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Loss of spinal glycinergic neurons is not necessary for development of neuropathic pain in transgenic mice expressing enhanced green fluorescent protein in glycinergic neurons.
Neuroscience 2009; 159(3):1148-53N

Abstract

It has been proposed that alterations in spinal inhibitory neurotransmission are critically involved in the pathophysiology of neuropathic pain. The mechanisms by which a relief from inhibitory tone contributes to pathological pain are not fully understood. Hitherto it is still under debate whether there is a loss of inhibitory neurons in the spinal cord in neuropathic pain. The aim of the present study was to evaluate whether a specific loss of glycinergic neurons is necessary to develop hyperalgesia and allodynia in the chronic constriction injury (CCI) model of neuropathic pain. The experiments were performed in bacterial artificial chromosome (BAC) transgenic mice which specifically express enhanced green fluorescent protein under the control of the promotor of the glycine transporter 2 gene, which is a reliable marker for glycinergic neurons. Thus, possible technical inconsistencies due to immunoreactivity in fixed tissues could be ruled out. Twelve days after CCI, in neuropathic animals and in sham-operated and naive animals, lumbar and thoracic segments were analyzed using the physical disector method. Although all animals that had undergone CCI showed pathological nociceptive behavior, stereology revealed no significant difference in glycinergic neurons-neither between the different groups nor between the ipsilateral and contralateral side of the thoracic and lumbar spinal segments. Our findings suggest that a loss of glycinergic neurons is not necessary for the development of pathological nociceptive behavior in the chronic constriction injury model of neuropathic pain in mice. A different mechanism may account for the decrease in inhibitory transmission in neuropathic pain.

Authors+Show Affiliations

Department of Anesthesiology, University of Duesseldorf, Moorenstrasse 5, Postfach 101007 40225, Duesseldorf, Germany. Henning.Hermanns@uni-duesseldorf.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19356695

Citation

Hermanns, H, et al. "Loss of Spinal Glycinergic Neurons Is Not Necessary for Development of Neuropathic Pain in Transgenic Mice Expressing Enhanced Green Fluorescent Protein in Glycinergic Neurons." Neuroscience, vol. 159, no. 3, 2009, pp. 1148-53.
Hermanns H, Muth-Selbach U, Lipfert P, et al. Loss of spinal glycinergic neurons is not necessary for development of neuropathic pain in transgenic mice expressing enhanced green fluorescent protein in glycinergic neurons. Neuroscience. 2009;159(3):1148-53.
Hermanns, H., Muth-Selbach, U., Lipfert, P., Braun, S., Werdehausen, R., & Bauer, I. (2009). Loss of spinal glycinergic neurons is not necessary for development of neuropathic pain in transgenic mice expressing enhanced green fluorescent protein in glycinergic neurons. Neuroscience, 159(3), pp. 1148-53. doi:10.1016/j.neuroscience.2009.01.037.
Hermanns H, et al. Loss of Spinal Glycinergic Neurons Is Not Necessary for Development of Neuropathic Pain in Transgenic Mice Expressing Enhanced Green Fluorescent Protein in Glycinergic Neurons. Neuroscience. 2009 Mar 31;159(3):1148-53. PubMed PMID: 19356695.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Loss of spinal glycinergic neurons is not necessary for development of neuropathic pain in transgenic mice expressing enhanced green fluorescent protein in glycinergic neurons. AU - Hermanns,H, AU - Muth-Selbach,U, AU - Lipfert,P, AU - Braun,S, AU - Werdehausen,R, AU - Bauer,I, Y1 - 2009/01/27/ PY - 2008/12/19/received PY - 2009/01/14/revised PY - 2009/01/16/accepted PY - 2009/4/10/entrez PY - 2009/4/10/pubmed PY - 2009/9/22/medline SP - 1148 EP - 53 JF - Neuroscience JO - Neuroscience VL - 159 IS - 3 N2 - It has been proposed that alterations in spinal inhibitory neurotransmission are critically involved in the pathophysiology of neuropathic pain. The mechanisms by which a relief from inhibitory tone contributes to pathological pain are not fully understood. Hitherto it is still under debate whether there is a loss of inhibitory neurons in the spinal cord in neuropathic pain. The aim of the present study was to evaluate whether a specific loss of glycinergic neurons is necessary to develop hyperalgesia and allodynia in the chronic constriction injury (CCI) model of neuropathic pain. The experiments were performed in bacterial artificial chromosome (BAC) transgenic mice which specifically express enhanced green fluorescent protein under the control of the promotor of the glycine transporter 2 gene, which is a reliable marker for glycinergic neurons. Thus, possible technical inconsistencies due to immunoreactivity in fixed tissues could be ruled out. Twelve days after CCI, in neuropathic animals and in sham-operated and naive animals, lumbar and thoracic segments were analyzed using the physical disector method. Although all animals that had undergone CCI showed pathological nociceptive behavior, stereology revealed no significant difference in glycinergic neurons-neither between the different groups nor between the ipsilateral and contralateral side of the thoracic and lumbar spinal segments. Our findings suggest that a loss of glycinergic neurons is not necessary for the development of pathological nociceptive behavior in the chronic constriction injury model of neuropathic pain in mice. A different mechanism may account for the decrease in inhibitory transmission in neuropathic pain. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/19356695/Loss_of_spinal_glycinergic_neurons_is_not_necessary_for_development_of_neuropathic_pain_in_transgenic_mice_expressing_enhanced_green_fluorescent_protein_in_glycinergic_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(09)00054-2 DB - PRIME DP - Unbound Medicine ER -