NDLI: Human autoantibodies specific for the α1A calcium channel subunit reduce both P-type and Q-type calcium currents in cerebellar neurons

Content Provider	PubMed Central
Author	Pinto, Ashwin Gillard, Samantha Moss, Fraser Whyte, Kathryn Brust, Paul Williams, Mark Ken, Stauderman Harpold, Michael Lang, Bethan Newsom-davis, John David, Bleakman Lodge, David Boot, John
Copyright Year	1998
Abstract	The pharmacological properties of voltage-dependent calcium channel (VDCC) subtypes appear mainly to be determined by the α1 pore-forming subunit but, whether P-and Q-type VDCCs are encoded by the same α1 gene presently is unresolved. To investigate this, we used IgG antibodies to presynaptic VDCCs at motor nerve terminals that underlie muscle weakness in the autoimmune Lambert–Eaton myasthenic syndrome (LEMS). We first studied their action on changes in intracellular free Ca2+ concentration [Ca2+]i in human embryonic kidney (HEK293) cell lines expressing different combinations of human recombinant VDCC subunits. Incubation for 18 h with LEMS IgG (2 mg/ml) caused a significant dose-dependent reduction in the K+-stimulated [Ca2+]i increase in the α1A cell line but not in the α1B, α1C, α1D, and α1E cell lines, establishing the α1A subunit as the target for these autoantibodies. Exploiting this specificity, we incubated cultured rat cerebellar neurones with LEMS IgG and observed a reduction in P-type current in Purkinje cells and both P- and Q-type currents in granule cells. These data are consistent with the hypothesis that the α1A gene encodes for the pore-forming subunit of both P-type and Q-type VDCCs.
Starting Page	8328
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	14
Volume Number	95
Language	English
Publisher	The National Academy of Sciences
Publisher Date	1998-07-07
Access Restriction	Open
Rights Holder	The National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Human autoantibodies specific for the $α_{1A}$ calcium channel subunit reduce both P-type and Q-type calcium currents in cerebellar neurons

Ablation of P/Q-type Ca2+ channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the α1A-subunit

Pentobarbital inhibition of human recombinant α1A P/Q-type voltage-gated calcium channels involves slow, open channel block

Interaction of Cysteine String Proteins with the α1A Subunit of the P/Q-type Calcium Channel

Genetic Background Influences P/Q-type Ca2+ Channel α1A Subunit mRNA Expression in Olfactory Bulb and Reproductive Ability of N-type Ca2+ Channel α1B Subunit-Deficient Mice

Differential modulation of N-type α1B and P/Q-type α1A calcium channels by different G protein β subunit isoforms

Antisense oligonucleotides against α1E reduce R-type calcium currents in cerebellar granule cells

Specific T-type calcium channel isoforms are associated with distinct burst phenotypes in deep cerebellar nuclear neurons

Deletion of the Ca2+ Channel Subunit α2δ3 Differentially Affects Cav2.1 and Cav2.2 Currents in Cultured Spiral Ganglion Neurons Before and After the Onset of Hearing

Human autoantibodies specific for the α1A calcium channel subunit reduce both P-type and Q-type calcium currents in cerebellar neurons

Similar Documents

Human autoantibodies specific for the $α_{1A}$ calcium channel subunit reduce both P-type and Q-type calcium currents in cerebellar neurons

Ablation of P/Q-type Ca2+ channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the α1A-subunit

Pentobarbital inhibition of human recombinant α1A P/Q-type voltage-gated calcium channels involves slow, open channel block

Interaction of Cysteine String Proteins with the α1A Subunit of the P/Q-type Calcium Channel

Genetic Background Influences P/Q-type Ca2+ Channel α1A Subunit mRNA Expression in Olfactory Bulb and Reproductive Ability of N-type Ca2+ Channel α1B Subunit-Deficient Mice

Differential modulation of N-type α1B and P/Q-type α1A calcium channels by different G protein β subunit isoforms

Antisense oligonucleotides against α1E reduce R-type calcium currents in cerebellar granule cells

Specific T-type calcium channel isoforms are associated with distinct burst phenotypes in deep cerebellar nuclear neurons

Deletion of the Ca2+ Channel Subunit α2δ3 Differentially Affects Cav2.1 and Cav2.2 Currents in Cultured Spiral Ganglion Neurons Before and After the Onset of Hearing

Human autoantibodies specific for the α1A calcium channel subunit reduce both P-type and Q-type calcium currents in cerebellar neurons