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Michel Bourin - One of the best experts on this subject based on the ideXlab platform.

  • Augmentation effect of combination therapy of aripiprazole and antidepressants on forced Swimming Test in mice.
    Psychopharmacology, 2009
    Co-Authors: Michel Bourin, Franck Chenu, Corina Prica, Martine Hascoët
    Abstract:

    Rationale A deficiency in brain monoamine systems (serotonin, dopamine, and/or norepinephrine) have long been hypothesized for the pathogenesis of depression. Drugs enhancing neurotransmission of those monoamines have been proven to have antidepressant effects. We hypothesized that aripiprazole, a partial D2 agonist, could increase the activity of various antidepressants in the mice forced Swimming Test (FST), an animal model of depression.

  • Antidepressant-like effects in various mice strains in the forced Swimming Test.
    Psychopharmacology, 2003
    Co-Authors: Denis J. David, Martine Hascoët, Caroline E. Renard, Pascale Jolliet, Michel Bourin
    Abstract:

    Rationale Strain differences in mice have been reported in response to drugs in the mouse forced Swimming Test (FST), even if few antidepressants were examined.

  • Clonidine potentiates the effects of tranylcypromine, phenelzine and two analogues in the forced Swimming Test in mice.
    Journal of psychiatry & neuroscience : JPN, 2002
    Co-Authors: Michel Bourin, Martine Hascoët, Marie Claude Colombel, Ronald T. Coutts, Glen B. Baker
    Abstract:

    Objective To compare tranylcypromine (TCP) and phenelzine (PLZ), two well-established inhibitors of monoamine oxidase (MAO), and 2 of their analogues, 4-fluorotranylcypromine (FTCP) and N2-acetylphenelzine (AcPLZ) respectively, with regard to effects in the forced Swimming Test, a behavioural Test used to screen for potential antidepressant drugs.

  • Involvement of 5-HT2C receptors in the anti-immobility effects of antidepressants in the forced Swimming Test in mice
    European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2001
    Co-Authors: Florence Clénet, Anouk De Vos, Michel Bourin
    Abstract:

    Abstract Several recent studies have demonstrated that 5-HT 1A , 5-HT 1B and 5-HT 3 receptors were implicated in the mechanism of action of antidepressants in the mouse forced Swimming Test. Despite extensive evidence for a role of 5-HT 2C receptors in depression, the precise role of these receptors in the effects of clinically established antidepressants was not directly investigated in the mouse forced Swimming Test. This work was aimed at exploring interactions between several doses of Ro 60-0175, a recently available, full and selective 5-HT 2C agonist, and antidepressant drugs in the mouse forced Swimming Test. Spontaneous locomotor activity was measured as an index of intact sensorimotor functions and the dose–effect of Ro 60-0175 alone, as well as interactions with several antidepressants, such as tricyclic antidepressants (imipramine, desipramine and maprotiline) and selective serotonin reuptake inhibitors (paroxetine, citalopram, fluoxetine, fluvoxamine and sertraline), were studied in the mouse forced Swimming Test. There was no intrinsic antidepressant-like effect of Ro 60-0175, but an impairment in locomotor function was detected when using doses higher than 4 mg/kg in the mouse. There was a synergistic effect of low doses of Ro 60-0175 with sub-active doses of imipramine, paroxetine, citalopram and fluvoxamine; an antagonism between the highest dose of Ro 60-0175 and the active doses of paroxetine and fluoxetine was also detected. There is evidence that 5-HT 2C receptors may be involved in the action of antidepressants which are able to boost the concentration of serotonin in the synapse, i.e. SSRIs and imipramine

  • Augmentation of Antidepressant Pharmacotherapy: A Preclinical Approach Using the Mouse Forced Swimming Test
    CNS Spectrums, 1999
    Co-Authors: John Paul Redrobe, Michel Bourin
    Abstract:

