Medical Journals

Expression of L-type Calcium Channel Alpha(1)-1.2 and Alpha(1)-1.3 Subunits on Rat Sacral Motoneurons Following Chronic Spinal Cord Injury.

Authors:
  • Anelli R
  • Sanelli L
  • Bennett D J
  • Heckman C J

From: Department of Physiology, Northwestern University Feinberg School of Medicine, Morton 5-666, 303 East Chicago Avenue (M211), Chicago, IL 60611, USA. ran806@northwestern.edu

Neuroscience

  • Publish Date: Mar 2007
  • ISSN: 0306-4522
  • Volume: 145
  • Issue: 2
  • Pages: 751-63
  • Medium: Print
  • Language: English
  • Citation (JAMA): Anelli R, Sanelli L, Bennett D J, et al. Expression of L-type Calcium Channel Alpha(1)-1.2 and Alpha(1)-1.3 Subunits on Rat Sacral Motoneurons Following Chronic Spinal Cord Injury.. Neuroscience Mar 2007;145:751-63

Abstract

In the presence of the monoamines serotonin and norepinephrine, motoneurons readily generate large persistent inward currents (PICs). The resulting plateau potentials amplify and sustain motor output. Monoaminergic input to the cord originates in the brainstem and the sharp reduction in monoamine levels that occurs following acute spinal cord injury greatly decreases motoneuron excitability. However, recent studies in the adult sacral cord of the rat have shown that motoneurons reacquire the ability to generate PICs and plateau potentials within 1-2 months following spinal transection. Ca(v)1.3 L-type calcium channels are involved in generating PICs in both healthy and injured animals. Additionally, expression of Ca(v)1.2 and Ca(v)1.3 L-type calcium channels is altered in several pathological conditions. Therefore, in this paper we analyzed the expression of L-type calcium channel alpha(1) subunits within the motoneuron pool following a complete transection of the spinal cord at the level of the sacral vertebra (S)2 segment. The analysis was done both caudally (S4 segment) and rostrally [thoracic vertebra (T)6 segment] from the injury site. The S4 segment was significantly reduced in diameter when compared with control animals, and this reduction was more evident in the white matter. Ca(v)1.2 alpha(1) subunit expression significantly increased (26%) in the motoneuron pool located caudally but not rostrally from the injury site. In contrast, the expression of Ca(v)1.3 alpha(1) subunit remained unchanged in both S4 and T6 segments. The differential expression of the two alpha(1) subunits in spinal injury suggests that Ca(v)1.2 and Ca(v)1.3 channels have different functions in neuronal adaptation following spinal cord injury.

Mesh Headings (Keywords): Animals, Biogenic Monoamines, Calcium Channels, Calcium Channels, L-Type, Chronic Disease, Efferent Pathways, Female, Membrane Potentials, Motor Neurons, Protein Subunits, Rats, Sacrum, Spinal Cord Injuries, Up-Regulation


Check for Full Text / PubMed Unique Identifier (PMID): 17291691


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.

The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


Advertisements

About | Privacy Policy | Business Solutions | Advertise | Contact | Add Healia to your site

©2012. Healia / Meredith Corporation  

Use of this site constitutes acceptance of our Terms of Service and Privacy Policy. All content on this Web site, including medical opinion and any other health-related information, is for informational purposes only and should not be used for a specific diagnosis or individual treatment plan for any situation. Use of this site and the information contained herein does not create a doctor-patient relationship. Always seek the direct advice of your doctor in connection with any questions or issues you may have regarding your own health or the health of others.