Time‐course of modifications elicited by reserpine on the density and mRNA synthesis of the vesicular monoamine transporter, and on the density of the membrane dopamine uptake complex

Naudon, Laurent; Leroux-Nicollet, Isabelle; Raisman‐Vozari, Rita; Botton, Damien; Costentin, Jean

doi:10.1002/syn.890210105

Cited by 28 publications

(18 citation statements)

References 32 publications

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“…This effect was observed up to 35 days after reserpine administration. This long-lasting increase in [ 11 C]raclopride binding is in agreement with the longlasting effect of reserpine on striatal DA levels, as previously demonstrated in rats (Naudon et al, 1995). Raclopride has affinity both for D 2 and D 3 receptors (Sokoloff et al, 1990).…”

Section: Discussionsupporting

confidence: 87%

Effect of reserpine-induced depletion of synaptic dopamine on [11C]Raclopride binding to D2-dopamine receptors in the monkey brain

Ginovart

Farde

Halldin

et al. 1997

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Positron emission tomography was used to examine the in vivo binding of [11C]raclopride to D2-dopamine (DA) receptors in the striatum of two Cynomolgus monkeys after a single dose of reserpine (1 mg/kg, i.v.). A Scatchard procedure was repeated five times to follow D2 receptor density and apparent affinity for 7 weeks after reserpine. Reserpine-induced depletion of DA lead to a marked increase in [11C]raclopride binding, which was still detectable 20 days after treatment. Scatchard analyses indicated that the measured increase in [11C]raclopride binding reflected an increase in receptor affinity but no evident change in receptor density (Bmax). Thus, the increase in [11C]raclopride binding after reserpine should correspond to a reduced competition with endogenous DA for binding to D2 receptors. The results were used to estimate the DA-induced D2 occupancy to be about 40% at physiological conditions.

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Section: Discussionsupporting

confidence: 87%

Effect of reserpine-induced depletion of synaptic dopamine on [11C]Raclopride binding to D2-dopamine receptors in the monkey brain

Ginovart

Farde

Halldin

et al. 1997

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“…Although it is possible that the reserpine treatment did not deplete all of the vesicles, one might expect that the responses would have been diminished if vesicles were strongly involved in these effects. Reserpine completely ablated [ 3 H]tetrabenazine binding to V M AT 2 in rat striatum 1 d after injection, suggesting that vesicles are not f unctional (Naudon et al, 1995). Therefore, the synaptic vesicles do not seem to be the source of the increased DA released by AM PH through the transporter.…”

Section: Vesicular Involvement In Enhanced Amph-mediated Da Releasementioning

confidence: 87%

Enhanced Amphetamine- and K⁺-Mediated Dopamine Release in Rat Striatum after Repeated Amphetamine: Differential Requirements for Ca²⁺- and Calmodulin-Dependent Phosphorylation and Synaptic Vesicles

1999

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After cessation of repeated, intermittent amphetamine, we detected an emergent Ca 2ϩ -dependent component of amphetamine-induced dopamine release and an increase in calmodulin and Ca 2ϩ -and calmodulin-dependent protein kinase activity in rat striatum. This study examined the involvement of calmodulin-dependent protein kinase II (CaM kinase II) and synaptic vesicles in the enhanced Ca 2ϩ -dependent dopamine release in response to amphetamine or K ϩ in rat striatum. Rats were pretreated for 5 d with 2.5 mg/kg amphetamine or saline and withdrawn from drug for 10 d. The selective CaM kinase II inhibitor KN-93 (1 M), but not the inactive analog KN-92, attenuated the Ca 2ϩ -dependent amphetaminemediated dopamine release from amphetamine-pretreated rats but had no effect in saline-pretreated controls.[ 3 H]Dopamine uptake was unaltered by repeated amphetamine or KN-93 and was Ca 2ϩ independent. Striatal dopamine release stimulated by 50 mM KCl was enhanced twofold after repeated amphetamine compared with that in saline controls but was unaffected by KN-93. To examine the requirement for dopaminergic vesicles in the Ca 2ϩ -dependent dopamine release, we administered reserpine to saline-and amphetamine-pretreated rats 1 d before killing. Reserpine pretreatment did not affect amphetamine-mediated dopamine release from either pretreatment group but completely ablated K ϩ -mediated dopamine release. Reserpine did not disrupt the ability of 1 M KN-93 to block the Ca 2ϩ -dependent amphetamine-mediated dopamine release from amphetamine-pretreated rats. The results indicate that the enhanced dopamine release elicited by amphetamine from chronically treated rats is dependent on Ca 2ϩ -and calmodulin-dependent phosphorylation and is independent of vesicular dopamine storage. On the contrary, the enhanced depolarization-mediated vesicular dopamine release is independent of Ca 2ϩ -and calmodulin-dependent phosphorylation.