    Until recently, several weeks of treatment were required in order to obtain a clinically significant antidepressant response using pharmacotherapy. The present study, using the mouse forced Swimming Test, investigated possible antidepressant augmentation strategies, together with the probable mechanisms involved in such potentiations. It is clear from this and other similar studies that it is possible to enhance the activity of antidepressant drugs with the addition of other compounds (ie, clonidine, quinine, glyburide, pindolol, or buspirone). These data indicate that direct/indirect manipulation of serotonergic receptor systems potentiates the effect antidepressant drugs (ie, selective serotonergic reuptake inhibitors) in the mouse forced Swimming Test, and thus establish this model as a reliable preclinical tool for the investigation of possible antidepressant augmentation strategies. It also appears that this model can be used as a method for identifying the mechanisms involved in such treatment strategies.

Zofia Rogóż - One of the best experts on this subject based on the ideXlab platform.

  • Enhancement of the anti-immobility action of antidepressants by risperidone in the forced Swimming Test in mice
    Pharmacological reports : PR, 2011
    Co-Authors: Zofia Rogóż, Marcin Kabziński
    Abstract:

    The aim of the present study was to examine the effect of antidepressants (ADs) belonging to different pharmacological groups and risperidone (an atypical antipsychotic drug), given separately or jointly, on immobility time in the forced Swimming Test in male C57BL/6J mice. The antidepressants: citalopram, fluvoxamine, sertraline, reboxetine, milnacipran (5 and 10 mg/kg), or risperidone in low doses (0.05 and 0.1 mg/kg) given alone did not change the immobility time of mice in the forced Swimming Test. Co-treatment with reboxetine or milnacipran (10 mg/kg) and risperidone in a lower dose of 0.05 mg/kg or with sertraline, reboxetine (5 and 10 mg/kg), citalopram, fluvoxamine, milnacipran (10 mg/kg) and risperidone in a higher dose of 0.1 mg/kg produced anti-depressant-like effect in the forced Swimming Test. WAY 100635 (a 5-HT1A receptor antagonist) inhibited the effects induced by co-administration of ADs and risperidone. Active behavior in the forced Swimming Test was not a consequence of an increased general activity, since the combined treatment with ADs and risperidone failed to enhance the locomotor activity of mice. The obtained results indicate that a low dose of risperidone enhances the activity of ADs in an animal model of depression, and that, among other mechanisms, 5-HT1A receptors may play a role in these effects.

  • effects of co treatment with mirtazapine and low doses of risperidone on immobility time in the forced Swimming Test in mice
    Pharmacological Reports, 2010
    Co-Authors: Zofia Rogóż
    Abstract:

    The aim of the present study was to examine the effect of mirtazapine (MIR) and risperidone (an atypical antipsychotic drug), given separately or jointly, on immobility time in the forced Swimming Test in male C57BL/6J mice. Fluoxetine (FLU) was used as a reference drug. MIR (2.5, 5 and 10 mg/kg) and FLU (5 and 10 mg/kg), or risperidone in low doses (0.05 and 0.1 mg/kg) given alone did not change the immobility time of mice in the forced Swimming Test. Joint administration of MIR (5 and 10 mg/kg) or FLU (10 mg/kg) and risperidone (0.1 mg/kg) produced antidepressant-like activity in the forced Swimming Test. WAY100636 (a 5-HT(1A) receptor antagonist) inhibited, while yohimbine (an α(2)-adrenergic receptor antagonist) potentiated the antidepressant-like effect induced by co-administration of MIR and risperidone. Active behavior in that Test did not reflect an increase in general activity, since combined administration of antidepressants and risperidone failed to enhance the locomotor activity of mice. The obtained results indicate that risperidone applied in a low dose enhances the antidepressant-like activity of MIR and that, among other mechanisms, 5-HT(1A)-, and α(2)-adrenergic receptors may play a role in this effect.

