Document Detail


Depletion of calcium stores in injured sensory neurons: anatomic and functional correlates.
MedLine Citation:
PMID:  19602957     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Painful nerve injury leads to disrupted Ca signaling in primary sensory neurons, including decreased endoplasmic reticulum (ER) Ca storage. This study examines potential causes and functional consequences of Ca store limitation after injury.
METHODS: Neurons were dissociated from axotomized fifth lumbar (L5) and the adjacent L4 dorsal root ganglia after L5 spinal nerve ligation that produced hyperalgesia, and they were compared to neurons from control animals. Intracellular Ca levels were measured with Fura-2 microfluorometry, and ER was labeled with probes or antibodies. Ultrastructural morphology was analyzed by electron microscopy of nondissociated dorsal root ganglia, and intracellular electrophysiological recordings were obtained from intact ganglia.
RESULTS: Live neuron staining with BODIPY FL-X thapsigargin (Invitrogen, Carlsbad, CA) revealed a 40% decrease in sarco-endoplasmic reticulum Ca-ATPase binding in axotomized L5 neurons and a 34% decrease in L4 neurons. Immunocytochemical labeling for the ER Ca-binding protein calreticulin was unaffected by injury. Total length of ER profiles in electron micrographs was reduced by 53% in small axotomized L5 neurons, but it was increased in L4 neurons. Cisternal stacks of ER and aggregation of ribosomes occurred less frequently in axotomized neurons. Ca-induced Ca release, examined by microfluorometry with dantrolene, was eliminated in axotomized neurons. Pharmacologic blockade of Ca-induced Ca release with dantrolene produced hyperexcitability in control neurons, confirming its functional importance.
CONCLUSIONS: After axotomy, ER Ca stores are reduced by anatomic loss and possibly diminished sarco-endoplasmic reticulum Ca-ATPase. The resulting disruption of Ca-induced Ca release and protein synthesis may contribute to the generation of neuropathic pain.
Authors:
Geza Gemes; Marcel Rigaud; Paul D Weyker; Stephen E Abram; Dorothee Weihrauch; Mark Poroli; Vasiliki Zoga; Quinn H Hogan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anesthesiology     Volume:  111     ISSN:  1528-1175     ISO Abbreviation:  Anesthesiology     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-24     Completed Date:  2009-08-25     Revised Date:  2011-05-02    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  393-405     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Boron Compounds
Calcium / metabolism*,  pharmacology
Calcium Signaling / drug effects
Calcium-Binding Protein, Vitamin D-Dependent / metabolism
Cytoplasm / drug effects,  metabolism
Dantrolene / pharmacology
Electrophysiology
Endoplasmic Reticulum / drug effects,  metabolism,  ultrastructure
Fluorescent Dyes
Hyperalgesia / pathology
Immunohistochemistry
Ligation
Male
Microscopy, Electron
Pain Measurement / drug effects
Rats
Rats, Sprague-Dawley
Sensory Receptor Cells / drug effects,  metabolism*,  ultrastructure
Spinal Nerves / drug effects,  metabolism,  ultrastructure
Grant Support
ID/Acronym/Agency:
NS-42150/NS/NINDS NIH HHS; R01 NS042150-07S1/NS/NINDS NIH HHS; R01 NS042150-09/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/4,4-difluoro-4-bora-3a,4a-diaza-s-indacene; 0/Boron Compounds; 0/Calcium-Binding Protein, Vitamin D-Dependent; 0/Fluorescent Dyes; 0/calretinin; 7261-97-4/Dantrolene; 7440-70-2/Calcium
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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