Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE

User menu

  • Log out
  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log out
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE
PreviousNext
ARTICLE, Cellular/Molecular

The Status of Voltage-Dependent Calcium Channels in α1E Knock-Out Mice

Scott M. Wilson, Peter T. Toth, Seog Bae Oh, Samantha E. Gillard, Steven Volsen, Dongjun Ren, Louis H. Philipson, E. Chiang Lee, Colin F. Fletcher, Lino Tessarollo, Neal G. Copeland, Nancy A. Jenkins and Richard J. Miller
Journal of Neuroscience 1 December 2000, 20 (23) 8566-8571; https://doi.org/10.1523/JNEUROSCI.20-23-08566.2000
Scott M. Wilson
1Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Peter T. Toth
2Department of Neurobiology, Pharmacology, and Physiology, The University of Chicago, Chicago, Illinois 60637,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Seog Bae Oh
2Department of Neurobiology, Pharmacology, and Physiology, The University of Chicago, Chicago, Illinois 60637,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Samantha E. Gillard
3Eli Lilly and Company, Lilly Corporate Center, Indianapolis, Indiana 46285, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Steven Volsen
4Eli Lilly and Company, Erl Wood, Manor, Windlesham, Surrey GU20 6PH, United Kingdom
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Dongjun Ren
2Department of Neurobiology, Pharmacology, and Physiology, The University of Chicago, Chicago, Illinois 60637,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Louis H. Philipson
2Department of Neurobiology, Pharmacology, and Physiology, The University of Chicago, Chicago, Illinois 60637,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
E. Chiang Lee
1Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Colin F. Fletcher
1Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Lino Tessarollo
1Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Neal G. Copeland
1Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Nancy A. Jenkins
1Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Richard J. Miller
2Department of Neurobiology, Pharmacology, and Physiology, The University of Chicago, Chicago, Illinois 60637,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Article Figures & Data

Figures

  • Tables
  • Fig. 1.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 1.

    Generation of a mouse with a disrupted allele of the Cacna1e gene. A, Targeting of theCacna1e gene is shown. Top, The genomic structure of the wild-type allele of the Cacna1e gene is shown with exons indicated by black boxes. Restriction sites used for determination of the disrupted allele are indicated.Bottom, A PGK neolURA3 expression cassette replaced the fourth through eighth exons of this fragment. The locations of probes used for genomic blot hybridization are shownbelow the disrupted allele. B, Genomic blot hybridization of DNA derived from neomycin-resistant ES cell clones is shown. ES cell DNA was probed with a 3′-flanking probe (left) and 5′ internal probe (right). Hybridization with the 3′ probe shows a 6 kb wild-type band and 6.6 kb mutant band, whereas the 5′ internal probe revealed an 8.7 kb wild-type band and 12 kb mutant band. C, Tail tip DNA from three intercross littermates was probed with the 3′-flanking probe and showed the expected size for wild-type, heterozygous, and homozygous mutant.ko, Knock-out.

  • Fig. 2.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 2.

    Western blot analysis of α1E protein in wild-type and α1E-deficient mice. Brain lysates from 129/SV and C57BL/6J wild-type mice show the expression of the 230 kDa α1E protein, whereas the protein is clearly absent from brain tissue of α1E KO mice. Specificity of the antibody was confirmed by detection of a band in α1E-transfected HEK cell membranes and the lack of staining in untransfected HEK cell membranes.

  • Fig. 3.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 3.

    Effects of drugs and toxins on the cerebellar granule cell IBa. A, Plot of the peak IBa versus time in an α1E KO mouse shows a resistant component of the high voltage-activated IBa remaining after consecutive bath application of specific drugs and toxins. SNX-482 had no effect on the toxin-resistant current. Inset,Representative traces at numbered points are shown. B, Plot of the peakIBa versus time from a wild-type C57BL/6J mouse is shown. Inset, Representativetraces are shown. SNX-482 inhibited a component of the R current remaining after nimodipine, ω-agatoxin IVA (ω-Aga IVA), and ω-conotoxin GVIA (ω-CTx GVIA) application. C, Plot of the peakIBa versus time from a wild-type 129/SV mouse is shown. SNX-482 also inhibited part of the R current in this case. Inset, Representative traces are shown. D, Comparison of inhibitory effects of specific drugs and toxins on the granule cell IBa in α1E KO and control mice is shown. Drugs and toxins were used in the following concentrations: nimodipine (Nimo), 500 nm; ω-conotoxin GVIA (CTx), 500 nm; ω-Aga IVA (Aga), 200 nm; SNX-482 (SNX), 1 μm; Cd2+, 100 μm. The data from the two parental control mouse strains were pooled. SNX-482 was only effective in inhibiting the IBa from control mice (**p < 0.01). The numbers inparentheses represent the number of experiments.E, The effects of the specific drugs and toxins on theIBa from the two control mouse strains did not differ significantly from each other. The numbers inparentheses represent the number of experiments.Resist, Resistant; wt, wild type.