  • Mechanism of synergistic action following co- treatment with pramipexole and fluoxetine or sertraline in the forced Swimming Test in rats
    Pharmacological reports : PR, 2006
    Co-Authors: Zofia Rogóż, Grazyna Skuza
    Abstract:

    The aim of the present study was to examine the effect of combined treatment of male Wistar rats with pramipexole and fluoxetine or sertraline in the forced Swimming Test. The obtained results showed that co-treatment with pramipexole (0.1 mg/kg) and fluoxetine (10 mg/kg) or sertraline (5 mg/kg) (in doses inactive per se) exhibited antidepressant-like activity in the forced Swimming Test. Sulpiride (a dopamine D(2/3) receptor antagonist) and WAY 100635 (a 5-HT(1A) receptor antagonist), either being ineffective in the forced Swimming Test, inhibited the antidepressant-like effect induced by co-administration of pramipexole and fluoxetine or sertraline. However, SCH 23390 (a dopamine D(1) receptor antagonist) only partly did not alter the effect of pramipexole given jointly with antidepressant drugs; on the other hand, S 33084 (a dopamine D(3) receptor antagonist) only partly decreased (in a statistically insignificant manner) that effect. Moreover, progesterone and BD 1047 (a sigma(1) receptor antagonist) counteracted the antidepressant-like effect induced by co-administration of pramipexole and sertraline (but not pramipexole and fluoxetine). In that Test, active behavior did not reflect the increases in general activity, since combined administration of pramipexole and fluoxetine or sertraline failed to enhance the locomotor activity of rats. None of the Tested drugs (SCH 23390, sulpiride, S 33084, WAY 100635, BD 1047 and progesterone) - alone or in combination with pramipexole and fluoxetine or sertraline - changed locomotor activity. The results described in the present paper indicate that co-administration of pramipexole and fluoxetine or sertraline may induce a more pronounced antidepressive activity than does treatment with pramipexole alone, and that in addition to other mechanisms, dopamine D(2/3) and 5-HT(1A) receptors may contribute to the antidepressant-like activity of pramipexole and fluoxetine or sertraline in the forced Swimming Test in rats. Moreover, sigma(1) receptors may constitute one of the possible mechanisms by which co-administration of pramipexole and sertraline induces antidepressant-like activity in that Test.

  • Synergistic effect of imipramine and amantadine in the forced Swimming Test in rats. Behavioral and pharmacokinetic studies.
    Polish journal of pharmacology, 2004
    Co-Authors: Zofia Rogóż, Grazyna Skuza, Maciej Kuśmider, Jacek Wójcikowski, Marta Kot, Władysława A. Daniel
    Abstract:

    Our previous studies demonstrated that joint administration of a tricyclic antidepressant drug, imipramine (IMI) with the uncompetitive antagonist of NMDA receptor, amantadine (AMA), produced stronger "antidepressant" effect in the forced Swimming Test (Porsolt's Test) than the treatment with either of drugs given alone. Since it has been suggested that, in addition to their other functions, dopamine and alpha(1)-adrenergic receptors may play a role in behavioral response in the forced Swimming Test, in the present study we examined the effect of sulpiride (dopamine D(2/3) receptor antagonist) and prazosin (alpha(1)-adrenergic receptor antagonist) on the effect of AMA given alone or in combination with IMI in the forced Swimming Test in rats. We also measured the level of IMI and its metabolite, desipramine, in the rat plasma and brain, 1 h after the forced Swimming Test. Joint treatment with IMI (5 or 10 mg/kg) and AMA (20 mg/kg) produced stronger antidepressant-like effect than either of agents given alone. Sulpiride (10 mg/kg) or prazosin (1 mg/kg) (ineffective in the forced Swimming Test) inhibited an antidepressant-like effect induced by co-administration of IMI and AMA. The active behaviors in that Test did not reflect an increase in general activity, since combined administration of IMI and AMA failed to enhance the locomotor activity of rats, measured in the open field Test. Also sulpiride and prazosin did not decrease the exploratory activity induced by co-administration of IMI and AMA. The above result suggests that the dopamine D(2/3) and alpha(1)-adrenergic receptors may contribute to the mechanism of synergistic action of IMI and AMA in the forced Swimming Test in rats. The pharmacokinetic interaction can be excluded, since AMA did not change significantly the antidepressant level in the rat plasma and brain, measured 1 h after exposure to the forced Swimming Test.

