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Biomedical subjects

M Bourin

Publications and source records attributed to M Bourin.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

[Mechanism of action of antidepressants and therapeutic perspectives].

Depression is an incapacitating disease which needs appropriate treatment. This article reviews the pharmacology of antidepressant drugs and the future perspectives of treating mood disorders such as depression. The foremost theory for explaining the biological basis of depression has been the monoamine hypothesis. Depression is due to a deficiency in one or other biogenic monoamines (serotonin, 5-HT; noradrenaline, NA; dopamine, DA). Antidepressant drugs are therefore classified according to their ability to improve monoaminergic transmission. Since this first theory, other explanations based on abnormal function of monoamine receptors or associated with impaired signalling pathways have been suggested. Notable progress has been accomplished in the treatment of major depressive disorders with new compounds recently discovered (selective serotonin reuptake inhibitors: SSRI; serotonin noradrenaline reuptake inhibitors: SNRI). Behavioural, electrophysiological and microdialysis studies have shown that serotonin (5-HT) receptors, mainly 5-HT1A, 5-HT1B and 5-HT2C sub-types, exert a key role in modulating antidepressant activity. Indirect activation of neurotransmitter receptors by antidepressants may also lead, via increases in endogenous levels of serotonin in synapses in specific brain regions, to activation of various G proteins coupled to a receptor, signal of transduction, transcription factors and neurotrophic factors such as brain-derived neurotrophic factor (BDNF). Thus, depression may be considered as a transduction mechanism anomaly. This hypothesis needs to be clarified by molecular biology. Although antidepressants have improved the therapeutic potential compared to tricyclics (TCA) in terms of reduced side effects, a number of problems still occur with these drugs. Clinical effects are not always observed until after this time has elapsed (4-6 weeks) and a substantial proportion of depressed patients show only partial or no response to antidepressants. Knowledge of the existence of links between neurotransmitter systems and the discovery of the most specific target, 5-HT receptors, should lead to improvements in antidepressant therapy. Developing drugs using innovative mechanisms such as directly acting on 5-HT receptors (5-HT1A agonists or 5-HT2 antagonists), would appear to be useful in the treatment of depression. The use of antidepressants in anxiety disorders such as obsessional compulsive disorders and even generalised anxiety, highlights the distinction between antidepressants and classic anxiolytics such as benzodiazepines, or even buspirone.

Antidepressive Agents↗
PubMedDate not supplied

[Hormone effects of the administration of 50 mg of dehydroepiandrosterone (DHEAS) intravenously in pregnant women (author's transl)].

The DHEAS overload test has been regarded by C. Lauritzen as reflecting the conditions of placental function. Some will support and some will oppose that test. We have merely concerned ourselves with conducting an examination into the metabolic outcome of the DHEAS overload. --by defining the way in which oestriolury variations are best express themselves. --by estimating how reliable such variations are in cases where foetal pain and hypotrophy are diagnosed. --by going through a statistical analysis of other hormonal variations.

17-Ketosteroids↗
PubMedDate not supplied

[Is cholecystokinin a biological support in panic attacks?].

Cholecystokinin (CCK) is a peptide found high density in the cerebral cortex, the amygdala and the hippocampus of the mammalian brain. Molecular forms of varying amino acid lengths of CCK have been isolated. The sulphated octapeptide (CCK-8S) is the most abundant form and shorter molecular forms are also present in the brain. CCK-8S has been shown to coexist with neurotensin and dopamine in neurons projecting from the ventral tegmental area to the nucleus accumbens, and to a lesser extent in neurons of the substantia nigra projecting to periventricular regions of the caudate. Evidence suggests that CCK acts as a neurotransmitter in the NCS it is synthesized and stored in nerve terminals and cell bodies; it is released by depolarization; it has specific binding sites; it can affect the firing rate of CNS neurons; and its effects can be interfered with by analogues. Studies have found microiontophoretic application of CCK-8S and CCK-4 on cortical and hippocampal neurons to elicit a strong excitatory action. CCK receptors are widely distributed throughout the central nervous system with high densities in the striatum and nucleus accumbens. Considerable effort has been devoted to characterizing the specificity of brain CCK receptors. So far, two types of CCK receptors have been described: CCK-A receptors which have a higher affinity for sulphated CCK-8 than for de-sulphated CCK-8 (CCK-8US), CCK 4 or gastrin, and CCK-B receptors have a high affinity for all of these compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholecystokinin↗
PubMedDate not supplied

[Results of a survey on the use of delayed-action neuroleptics in psychiatry].

Depot neuroleptics have been empirically used for 30 years by psychiatrists. An inquiry was performed among private and public psychiatrists. The goal of the study was to understand the prescription rules of depot neuroleptics. A questionnaire was systematically sent to all psychiatrists working in Loire-Atlantique. The answer rate was 41.4% which is quite good for this kind of inquiry. The main indications of depot neuroleptics were chronic deliria and schizophrenia. Dosages are not accorded to negative or productive symptoms. Therapists do not think that there are efficacy differences between marketed drugs. Few of them use therapeutic windows. Prescriptions were not adjusted following drug pharmacokinetic parameters. So this work lays down rules about rational prescriptions and drug monitoring of depot neuroleptic concentrations.

