clinical evaluation that neurotic mechanisms (hysterical, phobic or obsessionnal features) are unusual in anorexia nervosa. Within the primary anorectics, the major clinical predictors of a poor outcome were: age (greater than 20 years), persistant amenorrhea and importance of weight loss. Within the 33 patients, the other predictors of a poor outcome were: small weight gain during treatment, absence of manifest distress (denial or satisfaction) and bulimia associated with self-induced vomiting. On the other hand, anxiety, depression and premorbid personality traits were not systematically associated with a poor prognosis. The population studied was heterogeneous in terms of MMPI profiles and Rorschach scores. The extent to which all our patients deviated from the norm on the Rorschach scores was not negligeable. The Rorschach variables linked to a clinical severity were the percentage of responses F (Form) and F + (form quality). The combination of these scores with the MMPI Anxiety Index (WELSH) lead to identify different sub-groups with a poor prognosis. According to H. Bruch theories, cognitive and perceptual difficulties, disturbance of body image of internal sensations as well as deficiency in identifying emotional states were very common. Rorschach responses of anorectic patients were compared with those of schizophrenic and depressed control groups of F% and F + % mean scores. The results showed that the anorectic group was closer to the schizophrenic group than to the depressed one.

Adolescent↗

PubMed1976