Mesulergine antagonism towards the fluoxetine anti-immobility effect in the forced swimming test in mice

Cesana, Raffaele; Ceci, Angelo; Ciprandi, C; Borsini, Franco

doi:10.1111/j.2042-7158.1993.tb05578.x

Cited by 39 publications

(27 citation statements)

References 17 publications

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“…Therefore, it is possible to argue that acute fluoxetine reduces mesolimbic dopaminergic function by acting on 5-HT2C,2B receptors. This finding is consistent with a previous report showing that the anti-immobility effect of fluoxetine in the forced swimming test was blocked by mesulergine, but not by the mixed 5-HT2A/5-HT2C/2a antagonist ritanserin (Cesana et al, 1993) thus suggesting that this pharmacological effect was mediated by the 5-HT2C,2B receptor subtype.…”

Section: Discussionsupporting

confidence: 93%

“…It is now well established that fluoxetine is an effective antidepressant agent (Gram, 1994) which also has good therapeutic activity in the treatment of obsessive-compulsive disorders (Fontaine & Chouinard, 1986;Levine et al, 1989) and eating disorders (Freeman & Hampson, 1987;Kaye et al, 1991). There is evidence that the antidepressant effect of fluoxetine, assessed in the forced swimming test in mice, is antagonized by (±)-sulpiride a dopamine D2 receptor blocker (Cesana et al, 1993). These data are consistent with the general hypothesis that an enhancement of dopaminergic transmission in the mesolimbic system is involved in the antidepressant effect of several drugs (Cervo & Samanin, 1987;1988;Cervo et al, 1990).…”

Section: Introductionsupporting

confidence: 78%

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Differential effects of acute and chronic fluoxetine administration on the spontaneous activity of dopaminergic neurones in the ventral tegmental area

Prisco

Esposito

1995

British J Pharmacology

157

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1 Electrophysiological techniques were used to study the effects of fluoxetine and citalopram on the basal activity of dopaminergic neurones in the ventral tegmental area (VTA) and substantia nigra, pars compacta (SNc) of rats.2 Acute i.v. injection of fluoxetine (20-1280 ,ug kg-') caused a dose-dependent inhibition of the firing rate of VTA dopaminergic neurones, but did not affect the activity of dopaminergic cells in the SNc. Citalopram (20-1280 pg kg-', i.v.) inhibited the firing rate of dopaminergic neurones in the VTA, but its effect (maximal inhibition: 14 ± 7%) was less pronounced than that of fluoxetine (maximal inhibition: 34±7%).

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Section: Discussionsupporting

confidence: 93%

Section: Introductionsupporting

confidence: 78%

Differential effects of acute and chronic fluoxetine administration on the spontaneous activity of dopaminergic neurones in the ventral tegmental area

Prisco

Esposito

1995

British J Pharmacology

157

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“…Drug doses were 30 mg/kg fluoxetine, 20 mg/kg desipramine and 25 mg/kg imipramine. Doses were chosen on the basis of previous reports in mice of the anti-immobility effects of fluoxetine (Perrault et al 1992;Cesana et al 1993;Redrobe et al 1996;Eckeli et al 2000;Clenet et al 2001;Conti et al 2002), desipramine Vaugeois et al 1997;Srivastava and Nath 2000;Wong et al 2000;Clenet et al 2001;Cryan et al 2001;Lucki et al 2001;Conti et al 2002), and imipramine (Redrobe and Bourin 1997;Vaugeois et al 1997;Wong et al 2000;David et al 2001;Liu and Gershenfeld 2001;Do-Rego et al 2002).…”

Section: Drugsmentioning

confidence: 99%

Evaluation of Antidepressant-related Behavioral Responses in Mice Lacking the Serotonin Transporter