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“…The preparation of homogenates and HPLC determinations were made as described (16). Statistical Analyses.…”

Section: Measurement Of Tissue Levels Of 5-ht and Its Metabolitementioning

confidence: 99%

Behavioral, neurochemical, and electrophysiological characterization of a genetic mouse model of depression

Yacoubi

Bouali

Popa

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

239

173

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Depression is a multifactorial illness and genetic factors play a role in its etiology. The understanding of its physiopathology relies on the availability of experimental models potentially mimicking the disease. Here we describe a model built up by selective breeding of mice with strikingly different responses in the tail suspension test, a stress paradigm aimed at screening potential antidepressants. Indeed, ''helpless'' mice are essentially immobile in the tail suspension test, as well as the Porsolt forced-swim test, and they show reduced consumption of a palatable 2% sucrose solution. In addition, helpless mice exhibit sleep-wakefulness alterations resembling those classically observed in depressed patients, notably a lighter and more fragmented sleep, with an increased pressure of rapid eye movement sleep. Compared with ''nonhelpless'' mice, they display higher basal seric corticosterone levels and lower serotonin metabolism index in the hippocampus. Remarkably, serotonin 1A autoreceptor stimulation induces larger hypothermia and inhibition of serotoninergic neuronal firing in the nucleus raphe dorsalis in helpless than in nonhelpless mice. Thus, helpless mice exhibit a decrease in serotoninergic tone, which evokes that associated with endogenous depression in humans. Finally, both the behavioral impairments and the serotoninergic dysfunction can be improved by chronic treatment with the antidepressant fluoxetine. The helpless line of mice may provide an opportunity to approach genes influencing susceptibility to depression and to investigate neurophysiological and neurochemical substrates underlying antidepressant effects.T he prevalence of depression worldwide is such that this disorder represents a major health problem. It is estimated, for example, that Ϸ10% of men and 20% of women in Western Europe will suffer from a major depressive episode at some time in their life. The monoamine hypothesis of depression suggests that one of the biological bases of affective disorders is a deficiency in the neurotransmitter serotonin (5-HT). During the past 40 yr, this hypothesis has been refined, as more experimental and clinical evidence has emerged. The selective 5-HT reuptake inhibitors, in particular, allowed important progress in our understanding of the role of 5-HT in depression. To some extent, the mechanism of action of 5-HT reuptake inhibitors, which are the most widely prescribed antidepressant drugs today, can be anticipated from our knowledge of the anatomy and chemistry of the central serotoninergic system. However, it must be accepted that extensive investigations have so far failed to find convincing evidence of a primary dysfunction of the serotoninergic system in patients with depression. Disturbances of sleep are typical for most depressed patients and belong to the core symptoms of the disorder. Polysomnographic sleep research has demonstrated that, besides disturbances of sleep continuity, depression is associated with a reduction of slow-wave sleep and a shortening of rapid eye movement (REM...

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Time‐course of modifications elicited by reserpine on the density and mRNA synthesis of the vesicular monoamine transporter, and on the density of the membrane dopamine uptake complex

Cited by 28 publications

References 32 publications

Effect of reserpine-induced depletion of synaptic dopamine on [11C]Raclopride binding to D2-dopamine receptors in the monkey brain

Effect of reserpine-induced depletion of synaptic dopamine on [11C]Raclopride binding to D2-dopamine receptors in the monkey brain

Enhanced Amphetamine- and K⁺-Mediated Dopamine Release in Rat Striatum after Repeated Amphetamine: Differential Requirements for Ca²⁺- and Calmodulin-Dependent Phosphorylation and Synaptic Vesicles

Behavioral, neurochemical, and electrophysiological characterization of a genetic mouse model of depression

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Time‐course of modifications elicited by reserpine on the density and mRNA synthesis of the vesicular monoamine transporter, and on the density of the membrane dopamine uptake complex

Cited by 28 publications

References 32 publications

Effect of reserpine-induced depletion of synaptic dopamine on [11C]Raclopride binding to D2-dopamine receptors in the monkey brain

Effect of reserpine-induced depletion of synaptic dopamine on [11C]Raclopride binding to D2-dopamine receptors in the monkey brain

Enhanced Amphetamine- and K+-Mediated Dopamine Release in Rat Striatum after Repeated Amphetamine: Differential Requirements for Ca2+- and Calmodulin-Dependent Phosphorylation and Synaptic Vesicles

Behavioral, neurochemical, and electrophysiological characterization of a genetic mouse model of depression

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Enhanced Amphetamine- and K⁺-Mediated Dopamine Release in Rat Striatum after Repeated Amphetamine: Differential Requirements for Ca²⁺- and Calmodulin-Dependent Phosphorylation and Synaptic Vesicles