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Phagocytic microglial phenotype induced by glibenclamide improves functional recovery but worsens hyperalgesia after spinal cord injury in adult rats
Author(s) -
RedondoCastro Elena,
Hernández Joaquim,
Mahy Nicole,
Navarro Xavier
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12382
Subject(s) - microglia , neuropathic pain , neuroprotection , medicine , spinal cord , hyperalgesia , spinal cord injury , neuroscience , pharmacology , chronic pain , anesthesia , glibenclamide , inflammation , nociception , immunology , biology , receptor , endocrinology , diabetes mellitus
Microglial cell plays a crucial role in the development and establishment of chronic neuropathic pain after spinal cord injuries. As neuropathic pain is refractory to many treatments and some drugs only present partial efficacy, it is essential to study new targets and mechanisms to ameliorate pain signs. For this reason we have used glibenclamide ( GB ), a blocker of K ATP channels that are over expressed in microglia under activation conditions. GB has already been used to trigger the early scavenger activity of microglia, so we administer it to promote a better removal of dead cells and myelin debris and support the microglia neuroprotective phenotype. Our results indicate that a single dose of GB (1 μg) injected after spinal cord injury is sufficient to promote long‐lasting functional improvements in locomotion and coordination. Nevertheless, the Randall–Selitto test measurements indicate that these improvements are accompanied by enhanced mechanical hyperalgesia. In vitro results indicate that GB may influence microglial phagocytosis and therefore this action may be at the basis of the results obtained in vivo .