Spinal Nerve Ligation Does Not Alter the Expression or Function of GABAB Receptors in Spinal Cord and Dorsal Root Ganglia of the Rat

Mitchell P Engle; Martin Gassman; Kenneth T Sykes; Bernhard Bettler; Donna L Hammond

doi:10.1016/j.neuroscience.2005.11.064

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Spinal Nerve Ligation Does Not Alter the Expression or Function of GABAB Receptors in Spinal Cord and Dorsal Root Ganglia of the Rat

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Spinal Nerve Ligation Does Not Alter the Expression or Function of GABAB Receptors in Spinal Cord and Dorsal Root Ganglia of the Rat

Mitchell P Engle, Martin Gassman, Kenneth T Sykes, Bernhard Bettler and Donna L Hammond

Neuroscience, Vol.138(4), pp.1277-1287

2006

DOI: 10.1016/j.neuroscience.2005.11.064

PMCID: PMC1471878

PMID: 16427742

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Abstract

Loss of γ-aminobutyric acid (GABA)-mediated inhibition in the spinal cord is thought to mediate allodynia and spontaneous pain after nerve injury. Despite extensive investigation of GABA itself, relatively little is known about how nerve injury alters the receptors at which GABA acts. This study examined levels of GABA B receptor protein in the spinal cord dorsal horn, and in the L4 and L5 dorsal root ganglia (DRG) one to 18 weeks L5 spinal nerve ligation. Mechanical allodynia was maximal by 1 week and persisted at blunted levels for at least 18 weeks after injury. Spontaneous pain behaviors were evident for 6 weeks. Western blotting of dorsal horn detected two isoforms of the GABA B(1) subunit and a single GABA B(2) subunit. High levels of GABA B(1a) and low levels of GABA B(1b) protein were present in the DRG. However, GABA B(2) protein was not detected in the DRG, consistent with the proposed existence of an atypical receptor comprised of GABA B(1) homodimers. The levels of GABA B(1a) , GABA B(1b) , and GABA B(2) protein in the ipsilateral dorsal horn were unchanged at any time after injury. Immunohistochemical staining also did not detect a change in GABA B(1) or GABA B(2) subunits in dorsal horn segments having a robust loss of isolectin B4 staining. The levels of GABA B(1a) protein were also unchanged in the L4 or L5 DRG at any time after spinal nerve ligation. Levels of GABA B(2) remained undetectable. Finally, baclofen-stimulated binding of GTPγS in dorsal horn did not differ between sham and ligated rats. Collectively, these results argue that a loss of GABA B receptor-mediated inhibition, particularly of central terminals of primary afferents, is unlikely to mediate the development or maintenance of allodynia or spontaneous pain behaviors after spinal nerve injury.

Allodynia

Pain

GABA: γ-aminobutyric acid

ANOVA: analysis of variance

L: lumbar

DRG: dorsal root ganglia

Neuropathic

Details

Title: Subtitle: Spinal Nerve Ligation Does Not Alter the Expression or Function of GABAB Receptors in Spinal Cord and Dorsal Root Ganglia of the Rat
Creators: Mitchell P Engle - Pharmacology The University of Iowa, Iowa City, IA 52242, USA
Martin Gassman - Pharmazentrum University of Basel, Basel CH-4056 Switzerland
Kenneth T Sykes - Pharmacology The University of Iowa, Iowa City, IA 52242, USA
Bernhard Bettler - Pharmazentrum University of Basel, Basel CH-4056 Switzerland
Donna L Hammond - Departments of Anesthesia and
Resource Type: Journal article
Publication Details: Neuroscience, Vol.138(4), pp.1277-1287
DOI: 10.1016/j.neuroscience.2005.11.064
PMID: 16427742
PMCID: PMC1471878
NLM abbreviation: Neuroscience
ISSN: 0306-4522
eISSN: 1873-7544
Language: English
Date published: 2006
Academic Unit: Iowa Neuroscience Institute; Nursing; Anesthesia; Neuroscience and Pharmacology
Record Identifier: 9984006486102771

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