  • Effects of combined treatment with imipramine and metyrapone in the forced Swimming Test in rats. Behavioral and pharmacokinetic studies.
    Polish journal of pharmacology, 2003
    Co-Authors: Zofia Rogóż, Grazyna Skuza, Jacek Wójcikowski, Władysława A. Daniel
    Abstract:

    In the present study, we examined the effects of imipramine (IMI) and metyrapone (MET) given alone or in combination of IMI and MET in the forced Swimming Test in rats. We also measured pharmacokinetic parameters: the level of IMI and its metabolite, desipramine (DMI), in the rat plasma and brain (1 h after the forced Swimming Test). The present studies indicate that MET (50 mg/kg) reduced immobility time. Combined treatment with MET (50 mg/kg) and IMI (5 or 10 mg/kg) produced stronger antidepressant-like effect than either of drugs given alone. Sulpiride (dopamine D 2 / 3 antagonist), or WAY 100635 (5-HT 1 A antagonist) but not prazosin, (α 1 -adrenergic antagonist), at doses ineffective in the forced Swimming Test, inhibited an antidepressant-like effect induced by co-administration of IMI with MET. The active behaviors in that Test did not reflect an increase in general activity, since combined administration of IMI and MET failed to alter the locomotor activity of rats, measured in the open field Test. MET elevated the concentrations of IMI and DMI in plasma, and the total drug concentration (IMI + DMI) was doubled by MET. In the brain, MET enhanced the concentration of IMI, but decreased that of DMI, consequently, the brain IMI/DMI ratio increased twice. The total drug concentration in the brain (IMI + DMI) was not changed significantly by MET treatment. The obtained results suggest that dopamine D 2 / 3 and 5-HT 1 A receptors may contribute to the mechanism of synergistic action of IMI and MET in the forced Swimming Test in rats, and that pharmacokinetic interaction should not have a substantial impact on the MET-induced potentiation of IMI effect, observed in vivo. These findings may be of particular importance to pharmacotherapy of drug-resistant depression.

Ahmad Reza Dehpour - One of the best experts on this subject based on the ideXlab platform.

Ana Lúcia S. Rodrigues - One of the best experts on this subject based on the ideXlab platform.

  • Antidepressant-like responses in the forced Swimming Test elicited by glutathione and redox modulation.
    Behavioural brain research, 2013
    Co-Authors: Juliana M. Rosa, Alcir Luiz Dafre, Ana Lúcia S. Rodrigues
    Abstract:

    Abstract Glutathione (GSH) displays a broad range of functions, among them a role as a neuromodulator with some neuroprotective properties. Taking into account that oxidative stress has been associated with depressive disorders, this study investigated the possibility that GSH, a major cell antioxidant, elicits an antidepressant-like effect in mice. Thus, GSH was administered by i.c.v. route to mice that were Tested in the forced Swimming Test and in the tail suspension Test, two predictive Tests for antidepressant drug activity. In addition, GSH metabolism and the redox environment were modulated in order to study the possible mechanisms underlying the effects of GSH in the forced Swimming Test. The administration of GSH decreased the immobility time in the forced Swimming Test (300–3000 nmol/site) and tail suspension Test (100–1000 nmol/site), consistent with an antidepressant-like effect. GSH depletion elicited by l -buthionine sulfoximine (3.2 μmol/site, i.c.v.) did not alter the antidepressant-like effect of GSH, whereas the inhibition of extracellular GSH catabolism by acivicin (100 nmol/site, i.c.v.) prevented the antidepressant-like effect of GSH. Moreover, a sub-effective dose (0.01 nmol/site, i.c.v.) of the oxidizing agent DTNB (5,5′-dithiobis(2-nitrobenzoic acid)) potentiated the effect of GSH (100 nmol/site, i.c.v.), while the pretreatment (25–100 mg/kg, i.p.) with the reducing agent DTT ( dl -dithiothreitol) prevented the antidepressant-like effect of GSH (300 nmol/site, i.c.v.). DTNB (0.1 nmol/site, i.c.v.), produced an antidepressant-like effect, per se, which was abolished by DTT (25 mg/kg, i.p.). The results show, for the first time, that centrally administered GSH produces an antidepressant-like effect in mice, which can be modulated by the GSH metabolism and the thiol/disulfide reagents. The redox environment may constitute a new venue for future antidepressant-drug development.

