Increased expression of L-type high voltage-gated calcium channel α1 and α2/δ subunits in mouse brain after chronic nicotine administration

Hayashida, Shinsuke; Katsura, Masashi; Torigoe, Fumiko; Tsujimura, Akira; Ohkuma, Seitaro

doi:10.1016/j.molbrainres.2004.11.002

Cited by 24 publications

(20 citation statements)

References 22 publications

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“…In animal studies, long-term ethanol consumption and alcohol dependence as well as chronic administration of other GABA-A receptor positive allosteric modulators, such asmorphine and nicotine, have been associated with up-regulation of L-type high-voltage-gated calcium channels (HVCCs), increased expression of specific subunits, and more available binding sites of DHPs [Messing et al, 1986;Grant et al, 1993;Walter and Messing, 1999;Hayashida et al, 2005;Katsura et al, , 2007Shibasaki et al, 2007;Xiang et al, 2008]. A decrease in protein levels with chronic administration of morphine has been shown for the CaV1.3 subunit, underscoring the selectivity of adaptive changes within the LTCC family [Haller et al, 2008].…”

Section: Substance Abuse and Dependencementioning

confidence: 99%

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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Section: Substance Abuse and Dependencementioning

confidence: 99%

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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“…LTCC antagonists block acute nicotine-dependent locomotor activation and attenuate chronic nicotine-mediated locomotor sensitization (Hart et al, 1996;Biala, 2003). In addition, chronic nicotine administration increases the expression of various LTCC subunits in the cortex (Hayashida et al, 2005). Thus, calcineurin may serve as one of the critical effector proteins downstream of chronic nicotine-mediated LTCC activation to support nicotine-mediated behavior.…”

mentioning

confidence: 99%

Role of Calcineurin in Nicotine-Mediated Locomotor Sensitization

Addy¹,

Fornasiero²,

Stevens³

et al. 2007

J. Neurosci.

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Calcineurin is a serine/threonine phosphatase that contributes to the effects of nicotine on calcium signaling in cultured cortical neurons; however, the role of calcineurin in behavioral responses to nicotine in vivo has not been examined. We therefore determined whether calcineurin blockade could alter nicotine-mediated locomotor sensitization in Sprague Dawley rats using systemic or brain regionspecific administration of the calcineurin inhibitors cyclosporine or FK506. Systemic cyclosporine administration decreased calcineurin activity in the brain, attenuated nicotine-mediated locomotor sensitization, and blocked the effects of nicotine on DARPP32 (dopamineand cAMP-regulated phosphoprotein-32) activation in the striatum. Direct infusion of calcineurin inhibitors cyclosporine or FK506 into the ventral tegmental area (VTA) also attenuated nicotine-mediated locomotor sensitization, whereas infusion of rapamycin, which binds to FK-binding protein but does not inhibit calcineurin, did not affect sensitization. Together, the data suggest that activation of calcineurin, particularly in the VTA, is a novel signaling event important for nicotine-mediated behavior and intracellular signaling.

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“…It will be of significant interest to investigate the expression of Ca V 1.2␣1 and Ca V 1.3␣1 subunit proteins in hippocampal CA1 region in FZP-withdrawn rats in relation to changes in L-VGCC single-channel function. Importantly, increased DHP-binding site number and increased expression of L-VGCC Ca V 1.2␣1 and Ca V 1.3␣1 subunits were also demonstrated in animals physically dependent on ethanol, morphine, or nicotine (Katsura et al, 2002Hayashida et al, 2005;Shibasaki et al, 2007). Increases in expression of specific L-type channel subunits associated with enhanced HVA Ca 2ϩ channel function may provide a common mechanism underlying dependence on and addiction to a variety of drugs of abuse.…”

Section: Discussionmentioning

confidence: 93%

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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Increased expression of L-type high voltage-gated calcium channel α1 and α2/δ subunits in mouse brain after chronic nicotine administration

Cited by 24 publications

References 22 publications

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

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

Role of Calcineurin in Nicotine-Mediated Locomotor Sensitization

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

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