Antipsychotic Agents↗
PubMedDate not supplied

[Acute poisoning. Apropos of 1200 cases].

The team studied 1 200 cases of acute intoxications both accidental and self inflicted, self inflicted poisonings are much more frequent than accidental ones and in general occur more often amongst the young and by women; the median age is about thirty. Barbituric are often the means. There is a progressive increase in the use of tranquilizers and of thymo-analeptics as their use becomes greater. A mixture of poisons increases the dangers because this frequently results in more rapid loss of consciousness; also more than one poison increases the risk of shock and of thermo-regulation, respiratory problems necessitate intubation and artificial respiration which both increase the risk of assification. The characteristics of certain poisons are stressed and in particular the thymo-analeptics; also the supervision of the patients in an intensive care unit.

Acid-Base Imbalance↗
PubMedDate not supplied

[Cure of amineptine dependence with clonidine?].

Two patients with dependence to amineptine were treated with clonidine which is used in morphine withdrawals. After some days, the two patients stopped amineptine intake. The only way of action seems to be the potentialization of amineptine by clonidine, as probed in mice, or the increase of sensibilization of alpha 2 adrenoreceptors.

Adult↗
PubMedDate not supplied

[Triazolam 0.25 mg versus loprazolam 1 mg in the treatment of common insomnia treated in general practice. Double-blind cross-over randomized trial].

In a double-blind cross over randomized study for the first two nights efficacy and safety of triazolam 0.25 mg and loprazolam 1 mg have been compared in 67 out-patients complaining of common insomnia and treated by general practitioners. After the second night patients had to choose one of the two treatments and were continuing a 3-week treatment period with the preferred one. In case of no preference they received one of the 2 drugs according to a new randomization. Cross over administration of the two drugs for the first two nights shows that with triazolam global help to get in sleep is greater (p = 0.016) and sleep latency is shorter (p = 0.07) than with loprazolam, and number of night awakenings is decreased (p = 0.02) compared to loprazolam. Patients felt more rested under triazolam (p = 0.015) than loprazolam. Triazolam (N = 31) is more frequently preferred than loprazolam (N = 19) p = 0.09. Preferred treatment continued to be effective during the following three weeks and quality of sleep improved drastically for all items compared to baseline data (p = 0.01). Both treatments are well tolerated (4 drop-outs for side-effects: 2 under each treatment). The one-week tapering period allows progressive withdrawal with rare reappearance of minimum sleep disorders (5 cases: 2 under triazolam, 3 under loprazolam).

Adult↗
PubMedDate not supplied

[Mechanism of action of clonidine in the forced-swimming test in mice].

Clonidine displays immobility-reducing effects in the mouse swimming model at doses (0.06-16 mg/kg IP) which decrease spontaneous motility. Tricyclic antidepressants evoke a similar dissociation in motor activity. The immobility-reducing effect of clonidine (1 mg/kg at 30 min pretesting) was reversed by yohimbine (4 mg/kg) but was unaffected by prazosin (2 mg/kg) or alpha-methyl-paratyrosine (100 mg/kg), and was enhanced by reserpine (2.5 mg/kg). Mediation by alpha-2 postjunctional receptors was thus suggested. However, two 5-HT receptor blockers--methysergide (2 mg/kg) and ketanserin (8 mg/kg)--increased this effect of clonidine whereas the non selective agonist 5-MeODMT (1 mg/kg) reduced clonidine action. Conversely, pretreatment with a subthreshold dose of clonidine (0.06 mg/kg at 45 min pretesting) made effective subthreshold doses of three 5-HT uptake inhibitors (citalopram 2 mg/kg, indalpine and fluvoxamine 4 mg/kg) and of the 5-HT1 receptor agonist 8-OH-DPAT (0.5 mg/kg). According to these data, the mouse swimming model would trigger functional relationships between central alpha-noradrenergic and serotonergic mechanisms.

Animals↗
PubMedDate not supplied

[A scale for evaluating withdrawal symptoms induced by anxiolytic agents].

A scale to evaluate the withdrawal syndrome induced by tranquilizers (TWS) is proposed to distinguish between anxiety induced symptoms and withdrawal induced symptoms. This scale was established and validated by Lader, the french translation was performed by the author. The most frequently observed symptoms during a withdrawal syndrome are physical tiredness, headache, vertigo and tremor but other symptoms are evaluated by this tranquilizers withdrawal scale.

Anti-Anxiety Agents↗
PubMedDate not supplied

[Blood concentrations of maprotiline in depressive patients].

Blood levels of Maprotiline were analysed and their relationship to the clinical response was examined in 89 depressed inpatients, according DSM III criteria for Major Depressive Episode, given the drug treatment for 3 weeks. Maprotiline produced marked decreases in mean MADRS and COVI scale scores by the end of treatment. On day 21, no correlation between blood levels of Maprotiline and MADRS or COVI scores were found when all patients were considered. Nevertheless, significant correlations were observed on day 14 (r = .22; p less than .05 for MADRS and r = .23; p less than .05 for COVI scale). In addition, a significant correlation between MADRS or COVI scale scores and Maprotiline blood levels were observed on days 14 and 21 in subgroups of young patients, severe depression (high scores to clinical global investigations), during of at least 3 months, treated without other drug than Maprotiline and good responders.

Adult↗