Prevention of diazepam withdrawal syndrome by nifedipine—behavioural and neurochemical studies

Ganouni, Soumaya El; Hanoun, Naı̈ma; Boni, Claudette; Tazi, A.; Hakkou, F.; Hamon, Michel

doi:10.1016/j.pbb.2004.07.007

Cited by 11 publications

(8 citation statements)

References 28 publications

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“…Notably, acute systemic injection of the L-VGCC antagonist nimodipine, before AMPAR current enhancement, prevented both the augmentation of AMPAR currents in hippocampal CA1 neuron and anxiety-like behavior in benzodiazepine-withdrawn rats (Xiang and Tietz, 2007). These findings are consistent with other studies showing that administration of L-VGCC antagonists can interrupt withdrawal symptoms following benzodiazepine treatment (Gupta et al, 1996;El Ganouni et al, 2004;Cui et al, 2007), pointing to a role for regulation of L-VGCCs in mediating benzodiazepine dependence. However, little is known about the possible underlying mechanisms by which such adaptations may occur.…”

supporting

confidence: 89%

“…The finding that chronic, but not acute, benzodiazepine administration enhances HVA Ca 2ϩ currents suggests that a similar effect may occur in hippocampal CA1 pyramidal neurons associated with benzodiazepine withdrawal symptoms (Van Sickle et al, 2004). Indeed, L-type calcium channel blockers such as nimodipine, nifedipine, and verapamil were reported to block a variety of benzodiazepine withdrawal signs (Gupta et al, 1996;El Ganouni et al, 2004). These studies raise the possibility of a potential role for L-VGCC activation in benzodiazepine dependence.…”

Section: Discussionmentioning

confidence: 99%

“…The effect was not through a direct interaction between the antagonist and AMPARs, because nimodipine had no direct effect on AMPAR-mediated mEPSCs (Xiang and Tietz, 2007). These findings may also explain the ability of L-type calcium channel blockers to block a variety of benzodiazepine withdrawal signs, including hyperkinesia, hyperthermia, hyperaggression, and audiogenic seizures (Gupta et al, 1996;El Ganouni et al, 2004). The accumulated evidence supports the possibility that L-type VGCCs may be a major Ca 2ϩ source for diverse intracellular messengers or transcription factors to increase glutamatergic strength during benzodiazepine withdrawal and contribute to benzodiazepine physical dependence.…”

Section: Benzodiazepine Effect On Voltage-gated Calcium Currents 881mentioning

confidence: 99%

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Chronic Benzodiazepine Administration Potentiates High Voltage-Activated Calcium Currents in Hippocampal CA1 Neurons

Kong¹,

Earl²,

Davis³

et al. 2008

J Pharmacol Exp Ther

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Signs of physical dependence as a consequence of long-term drug use and a moderate abuse liability limit benzodiazepine clinical usefulness. Growing evidence suggests a role for voltage-gated calcium channel (VGCC) regulation in mediating a range of chronic drug effects from drug withdrawal phenomena to dependence on a variety of drugs of abuse. High voltageactivated (HVA) calcium currents were measured in whole-cell recordings from acutely isolated hippocampal CA1 neurons after a 1-week flurazepam (FZP) treatment that results in withdrawal-anxiety. An ϳ1.8-fold increase in Ca 2ϩ current density was detected immediately after and up to 2 days but not 3 or 4 days after drug withdrawal. Current density was unchanged after acute desalkyl-FZP treatment. A significant negative shift of the half-maximal potential of activation of HVA currents was also observed but steady-state inactivation remained unchanged. FZP and diazepam showed use-and concentration-

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supporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Benzodiazepine Effect On Voltage-gated Calcium Currents 881mentioning

confidence: 99%

See 1 more Smart Citation

Chronic Benzodiazepine Administration Potentiates High Voltage-Activated Calcium Currents in Hippocampal CA1 Neurons

Kong¹,

Earl²,

Davis³

et al. 2008

J Pharmacol Exp Ther

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“…Consistent with these data, Ltype calcium channels are found on the nerve terminals in the basal forebrain, and activation of nAChRs is known to increase calcium conductance of membranes of central neurons (Prince et al, 1996). In order to further discuss the influence of calcium homeostasis in anxiety-related behavior, it can be mentioned that some modest anxiolytic-like effects of certain CCAs can be observed, especially under conditions of high degree of behavioral inhibition due to increased fear (Pucilowski, 1992;El Ganouni et al, 2004). For instance, L-type VDCC plays a role in the amygdala in cued fear conditioning (ShinnickGallagher et al, 2003).…”

Section: Discussionmentioning

confidence: 65%

“…For instance, L-type VDCC plays a role in the amygdala in cued fear conditioning (ShinnickGallagher et al, 2003). Recent studies have also investigated an anti-withdrawal-like effect of CCAs after chronic ethanol or diazepam administration, when the anxiolytic properties of CCAs have been described during benzodiazepine and ethanol withdrawal (El Ganouni et al, 2004). The mechanism of action of CCAs does not appear to be linked with the function of the GABA-A receptor, but may be due to their non-specific antiserotonergic activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of acute and chronic nicotine on elevated plus maze in mice: Involvement of calcium channels

Biała

Budzyńska

2006

Life Sciences

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L‐type calcium channels and psychiatric disorders: A brief review

Casamassima

Hay

Benedetti

et al. 2010

American J of Med Genetics Pt B

116

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Emerging evidence from genome-wide association studies (GWAS) support the association of polymorphisms in the alpha 1C subunit of the L-type voltage-gated calcium channel gene (CACNA1C) with bipolar disorder. These studies extend a rich prior literature implicating dysfunction of L-type calcium channels (LTCCs) in the pathophysiology of neuropsychiatric disorders. Moreover, calcium channel blockers reduce Ca(2+) flux by binding to the α1 subunit of the LTCC and are used extensively for treating hypertension, preventing angina, cardiac arrhythmias and stroke. Calcium channel blockers have also been studied clinically in psychiatric conditions such as mood disorders and substance abuse/dependence, yielding conflicting results. In this review, we begin with a summary of LTCC pharmacology. For each category of disorder, this article then provides a review of animal and human data. In particular, we extensively focus on animal models of depression and clinical trials in mood disorders and substance abuse/dependence. Through examining rationale and study design of published clinical trials, we provide some of the possible reasons why we still do not have definitive evidence of efficacy of calcium-channel antagonists for mood disorders. Refinement of genetic results and target phenotypes, enrollment of adequate sample sizes in clinical trials and progress in physiologic and pharmacologic studies to synthesize tissue and isoform specific calcium channel antagonists, are all future challenges of research in this promising field. © 2010 Wiley-Liss, Inc.

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Prevention of diazepam withdrawal syndrome by nifedipine—behavioural and neurochemical studies

Cited by 11 publications

References 28 publications

Chronic Benzodiazepine Administration Potentiates High Voltage-Activated Calcium Currents in Hippocampal CA1 Neurons

Chronic Benzodiazepine Administration Potentiates High Voltage-Activated Calcium Currents in Hippocampal CA1 Neurons

Effects of acute and chronic nicotine on elevated plus maze in mice: Involvement of calcium channels

L‐type calcium channels and psychiatric disorders: A brief review

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