  • Role of different types of potassium channels in the antidepressant-like effect of agmatine in the mouse forced Swimming Test
    European journal of pharmacology, 2007
    Co-Authors: Josiane Budni, Manuella P. Kaster, Vinicius M. Gadotti, Adair R.s. Santos, Ana Lúcia S. Rodrigues
    Abstract:

    Abstract The administration of agmatine elicits an antidepressant-like effect in the mouse forced Swimming Test by a mechanism dependent on the inhibition of the NMDA receptors and the l -arginine-nitric oxide (NO) pathway. Since it has been reported that the NO can activate different types of potassium (K+) channels in several tissues, the present study investigates the possibility of synergistic interactions between different types of K+ channel inhibitors and agmatine in the forced Swimming Test. Treatment of mice by i.c.v. route with subeffective doses of tetraethylammonium (a non specific inhibitor of K+ channels, 25 pg/site), glibenclamide (an ATP-sensitive K+ channels inhibitor, 0.5 pg/site), charybdotoxin (a large- and intermediate-conductance calcium-activated K+ channel inhibitor, 25 pg/site) or apamin (a small-conductance calcium-activated K+ channel inhibitor, 10 pg/site), augmented the effect of agmatine (0.001 mg/kg, i.p.) in the forced Swimming Test. Furthermore, the administration of agmatine and the K+ channel inhibitors, alone or in combination, did not affect locomotion in the open-field Test. Moreover, the reduction in the immobility time elicited by an active dose of agmatine (10 mg/kg, i.p.) in the forced Swimming Test was prevented by the pre-treatment of mice with the K+ channel openers cromakalim (10 μg/site, i.c.v.) and minoxidil (10 μg/site, i.c.v.), without affecting locomotion. Together these data raise the possibility that the antidepressant-like effect of agmatine in the forced Swimming Test is related to its modulatory effects on neuronal excitability, via inhibition of K+ channels.

  • Evidence for imidazoline receptors involvement in the agmatine antidepressant-like effect in the forced Swimming Test
    European Journal of Pharmacology, 2007
    Co-Authors: Mariana P. Zeidan, Andréa D.e. Zomkowski, Angelo O. Rosa, Ana Lúcia S. Rodrigues, Nelson H Gabilan
    Abstract:

    Abstract This study investigated the involvement of the imidazoline receptors in the antidepressant-like effect of agmatine in the forced Swimming Test. The antidepressant-like effects of agmatine (10 mg/kg, i.p.) in the forced Swimming Test was blocked by pretreatment of mice with efaroxan (1 mg/kg, i.p., an imidazoline I1/α2-adrenoceptor antagonist), idazoxan (0.06 mg/kg, i.p., an imidazoline I2/α2-adrenoceptor antagonist) and antazoline (5 mg/kg, i.p., a ligand with high affinity for the I2 receptor). A subeffective dose of agmatine (0.001 mg/kg, i.p.) produced a synergistic antidepressant-like effect with clonidine (0.06 mg/kg, i.p, an imidazoline I1/α2-adrenoceptor agonist), moxonidine (0.5 mg/kg, i.p., an imidazoline I1/α2-adrenoceptor agonist), antazoline (1 mg/kg, i.p.) and MK-801 (0.001 mg/kg, i.p., a non-competitive NMDA receptor antagonist), but not with efaroxan (1 mg/kg, i.p.) and idazoxan (0.06 mg/kg, i.p.). Pretreatment of mice with yohimbine (1 mg/kg, i.p., an α2-adrenoceptor antagonist) blocked the synergistic antidepressant-like effect of agmatine (0.001 mg/kg, i.p.) with clonidine (0.06 mg/kg, i.p). A subeffective dose of MK-801 (0.001 mg/kg, i.p.) produced a synergistic antidepressant-like effect with antazoline (5 mg/kg, i.p.), but not with efaroxan (1 mg/kg, i.p.) or idazoxan (0.06 mg/kg, i.p.). In conclusion, this study suggests that the anti-immobility effect of agmatine in the forced Swimming Test is dependent on its interaction with imidazoline I1 and I2 receptors.