Holmes

Yang

Murphy

et al. 2002

Neuropsychopharmacology

263

181

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Inhibition of the serotonin transporter (5-HTT) is a principal initial target of many antidepressants. However, the contribution of the 5-HTT to their therapeutic efficacy is incompletely understood. We utilized a targeted gene mutation approach to examine the role of the 5-HTT in the behavioral actions of antidepressants. The 5-HTT mutation was bred onto two separate genetic backgrounds, C57BL/6J and 129S6. On a preliminary screen for gross physical, neurological and behavioral functions, all measures were normal with the exception that 5-HTT 5-HTT Ϫ / Ϫ mice on the C57BL/6J background showed no baseline antidepressant-related phenotype on either test. The behavioral effects of three antidepressants were tested in 5-HTT mutant mice (C57BL/6J background) in the tail suspension test. The anti-immobility effects of the serotonin reuptake inhibitor, fluoxetine (30 mg/kg), were abolished in 5-HTT Ϫ / Ϫ mice, confirming that the 5-HTT gene is required for the behavioral effects of fluoxetine. In contrast, 5-HTT Ϫ / Ϫ mice retained sensitivity to the anti-immobility effects of the norepinephrine reuptake inhibitor, desipramine (20 mg/kg), and the mixed serotonin/norepinephrine reuptake inhibitor, imipramine (25 mg/kg Antidepressants are thought to normalize the disturbances in monoamine function that occur in affective disorders (Feighner and Boyer 1996;Frazer 1997; Montgomery and Den Boer 2001). While dysfunctions in noradrenergic and dopaminergic systems are putative etiological factors in depression, there is considerable evidence indicating that perturbation of central serotonergic activity is a major etiological component of depression (Willner 1985;Murphy 1990;Maes and Meltzer 1995;Charney 1998 NO . 6 Antidepressant Responses in 5-HTT KO Mice 915 (for reviews see Brown and Linnoila 1990;Owens and Nemeroff 1998;Mann 1999). The serotonin transporter (5-HTT) acts as a key regulator of serotonin signaling. By regulating reuptake of released serotonin, the 5-HTT controls the duration and intensity of serotoninergic activity at the synapse. The 5-HTT has been directly implicated in depression by the finding that brain 5-HTT binding density is reduced in brains and platelets of depressed patients (e.g., Nemeroff et al. 1994;Malison et al. 1998;Mann et al. 2000). Moreover, a number of studies have found an association between genetic variation in the regulatory region of the 5-HTT gene and depression (e.g., Battersby et al. 1996; Collier et al. 1996a,b;Furlong et al. 1998;Rees et al. 1997;Menza et al. 1999; but see Seretti et al. 1999). The 5-HTT is also a major target for many antidepressant drug treatments (Blakely et al. 1991;Ramamoorthy et al. 1993). It is well known that the serotonin reuptake inhibitor (SRI) class of antidepressants increase concentrations of serotonin in the synapse by blocking the serotonin transporter (5-HTT) (Blakely et al. 1991;Ramamoorthy et al. 1993). However, given the time lag between the initial inhibitory effects of antidepressants on the 5-HTT and an observable improvement in sympt...

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“…was administered twice daily for 3 days, with the last dose given 18 h prior to behavioral testing (Cesana et al, 1993). Depletion of 5-HT was confirmed by killing mice 1 h after behavioral testing and dissecting the hippocampus from mouse brain.…”

Section: Drugsmentioning

confidence: 99%

Sex Differences in the Regulation of Serotonergic Transmission and Behavior in 5-HT Receptor Knockout Mice

Jones

Lucki

2005

Neuropsychopharmacol

100

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Few studies have examined the relationship between genetics, stress, and sex-linked differences in neurotransmitter systems. Examining serotonin (5-HT) receptor knockout mice on stress-induced behavioral depression, female 5-HT 1B receptor knockout mice demonstrated significantly reduced immobility than either male 5-HT 1B receptor knockout mice or male and female wild-type mice on the tail suspension test (TST) and forced swimming test. The behavioral phenotype was identified as likely due to a disinhibition of 5-HT release, because depletion of 5-HT with parachlorophenylalanine selectively reduced immobility of female 5-HT 1B receptor knockout mice in the TST. In contrast, male and female 5-HT 1A receptor knockout mice demonstrated reduced immobility compared with control mice, but the depletion of 5-HT with PCPA did not reverse the antidepressant-like phenotype. Microdialysis studies confirmed significantly higher baseline levels of hippocampal 5-HT in female, but not male, 5-HT 1B receptor knockout mice. Both male and female 5-HT 1B receptor knockout mice demonstrated augmented dialysate responses to fluoxetine. Also, both male and female 5-HT 1B receptor knockout mice demonstrated reductions of immobility in the TST after treatment with fluoxetine. Therefore, female 5-HT 1B receptor knockout mice demonstrate a sex-linked disinhibition of 5-HT release that sustained higher baseline levels of hippocampal 5-HT and behavioral vulnerability to 5-HT depletion.

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Mesulergine antagonism towards the fluoxetine anti-immobility effect in the forced swimming test in mice

Cited by 39 publications

References 17 publications

Differential effects of acute and chronic fluoxetine administration on the spontaneous activity of dopaminergic neurones in the ventral tegmental area

Differential effects of acute and chronic fluoxetine administration on the spontaneous activity of dopaminergic neurones in the ventral tegmental area

Evaluation of Antidepressant-related Behavioral Responses in Mice Lacking the Serotonin Transporter

Sex Differences in the Regulation of Serotonergic Transmission and Behavior in 5-HT Receptor Knockout Mice

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