  • Fig. 4.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 4.

    Effects of drugs and toxins on theIBa in DRG neurons from wild-type and α1E KO mice. A, Plot of the peakIBa versus time in a DRG neuron from an α1E KO mouse. An R current still remained after sequential application of the different drugs and toxins. TheIBa from α1E KO mice was insensitive to SNX-482. Inset, Representative currents.B, Time course of the peakIBa from a wild-type DRG neuron exhibiting sensitivity to SNX-482. C, Time course of the peakIBa from a wild-type DRG neuron that was insensitive to SNX-482. D, Average inhibition (mean ± SEM) of the peak IBa by specific drugs and toxins. Drugs and toxins were used in the following concentrations: nimodipine, 2 μm; ω-conotoxin GVIA, 1 μm; ω-Aga IVA, 200 nm; SNX-482, 1 μm. DRG neurons from α1E KO mice (n = 7) and a population of DRG neurons from wild-type mice (n= 8) were insensitive to SNX-482 application. TheIBa inhibition by SNX-482 in sensitive DRG neurons (n = 10) was significant (p < 0.01). E, Interrelationship between sensitivity to ω-Aga IVA and SNX-482 in wild-type DRG neurons (n = 8). The correlation was significant (p = 0.0265) using the Spearman rank correlation test.

Tables

  • Figures
    • View popup
    Table 1.

    Ba2+ currents in cultured mouse neurons

    KOWild type
    Total current364.9  ± 50.4375.8  ± 47.6
    Nimodipine36.1  ± 8.244.7  ± 8.4
    ω-Aga IVA75.0  ± 15.0105.3  ± 15.6
    ω-CTx GVIA139.2  ± 30.795.4  ± 22.1
    SNX-4821.8  ± 1.345.5  ± 6.9
    Resistant112.8  ± 26.884.9  ± 20.54
    • Comparison of the peak IBa (pA) from cultured mouse cerebellar granule cells (α1E knock-out,n = 5; wild type, n = 9). Data represent peak current amplitudes (pA) blocked by the specific toxin or drug indicated and the remaining resistant current. Data are given as mean ± SEM.

Back to top

In this issue

The Journal of Neuroscience: 20 (23)
Journal of Neuroscience
Vol. 20, Issue 23
1 Dec 2000
  • Table of Contents
  • Index by author
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
The Status of Voltage-Dependent Calcium Channels in α1E Knock-Out Mice
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
The Status of Voltage-Dependent Calcium Channels in α1E Knock-Out Mice
Scott M. Wilson, Peter T. Toth, Seog Bae Oh, Samantha E. Gillard, Steven Volsen, Dongjun Ren, Louis H. Philipson, E. Chiang Lee, Colin F. Fletcher, Lino Tessarollo, Neal G. Copeland, Nancy A. Jenkins, Richard J. Miller
Journal of Neuroscience 1 December 2000, 20 (23) 8566-8571; DOI: 10.1523/JNEUROSCI.20-23-08566.2000

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
The Status of Voltage-Dependent Calcium Channels in α1E Knock-Out Mice
Scott M. Wilson, Peter T. Toth, Seog Bae Oh, Samantha E. Gillard, Steven Volsen, Dongjun Ren, Louis H. Philipson, E. Chiang Lee, Colin F. Fletcher, Lino Tessarollo, Neal G. Copeland, Nancy A. Jenkins, Richard J. Miller
Journal of Neuroscience 1 December 2000, 20 (23) 8566-8571; DOI: 10.1523/JNEUROSCI.20-23-08566.2000
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • MATERIALS AND METHODS
    • RESULTS
    • DISCUSSION
    • Footnotes
    • REFERENCES
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Keywords

  • dorsal root ganglia
  • cerebellar granule cells
  • pain
  • synaptic transmission
  • voltage-dependent calcium channels
  • α1E knock-out mice

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

ARTICLE

  • Single-Cell Microarray Analysis in Hippocampus CA1: Demonstration and Validation of Cellular Heterogeneity
  • Heme Oxygenase-2 Protects against Lipid Peroxidation-Mediated Cell Loss and Impaired Motor Recovery after Traumatic Brain Injury
  • Gene Microarrays in Hippocampal Aging: Statistical Profiling Identifies Novel Processes Correlated with Cognitive Impairment
Show more ARTICLE

Cellular/Molecular

  • Single-Cell Microarray Analysis in Hippocampus CA1: Demonstration and Validation of Cellular Heterogeneity
  • Heme Oxygenase-2 Protects against Lipid Peroxidation-Mediated Cell Loss and Impaired Motor Recovery after Traumatic Brain Injury
  • Gene Microarrays in Hippocampal Aging: Statistical Profiling Identifies Novel Processes Correlated with Cognitive Impairment
Show more Cellular/Molecular
  • Home
  • Alerts
  • Follow SFN on BlueSky
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Notice
  • Contact
  • Accessibility
(JNeurosci logo)
(SfN logo)

Copyright © 2025 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.