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PubMed1990

Continuation and maintenance therapy with antidepressive agents. An overview of research.

The literature was reviewed in order to ascertain the clinical benefits of long-term antidepressant drug treatment in recurrent major depression. Articles describing randomized, controlled, double-blind trials of long-term antidepressant drug treatment, starting at a specified period after recovery from an affective episode, in patients with major depression, were identified and reviewed. The authors describe, evaluate and comment on the design and quality of over 25 identified studies, 18 studies of continuation therapy and 7 of maintenance treatment. The methodological problems which are encountered in this type of research and the sources of bias which invalidate study results, are dealt with systematically. On the basis of this survey, some treatment guidelines and suggestions for future research are given.

Antidepressive Agents↗
PubMed1993

[Contributions of pharmacology in the treatment of resistance to antidepressive agents].

Pharmacology can contribute in four ways to our understanding and to the management of resistant depression: 1) Dosage: some antidepressants have an inverted-U dose-response curve, i.e. the response disappears when dosage is increased. In man, dose-response relationships are not well established because the curves are obtained with groups of patients and they reflect an overall mean rather than the reality of each individual patient. 2) Secondary regulatory adaptive mechanism such as: down regulation of beta, 5-HT2, alpha-2 receptors--increased reactivity of 5-HT1A, alpha-1 and dopaminergic systems. Defective development of these mechanisms is thought to originate resistance in certain cases, which could therefore be corrected more or less specifically by adding thyroid hormone, lithium, an alpha-2 agonist or even by switching to a 5-HT1A agonist or a dopaminergic drug. 3) Biological resistance factors: it has been shown in the rat that hypothyroidism, diabetes, weight loss cause a decrease in beta-adrenergic system reactivity, and therefore a resistance to noradrenergic antidepressants. 4) Co-prescription: the efficacy of noradrenergic antidepressants is known to involve the activation of beta-adrenergic receptors. Animal studies have shown that the co-prescription of a beta-blocker nullifies this efficacy. Benzodiazepines decrease serotonergic and noradrenergic neuronal activity: animal studies have shown that they antagonize most antidepressants. What happens in depressed humans who are often co-prescribed these drugs? I would like to share with you a few data from experimental pharmacology which may help us to think differently, not when faced to a patient with resistant depression, but when confronted with the failure of a well conducted antidepressant treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

The mode of action of sulpiride as an atypical antidepressant agent.

It can be said that sulpiride exerts a disinhibitory effect in both depression and schizophrenia but this is not associated with mechanisms through which typical antidepressant or anxiolytic agents act. Sulpiride acts selectively as a dopamine receptor antagonist in the brain, its effects on other neuronal systems being extremely limited. Indeed, it may act even selectively within the dopamine systems in that it would appear it specifically interacts with one sub-population of cerebral dopamine receptors. Within a given dopamine receptor system sulpiride may exert a differential pre-synaptic action on dopamine neurones although the evidence for this remains controversial. The disinhibitory effects in depression may be due to a preferential pre-synaptic action of the drug on dopamine neurones causing over-activation of cerebral dopamine post-synaptic receptors causing behavioural arousal and motor facilitation. On the other hand, the disinhibitory effect of sulpiride in schizophrenia may also involve the preferential pre-synaptic action of the drug coupled with the specificity of post-synaptic action to result in little sedation or motor retardation. Sulpiride may also differentially antagonise post-synaptic dopamine receptors in different brain areas and this may also be critically involves in its unusual spectrum of neuroleptic action.

Animals↗