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Journal ArticleDOI

Depression: a new animal model sensitive to antidepressant treatments

R D Porsolt, +2 more
- 21 Apr 1977 - 
- Vol. 266, Iss: 5604, pp 730-732
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TLDR
Results presented below indicate that immobility is reduced by different treatments known to be therapeutic in depression including three drugs, iprindole, mianserin and viloxazine which although clinically active show little or no ‘antidepressant’ activity in the usual animal tests.
Abstract
A MAJOR problem in the search for new antidepressant drugs is the lack of animal models which both resemble depressive illness and are selectively sensitive to clinically effective antidepressant treatments. We have been working on a new behavioural model in the rat which attempts to meet these two requirements. The method is based on the observation that a rat, when forced to swim in a situation from which there is no escape, will, after an initial period of vigorous activity, eventually cease to move altogether making only those movements necessary to keep its head above water. We think that this characteristic and readily identifiable behavioural immobility indicates a state of despair in which the rat has learned that escape is impossible and resigns itself to the experimental conditions. This hypothesis receives support from results presented below which indicate that immobility is reduced by different treatments known to be therapeutic in depression including three drugs, iprindole, mianserin and viloxazine which although clinically active1–3 show little or no ‘antidepressant’ activity in the usual animal tests4–6.

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Citations
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Journal ArticleDOI

Behavioural despair in rats: a new model sensitive to antidepressant treatments.

TL;DR: Positive findings with atypical antidepressant drugs such as iprindole and mianserin suggest that the method may be capable of discovering new antidepressants hitherto undetectable with classical pharmacological tests.
Journal ArticleDOI

A neurotrophic model for stress-related mood disorders.

TL;DR: Analysis of preclinical cellular and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies, are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation ofBDNF plays a role in the actions of antidepressant treatment.
Journal ArticleDOI

Brain-Derived Neurotrophic Factor Produces Antidepressant Effects in Behavioral Models of Depression

TL;DR: The hypothesis that BDNF in the hippocampus produces an antidepressant effect in behavioral models of depression, the learned helplessness (LH) and forced swim test (FST) paradigms is tested and provides further support for the hypothesis thatBDNF contributes to the therapeutic action of antidepressant treatment.
Journal ArticleDOI

NMDA receptor blockade at rest triggers rapid behavioural antidepressant responses

TL;DR: It is shown that ketamine and other NMDAR antagonists produce fast-acting behavioural antidepressant-like effects in mouse models, and that these effects depend on the rapid synthesis of brain-derived neurotrophic factor, suggesting the regulation of protein synthesis by spontaneous neurotransmission may serve as a viable therapeutic target for the development of fast- acting antidepressants.
Journal ArticleDOI

Assessing antidepressant activity in rodents: recent developments and future needs

TL;DR: This review focuses on recent findings regarding some of the most widely employed animal models used currently to predict antidepressant potential, and emphasis is placed on recent modifications to such paradigms that have increased their utility and reliability.
References
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Journal ArticleDOI

A Multiple Comparison Procedure for Comparing Several Treatments with a Control

TL;DR: In this article, a multiple comparison procedure for comparing several treatments with a control is presented, which is based on the Multiple Comparison Procedure for Comparing Several Treatments with a Control (MCPC).
Journal ArticleDOI

The catecholamine hypothesis of affective disorders: a review of supporting evidence

TL;DR: The "catecholamine hypothesis of affective disorders" as discussed by the authors suggests that depression is associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites.
Journal ArticleDOI

The pharmacology of iprindole, a new antidepressant

Gluckman Mi, +1 more
- 01 Jan 1969 - 
TL;DR: These findings suggest that iprindole enhances activity of adrenergic receptors through a mechanism unrelated to inhibition of reuptake of norepinephrine, and supports the contention that these effects are unnecessary for antidepressant activity.
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