Additive effects of clonidine and antidepressant drugs in the mouse forced-swimming test

Malinge, M.; Bourin, Michel; Colombel, M.C.; Larousse, C

doi:10.1007/bf02431541

Cited by 59 publications

(16 citation statements)

References 42 publications

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“…It is generally accepted that selective inhibitors of serotonin uptake do not show an antidepressant-like activity in the forced swimming test in rats (Borsini, 1995;G6rka et al, 1979;Maj et al, 1982;Porsolt et al, 1978), although some authors described positive effects, especially in mice (Cervo et al, 1991;Nixon et al, 1994;Malinge et al, 1988). The presently obtained results support the above data.…”

Section: Discussionsupporting

confidence: 92%

Antidepressant effects of pramipexole, a novel dopamine receptor agonist

Rogóż

Skuza

et al. 1997

J. Neural Transmission

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Pramipexole (2-amino-4,5,6,7-tetrahydro-6-propyl-amino-benzthiazole-dihydrochl oride), a new dopamine receptor agonist with preference for D3 compared to D2 and D4 receptors, was tested in rats in respect of its potential antidepressant activity. In the forced swimming test the drug under study, given three times in rats, reduced the immobility time. In the forced swimming test, joint treatment with antidepressants (imipramine, amitriptyline) and pramipexole evoked a more potent effect than any of the drugs given alone; however, the locomotor hyperactivity was weaker after joint administration. Citalopram and fluoxetine, inactive per se in the forced swimming tests, visibly enhanced the antidepressant-like effect of pramipexole but, on the other hand, they attenuated the locomotor hyperactivity evoked by the drug. Repeated treatment with pramipexole (0.3 or 1 mg/kg, twice daily for 14 days) increased the locomotor activity measured at 1 h after the last dose. Repeated administration of pramipexole (as above) potentiated the D-amphetamine- or quinpirole-induced locomotor hyperactivity. The obtained results indicate that, in the tests used, pramipexole evokes effects similar to those of typical antidepressants and, at the same time, enhances their activity (the forced swimming test in rats); therefore it may be regarded as a potential antidepressant drug.

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Section: Discussionsupporting

confidence: 92%

Antidepressant effects of pramipexole, a novel dopamine receptor agonist

Rogóż

Skuza

et al. 1997

J. Neural Transmission

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“…Two, 4, and 8 mEq/kg lithium were shown to have a small but significant effect on immobility time, and when the subactive 1 mEq/kg was administered 15 minutes before a subactive dose of the 5HT(1A) agonist gepirone, immobility time was also reduced. This adjunctive effect of lithium, which it shares (though not identically) with clonidine and quinine, has been shown for a number of different kinds of antidepressants, including SSRIs, MAOIs, tricyclic, and atypical antidepressants (Malinge et al, 1988;Bourin et al, 1991;Hascoet et al, 1994;Nixon et al, 1994;Guo et al, 1995;Bourin et al, 1996;Redrobe et al, 1998). This additive mechanism is likely to be mediated at least in part by the serotonergic system, as antidepressants specific for dopaminergic and noradrenergic transmission are not affected by lithium in this model (Nixon et al, 1994).…”

Section: Effect Of Lithium On the Forced Swim Testsupporting

confidence: 65%

The behavioral actions of lithium in rodent models: Leads to develop novel therapeutics

O’Donnell

Gould

2007

Neuroscience & Biobehavioral Reviews

121

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For nearly as long as lithium has been in clinical use for the treatment of bipolar disorder, depression, and other conditions, investigators have attempted to characterize its effects on behaviors in rodents. Lithium consistently decreases exploratory activity, rearing, aggression, and amphetamine-induced hyperlocomotion; and it increases the sensitivity to pilocarpine-induced seizures, decreases immobility time in the forced swim test, and attenuates reserpine-induced hypolocomotion. Lithium also predictably induces conditioned taste aversion and alterations in circadian rhythms. The modulation of stereotypy, sensitization, and reward behavior are less consistent actions of the drug. These behavioral models may be relevant to human symptoms and to clinical endophenotypes. It is likely that the actions of lithium in a subset of these animal models are related to the therapeutic efficacy, as well the side effects, of the drug. We conclude with a brief discussion of various molecular mechanisms by which these lithium-sensitive behaviors may be mediated, and comment on the ways in which rat and mouse models can be used more effectively in the future to address persistent questions about the therapeutically relevant molecular actions of lithium.

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“…However, even if a sedative effect is observed in the locomotor-activity measuring device, antidepressant-like activity may be perceived in the FST Malinge et al, 1988). The observed downregulation of a 1 -adrenoceptor in NET À/À mice together with their increased activity in the behavioral tests is an interesting finding, as blockade of a 1 -adrenoceptors by prazosin (Stone and Quartermain, 1999) or terazosin (Stone et al, 2003) has been reported to produce cessation of behavioral activity, also in the TST.…”

Section: Discussionmentioning

confidence: 90%

Effect of Antidepressant Drugs in Mice Lacking the Norepinephrine Transporter

Dziedzicka-Wasylewska

Faron-Górecka

Kuśmider

et al. 2006

Neuropsychopharmacol

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One of the main theories concerning the mechanism of action of antidepressant drugs (ADs) is based on the notion that the neurochemical background of depression involves an impairment of central noradrenergic transmission with a concomitant decrease of the norepinephrine (NE) in the synaptic gap. Many ADs increase synaptic NE availability by inhibition of the reuptake of NE. Using mice lacking NE transporter (NET À/À ) we examined their baseline phenotype as well as the response in the forced swim test (FST) and in the tail suspension test (TST) upon treatment with ADs that display different pharmacological profiles. In both tests, the NET À/À mice behaved like wild-type (WT) mice acutely treated with ADs. Autoradiographic studies showed decreased binding of the b-adrenergic ligand [ 3 H]CGP12177 in the cerebral cortex of NET À/À mice, indicating the changes at the level of b-adrenergic receptors similar to those obtained with ADs treatment. The binding of [ 3 H]prazosin to a 1 -adrenergic receptors in the cerebral cortex of NET À/À mice was also decreased, most probably as an adaptive response to the sustained elevation of extracellular NE levels observed in these mice. A pronounced NET knockout-induced shortening of the immobility time in the TST (by ca 50%) compared to WT mice was not reduced any further by NET-inhibiting ADs such as reboxetine, desipramine, and imipramine. Citalopram, which is devoid of affinity for the NET, exerted a significant reduction of immobility time in the NET À/À mice. In the FST, reboxetine, desipramine, imipramine, and citalopram administered acutely did not reduce any further the immobility time shortened by NET knockout itself (ca 25%); however, antidepressant-like action of repeatedly (7 days) administered desipramine was observed in NET À/À mice, indicating that the chronic presence of this drug may also affect other neurochemical targets involved in the behavioral reactions monitored by this test. From the present study, it may be concluded that mice lacking the NET may represent a good model of some aspects of depression-resistant behavior, paralleled with alterations in the expression of adrenergic receptors, which result as an adaptation to elevated levels of extracellular NE.

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Additive effects of clonidine and antidepressant drugs in the mouse forced-swimming test

Cited by 59 publications

References 42 publications

Antidepressant effects of pramipexole, a novel dopamine receptor agonist

Antidepressant effects of pramipexole, a novel dopamine receptor agonist

The behavioral actions of lithium in rodent models: Leads to develop novel therapeutics

Effect of Antidepressant Drugs in Mice Lacking the Norepinephrine Transporter

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