  • Veratrine blocks the lamotrigine-induced Swimming increase and immobility decrease in the modified forced Swimming Test.
    Progress in neuro-psychopharmacology & biological psychiatry, 2007
    Co-Authors: F.t. Codagnone, Ana Lúcia S. Rodrigues, F.t. Consoni, Maria A.b.f. Vital, Roberto Andreatini
    Abstract:

    Lamotrigine exhibits an anti-immobility effect in the modified forced Swimming Test, increasing Swimming and climbing, behaviors that are related to serotonergic and noradrenergic effects, respectively. However, these effects could be secondary to lamotrigine blockade of Na(+) sensitive channel. Thus, this study investigated the influence of veratrine (0.1 mg/kg, ip, 10 min before each lamotrigine administration), an Na(+) channel activator, in the effect of lamotrigine (20 mg/kg, ip, 24, 5, 1 h before the Test session) in the modified forced Swimming Test. Veratrine pre-treatment blocked lamotrigine-induced immobility decrease and Swimming increase but it did not change the effect of lamotrigine on climbing. These results suggest that the serotonergic effect of lamotrigine in the modified forced Swimming Test is dependent on Na(+) voltage sensitive channel blockade, whereas its noradrenergic effect is not.

  • Antidepressant-like effect of lamotrigine in the mouse forced Swimming Test: Evidence for the involvement of the noradrenergic system
    European Journal of Pharmacology, 2007
    Co-Authors: Manuella P. Kaster, Roberto Andreatini, Inara M. Raupp, Ricardo W. Binfaré, Ana Lúcia S. Rodrigues
    Abstract:

    Lamotrigine is an anticonvulsant drug that is also effective in the treatment of mood disorders, especially bipolar disorder. However, few studies have been conducted in animal models of depression to evaluate its mechanism of action. The present study investigated the effect of lamotrigine in the forced Swimming Test in mice and the involvement of the noradrenergic system in this effect. Lamotrigine (20-30 mg/kg, i.p.) decreased the immobility time in the forced Swimming Test and the number of crossings in the open-field Test. In addition, the pretreatment of mice with the inhibitor of the enzyme tyrosine hydroxylase, alpha-methyl-p-tyrosine (100 or 250 mg/kg), prevented the antidepressant-like effect of lamotrigine (30 mg/kg, i.p.) in the forced Swimming Test. Besides that, the pretreatment of mice with prazosin (1 mg/kg, i.p., an alpha1-adrenoceptor antagonist) or yohimbine (1 mg/kg, i.p., an alpha2-adrenoceptor antagonist) also prevented the anti-immobility effect of lamotrigine (30 mg/kg, i.p.). Moreover, the administration of subeffective doses of phenylephrine (5 mg/kg, i.p., an alpha1-adrenoceptor agonist) or clonidine (0.06 mg/kg, i.p., an alpha2-adrenoceptor agonist) was able to potentiate the action of a subeffective dose of lamotrigine (10 mg/kg, i.p.) in the forced Swimming Test. Thus, the present study suggests that the antidepressant-like effect of lamotrigine in the forced Swimming Test is related to the noradrenergic system, likely due to an activation of alpha1- and alpha2-postsynaptic adrenoceptors.

Farzad Ebrahimi - One of the best experts on this subject based on the ideXlab platform.

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