The antidepressant-like effect induced by the sigma1 (σ1) receptor agonist igmesine involves modulation of intracellular calcium mobilization

Urani, Alexandre; Romieu, Pascal; Portales-Casamar, Élodie; Roman, François J.; Maurice, Tangui

doi:10.1007/s00213-002-1150-y

Cited by 42 publications

(44 citation statements)

References 60 publications

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“…Present results suggest the possible involvement of RyR also in the induction of depressive conditions. Urani et al (2002) did not evidence any effect on mouse immobility time when xestospongin C and ryanodine were administered alone. In this study both compounds were used at concentrations at least 10 times higher than those resulted effective in the present study.…”

Section: Discussionmentioning

confidence: 69%

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

2006

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The role of intracellular calcium in the modulation of a depressant-like condition was investigated in the mouse forced swimming test. I.c.v. administration of TMB-8 (0.23e46.3 nmol per mouse), a blocker of Ca 2C release from intracellular stores, decreased the mouse immobility time. I.c.v. injection of thapsigargin (0.003e3 nmol per mouse), compound which selectively inhibits Ca 2C uptake into the endoplasmic reticulum, produced, 60 min after administration, a depressant-like condition. Xestospongin C (1e100 pmol per mouse i.c.v.), an InsP 3 -receptor antagonist, decreased the mouse immobility time. By contrast, D-myo-inositol (5.4e540 pmol per mouse i.c.v.), compound which produces InsP 3 , resulted in a depressant-like effect. Similarly, ryanodine (0.1e600 pmol per mouse i.c.v.), an RyR antagonist, decreased the immobility time values whereas the administration of 4-chloro-m-cresol (0.1e100 pmol per mouse i.c.v.), an RyR agonist, showed an opposite effect. The antidepressant-like effects observed with TMB-8, xestospongin C and ryanodine were comparable to that produced by the antidepressant drugs amitriptyline and clomipramine. The treatments employed did not produce any behavioural impairment of mice as revealed by the rota-rod and hole board tests indicating that the antidepressant-and depressant-like effects were not due to a compromised locomotor activity and spontaneous motility of the treated animals. These results indicate that a central variation in intracellular calcium contents is involved in the modulation of a depressive-like condition in the mouse forced swimming test. In particular, the blockade of both InsP 3 Rs and RyRs appears to play an important role in the induction of an antidepressant-like effect, whereas the stimulation of these receptors is involved in a depressant-like response of mice.

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Section: Discussionmentioning

confidence: 69%

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

2006

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“…In addition, a lower dose of JO-1784 had no effect by itself, but co-administered with the L-type voltage-dependent Ca 2+ channel (VDCC) positive modulator (-)-Bay K8644, it significantly reduced immobility. In agreement, the L-type VDCC antagonist verapamil and the N-type VDCC antagonist w-conotoxin blocked the effects of JO-1784 (211). Therefore, sigma 1 receptors may be interacting with pre-or postsynaptic VDCC's to exert "antidepressant-like" effects in the FST (211).…”

Section: +mentioning

confidence: 60%

The Role of Sigma Receptors in Depression

2005

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Abstract. Behavioral models used to test potential antidepressants have shown that ligands that bind to sigma receptors possess "antidepressant-like" properties. The focus of this review is to discuss the literature concerning sigma receptors and their ligands, with respect to their antidepressants properties. In addition to the behavioral data, we discuss electrophysiological and biochemical models demonstrating sigma receptors' ability to modulate important factors in the pathophysiology of depression and / or the mechanisms of action of antidepressants such as the serotonergic neurotransmission in the dorsal raphe nucleus (DRN) and the glutamatergic transmission in the hippocampus. We also discuss the significance of these two systems in the mechanism of action of antidepressants. Sigma ligands have potential as antidepressant medications with a fast onset of action as they produce a rapid modulation of the serotonergic system in the DRN and the glutamatergic transmission in the hippocampus. As these effects of sigma ligands may produce antidepressant properties by completely novel mechanisms of action, they may provide an alternative to the antidepressants currently available and may prove to be beneficial for treatment-resistant depressed patients.

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“…It has been reported that sigma-1 receptors regulate Ca 2 + release from intracellular Ca 2 + storage sites (Hayashi et al, 2000;Su, 2001, 2004), and that injections of inhibitors of intracellular Ca 2 + released into the brain could abolish the effects of sigma-1 receptor agonists in an animal model of depression (Urani et al, 2002). Therefore, it is likely that modulation of Ca 2 + signaling by a sigma-1 receptor agonist may play a role in the active mechanism of these drugs in the cognitive deficits paradigm, although further detailed studies are necessary.…”

Section: Discussionmentioning

confidence: 99%

Phencyclidine-Induced Cognitive Deficits in Mice are Improved by Subsequent Subchronic Administration of Fluvoxamine: Role of Sigma-1 Receptors

Hashimoto

Fujita

Iyo

2006

Neuropsychopharmacol

121

101

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This study was undertaken to examine the effects of the selective serotonin reuptake inhibitors fluvoxamine and paroxetine on cognitive deficits in mice after repeated administration of the N-methyl-D-aspartate receptor antagonist phencyclidine (PCP). In the novel object recognition test, repeated administration of PCP (10 mg/kg/day, 10 days) significantly decreased the exploratory preference in the retention test session, but not in the training test session. PCP-induced cognitive deficits were significantly improved by subsequent subchronic (2-week) administration of fluvoxamine (20 mg/kg/day), but not paroxetine (10 mg/kg/day). Furthermore, the effect of fluvoxamine on PCP-induced cognitive deficits was antagonized by co-administration of the selective sigma-1 receptor antagonist NE-100 (1 mg/kg/day). Moreover, PCP-induced cognitive deficits were also significantly improved by subsequent subchronic (2-week) administration of the selective sigma-1 receptor agonist SA4503 (1 mg/kg/day) or neurosteroid dehydroepiandrosterone 3-sulfate (DHEA-S; 25 mg/kg/day). The effects of SA4503 or DHEA-S were also antagonized by co-administration of NE-100 (1 mg/kg/day), suggesting the role of sigma-1 receptors in the active mechanisms of these drugs. In contrast, acute single administration of these drugs (fluvoxamine, paroxetine, SA4503) alone or combination with NE-100 did not alter PCP-induced cognitive deficits. The present study suggests that agonistic activity of fluvoxamine at sigma-1 receptors plays a role in the active mechanisms of fluvoxamine on PCP-induced cognitive deficits in mice. Therefore, sigma-1 receptor agonists such as fluvoxamine would be potential therapeutic drugs for the treatment of the cognitive deficits of schizophrenia.

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The antidepressant-like effect induced by the sigma1 (σ1) receptor agonist igmesine involves modulation of intracellular calcium mobilization

Abstract: The sigma(1) receptor-mediated behavioral effect is dependent not only on rapid Ca(2+) influx, as observed for a classical antidepressant, but also on intracellular Ca(2+) mobilization.

Cited by 42 publications

References 60 publications

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

The Role of Sigma Receptors in Depression

Phencyclidine-Induced Cognitive Deficits in Mice are Improved by Subsequent Subchronic Administration of Fluvoxamine: Role of Sigma-1 Receptors

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