Electroconvulsive Shock Reduces Inositol 1,4,5‐Trisphosphate 3‐Kinase mRNA Expression in Rat Dentate Gyrus

Kim, Hyun; Ko, Jae Pil; Kang, Ung Gu; Park, Joo‐Bae ‐B; Kim, Hyung‐Lae ‐L; Lee, Young Han; Kim, Yong Sik

doi:10.1046/j.1471-4159.1994.63051991.x

Cited by 32 publications

(12 citation statements)

References 16 publications

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“…These data indicate that a lower level of InsP3Rl protein expression inhibition is sufficient to obtain a phenotype resistant to the induction of a depressive state. To further support our results suggesting the importance of type 1 InsP3R in mood disorders, a reduction of InsP3Rl mRNA in rat brain was observed after a single electroconvulsive shock (Kim et al, 2001).…”

Section: Discussionsupporting

confidence: 84%

An antidepressant behaviour in mice carrying a gene-specific InsP3R1, InsP3R2 and InsP3R3 protein knockdown

et al. 2008

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a b s t r a c tEvidence has accumulated for the involvement of Ca 2þ in the pathophysiology of mood disorders.Elevations in both resting and stimulated intracellular Ca 2þ levels in patients with affective disorders have been reported. The role of inositol-1,4,5-trisphosphate receptors (InsP3Rs), which allow mobilization of intracellular Ca 2þ stores, was, then, investigated in the mouse forced swimming test. InsP3Rantagonists (heparin, xestospongin C) as well as an inositol monophosphatase inhibitor (LiCl) showed an antidepressant activity of intensity comparable to clinically used antidepressants. InsP3Rl, InsP3R2 and InsP3R3 knockdown mice were obtained to investigate the role of InsP3R isoforms. We generated mice carrying a cerebral knockdown of InsP3Rl, InsP3R2 and InsP3R3 proteins by administering antisense oligonucleotides complementary to the sequence of InsP3Rl, InsP3R2 and InsP3R3. These antisensetreated mice showed a specific InsP3R protein level reduction in the mouse cerebral cortex and hippocampus, demonstrated by immunoblotting, immunoprecipitation and immunocytochemistry experiments. Knockdown mice for each InsP3R isoforms showed an antidepressant behaviour and the induced phenotype was reversible disappearing 7 days after the end of the treatment. The absence of impairment of locomotor activity and spontaneous mobility in InsP3R knockdown mice was revealed. These results indicate the involvement of the InsP3R-mediated pathway in the modulation of depressive conditions and may be useful for the development of new therapeutical strategies for the treatment of mood disorders.

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Section: Discussionsupporting

confidence: 84%

An antidepressant behaviour in mice carrying a gene-specific InsP3R1, InsP3R2 and InsP3R3 protein knockdown

et al. 2008

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“…Specifically, antidepressant behavior was achieved by administering lithium chloride which presumably acted through the inhibition of inositol monophosphatase and caused phosphoinositol lipid turnover [Phiel and Klein, 2001]. As the authors underscored in their article [Galeotti et al, 2008], electroconvulsive therapy (ECT) is one of the most effective treatments for depression and it rapidly reduces the expression of InsP3R in rat brains as well [Kim et al, 2001]. Interestingly, nicardipine, a calcium-channel blocker, was found to enhance the antidepressant action of ECT in 26 patients affected by major depression [Dubovsky et al, 2001].…”

Section: Mood and Anxiety Disordersmentioning

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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“…Accumulating evidence suggests that direct treatment of brain slices with NMDA produces long-term depression-like phenomena (Lee et al, 1998), which promote the shrinkage of spines (Zhou et al, 2004). Furthermore, we have also previously shown that aberrant neuronal activations by chemical reagents (kainic acid) or electric stimulation (electroconvulsive shock) reduce the expression of IP 3 K-A (Kim et al, 1994; Sun et al, 2006). Because these conditions reduce synaptic efficacy and induce amnesia (Squire and Spanis, 1984; Holmes, 1991), these results collectively suggested that the expression and localization of IP 3 K-A might be dynamically regulated by neuronal plasticity.…”

Section: Discussionmentioning

confidence: 88%

Inositol 1,4,5-Trisphosphate 3-Kinase A Functions As a Scaffold for Synaptic Rac Signaling

Kim¹,

Park²,

Hong³

et al. 2009

J. Neurosci.

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Activity-dependent alterations of synaptic contacts are crucial for synaptic plasticity. The formation of new dendritic spines and synapses is known to require actin cytoskeletal reorganization specifically during neural activation phases. Yet the site-specific and timedependent mechanisms modulating actin dynamics in mature neurons are not well understood. In this study, we show that actin dynamics in spines is regulated by a Rac anchoring and targeting function of inositol 1,4

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Electroconvulsive Shock Reduces Inositol 1,4,5‐Trisphosphate 3‐Kinase mRNA Expression in Rat Dentate Gyrus

Cited by 32 publications

References 16 publications

An antidepressant behaviour in mice carrying a gene-specific InsP3R1, InsP3R2 and InsP3R3 protein knockdown

An antidepressant behaviour in mice carrying a gene-specific InsP3R1, InsP3R2 and InsP3R3 protein knockdown

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

Inositol 1,4,5-Trisphosphate 3-Kinase A Functions As a Scaffold for Synaptic Rac Signaling

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