Upregulation of the GABA transporter GAT-1 in the gracile nucleus in the spared nerve injury model of neuropathic pain.

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Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_B39D6B6F62E3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Upregulation of the GABA transporter GAT-1 in the gracile nucleus in the spared nerve injury model of neuropathic pain.
Périodique
Neuroscience Letters
Auteur⸱e⸱s
Gosselin R.D., Bebber D., Decosterd I.
ISSN
1872-7972[electronic], 0304-3940[linking]
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
480
Numéro
2
Pages
132-137
Langue
anglais
Résumé
Neuropathic pain is a major health issue and is frequently accompanied by allodynia (painful sensations in response to normally non-painful stimulations), and unpleasant paresthesia/dysesthesia, pointing to alterations in sensory pathways normally dedicated to the processing of non-nociceptive information. Interestingly, mounting evidence indicate that central glial cells are key players in allodynia, partly due to changes in the astrocytic capacity to scavenge extracellular glutamate and gamma-aminobutyric acid (GABA), through changes in their respective transporters (EAAT and GAT). In the present study, we investigated the glial changes occurring in the dorsal column nuclei, the major target of normally innocuous sensory information, in the rat spared nerve injury (SNI) model of neuropathic pain. We report that together with a robust microglial and astrocytic reaction in the ipsilateral gracile nucleus, the GABA transporter GAT-1 is upregulated with no change in GAT-3 or glutamate transporters. Furthermore, [(3)H] GABA reuptake on crude synaptosome preparation shows that transporter activity is functionally increased ipsilaterally in SNI rats. This GAT-1 upregulation appears evenly distributed in the gracile nucleus and colocalizes with astrocytic activation. Neither glial activation nor GAT-1 modulation was detected in the cuneate nucleus. Together, the present results point to GABA transport in the gracile nucleus as a putative therapeutic target against abnormal sensory perceptions related to neuropathic pain.
Pubmed
Web of science
Open Access
Oui
Création de la notice
21/07/2010 13:29
Dernière modification de la notice
20/08/2019 15:22
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