ArticleNeuroscience2006
Spinal nerve ligation does not alter the expression or function of GABA(B) receptors in spinal cord and dorsal root ganglia of the rat.
Article in Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Dysfunction of inhibitory interneurons contributes to synaptic plasticity via GABABR-pNR2B signaling in a chronic migraine rat model.Frontiers in molecular neuroscience · 2023Article
- GABACurrent topics in behavioral neurosciences · 2022Review
- Presynaptic GABAeLife · 2020Article
- Impaired Autophagy of GABAergic Interneurons in Neuropathic Pain.Pain research & management · 2018Review
- Peripheral nerve injury induces loss of nociceptive neuron-specific Gαi-interacting protein in neuropathic pain rat.Molecular pain · 2016Article
- Presynaptic inhibition of optogenetically identified VGluT3+ sensory fibres by opioids and baclofen.Pain · 2015Article
- GABAB receptor phosphorylation regulates KCTD12-induced K⁺ current desensitization.Biochemical pharmacology · 2014Article
- Spatiotemporal changes in NSF expression of DRG neurons in a rat model of spinal nerve ligation.Journal of molecular neuroscience : MN · 2014Article
- Up-regulation of GABA(B) receptor signaling by constitutive assembly with the K+ channel tetramerization domain-containing protein 12 (KCTD12).The Journal of biological chemistry · 2013Article
- GABAergic inhibition of histaminergic neurons regulates active waking but not the sleep-wake switch or propofol-induced loss of consciousness.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Spinal nerve ligation decreases γ-aminobutyric acidB receptors on specific populations of immunohistochemically identified neurons in L5 dorsal root ganglion of the rat.The Journal of comparative neurology · 2012Article
- Potential for Cell-Transplant Therapy with Human Neuronal Precursors to Treat Neuropathic Pain in Models of PNS and CNS Injury: Comparison of hNT2.17 and hNT2.19 Cell Lines.Pain research and treatment · 2012Article
- Vector-mediated release of GABA attenuates pain-related behaviors and reduces Na(V)1.7 in DRG neurons.European journal of pain (London, England) · 2011Article
- Src family kinases mediate the inhibition of substance P release in the rat spinal cord by μ-opioid receptors and GABA(B) receptors, but not α2 adrenergic receptors.The European journal of neuroscience · 2010Article
- Article
- Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010Article
- A Gut Feeling about GABA: Focus on GABA(B) Receptors.Frontiers in pharmacology · 2010Article
- Changes in expression of sensory organ-specific microRNAs in rat dorsal root ganglia in association with mechanical hypersensitivity induced by spinal nerve ligation.Neuroscience · 2009Article
- Conditional gene deletion reveals functional redundancy of GABAB receptors in peripheral nociceptors in vivo.Molecular pain · 2009Article
- A functional link between T-type calcium channels and mu-opioid receptor expression in adult primary sensory neurons.Journal of neurochemistry · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Loss of 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 (lumbar designations) dorsal root ganglia one to 18 weeks after 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 dorsal root ganglia. However, GABA(B(2)) protein was not detected in the dorsal root ganglia, consistent with the proposed existence of an atypical receptor composed 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 dorsal root ganglia at any time after spinal nerve ligation. Levels of GABA(B(2)) remained undetectable. Finally, baclofen-stimulated binding of guanosine-5'-(gamma-O-thio)triphosphate 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.
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