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The lesion of dorsolateral funiculus changes the antiallodynic effect of the intrathecal muscimol and baclofen in distinct phases of neuropathic pain induced by spinal nerve ligation in rats.
Brain Res Bull. 2016 06; 124:103-15.BR

Abstract

The abnormal firing of damaged primary afferents and the changes in the central nervous system (CNS) play important role in the initiation and maintenance phases of neuropathic pain. These phases of neuropathic pain involve changes in the GABAergic control of descending pathways that travel through the dorsolateral funiculus (DLF). The present study shows that unilateral DLF lesion increased the antiallodynic effect of muscimol (0.2μg/5μL) (a GABAA receptor agonist) in the initiation, but not maintenance phase of the mechanical allodynia induced by a spinal nerve ligation (SNL) of the ipsilateral hindpaw of rats. The unilateral DLF lesion increased the antiallodynic effect of baclofen (0.8μg/5μL) (a GABAB receptor agonist) in the initiation phase and reduced your effect in the maintenance phase of the mechanical allodynia induced by a spinal nerve ligation (SNL) of the ipsilateral paw of rats. The unilateral DLF lesion significantly reduced the proallodynic effect of an intrathecal injection of phaclofen (30μg/5μL) (a GABAB receptor antagonist), but not bicuculline (0.3μg/5μL) (a GABAA receptor antagonist). The effect of DLF lesion on the proallodynic effect of phaclofen was observed in the maintenance, but not in the initiation phase of the mechanical allodynia induced by SNL. We than conclude that the spinal GABAergic neurotransmission is negatively modulated by DLF using GABAA and GABAB receptors, in the initiation phase of mechanical allodynia induced by SNL. In addition, the integrity of DLF is necessary for the effectiveness of GABAergic transmission that occurs via spinal GABAB, but not GABAA receptors, in the maintenance phase of mechanical allodynia induced by SNL.

Authors+Show Affiliations

Oswaldo Cruz Foundation (FIOCRUZ), Porto Velho, Rondônia, Brazil.Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil. Electronic address: wadprado@fmrp.usp.br.

Pub Type(s)

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

Language

eng

PubMed ID

27063286

Citation

Dias, Quintino Moura, and Wiliam A. Prado. "The Lesion of Dorsolateral Funiculus Changes the Antiallodynic Effect of the Intrathecal Muscimol and Baclofen in Distinct Phases of Neuropathic Pain Induced By Spinal Nerve Ligation in Rats." Brain Research Bulletin, vol. 124, 2016, pp. 103-15.
Dias QM, Prado WA. The lesion of dorsolateral funiculus changes the antiallodynic effect of the intrathecal muscimol and baclofen in distinct phases of neuropathic pain induced by spinal nerve ligation in rats. Brain Res Bull. 2016;124:103-15.
Dias, Q. M., & Prado, W. A. (2016). The lesion of dorsolateral funiculus changes the antiallodynic effect of the intrathecal muscimol and baclofen in distinct phases of neuropathic pain induced by spinal nerve ligation in rats. Brain Research Bulletin, 124, 103-15. https://doi.org/10.1016/j.brainresbull.2016.04.001
Dias QM, Prado WA. The Lesion of Dorsolateral Funiculus Changes the Antiallodynic Effect of the Intrathecal Muscimol and Baclofen in Distinct Phases of Neuropathic Pain Induced By Spinal Nerve Ligation in Rats. Brain Res Bull. 2016;124:103-15. PubMed PMID: 27063286.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The lesion of dorsolateral funiculus changes the antiallodynic effect of the intrathecal muscimol and baclofen in distinct phases of neuropathic pain induced by spinal nerve ligation in rats. AU - Dias,Quintino Moura, AU - Prado,Wiliam A, Y1 - 2016/04/05/ PY - 2015/12/30/received PY - 2016/03/31/revised PY - 2016/04/04/accepted PY - 2016/4/12/entrez PY - 2016/4/12/pubmed PY - 2017/10/27/medline KW - Allodynia KW - Descending facilitatory mechanisms KW - Dorsolateral funiculus lesion KW - Neuropathic pain KW - Spinal GABAergic modulation SP - 103 EP - 15 JF - Brain research bulletin JO - Brain Res Bull VL - 124 N2 - The abnormal firing of damaged primary afferents and the changes in the central nervous system (CNS) play important role in the initiation and maintenance phases of neuropathic pain. These phases of neuropathic pain involve changes in the GABAergic control of descending pathways that travel through the dorsolateral funiculus (DLF). The present study shows that unilateral DLF lesion increased the antiallodynic effect of muscimol (0.2μg/5μL) (a GABAA receptor agonist) in the initiation, but not maintenance phase of the mechanical allodynia induced by a spinal nerve ligation (SNL) of the ipsilateral hindpaw of rats. The unilateral DLF lesion increased the antiallodynic effect of baclofen (0.8μg/5μL) (a GABAB receptor agonist) in the initiation phase and reduced your effect in the maintenance phase of the mechanical allodynia induced by a spinal nerve ligation (SNL) of the ipsilateral paw of rats. The unilateral DLF lesion significantly reduced the proallodynic effect of an intrathecal injection of phaclofen (30μg/5μL) (a GABAB receptor antagonist), but not bicuculline (0.3μg/5μL) (a GABAA receptor antagonist). The effect of DLF lesion on the proallodynic effect of phaclofen was observed in the maintenance, but not in the initiation phase of the mechanical allodynia induced by SNL. We than conclude that the spinal GABAergic neurotransmission is negatively modulated by DLF using GABAA and GABAB receptors, in the initiation phase of mechanical allodynia induced by SNL. In addition, the integrity of DLF is necessary for the effectiveness of GABAergic transmission that occurs via spinal GABAB, but not GABAA receptors, in the maintenance phase of mechanical allodynia induced by SNL. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/27063286/The_lesion_of_dorsolateral_funiculus_changes_the_antiallodynic_effect_of_the_intrathecal_muscimol_and_baclofen_in_distinct_phases_of_neuropathic_pain_induced_by_spinal_nerve_ligation_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(16)30075-2 DB - PRIME DP - Unbound Medicine ER -