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Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons
Author(s) -
Nadeau Joelle R.,
WilsonGerwing Tracy D.,
Verge Valerie M.K.
Publication year - 2014
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22640
Subject(s) - axotomy , glial fibrillary acidic protein , biology , neuroscience , nerve growth factor , peripheral nerve injury , microbiology and biotechnology , sensory neuron , gap junction , perineuronal net , sensory system , central nervous system , receptor , intracellular , immunology , regeneration (biology) , biochemistry , immunohistochemistry
Satellite glial cells (SGCs) surrounding primary sensory neurons are similar to astrocytes of the central nervous system in that they buffer the extracellular environment via potassium and calcium channels and express the intermediate filament glial fibrillary acidic protein (GFAP). Peripheral nerve injury induces a reactive state in SGCs that includes SGC proliferation, increased SGC/SGC coupling via gap junctions, decreased inward rectifying potassium channel 4.1 (K ir 4.1) expression and increased expression of GFAP and the common neurotrophin receptor, p75NTR. In contrast, neuronal p75NTR expression, normally detected in ∼80% of adult rat sensory neurons, decreases in response to peripheral axotomy. Given the differential regulation of p75NTR expression in neurons versus SGCs with injury, we hypothesized that reduced signaling via neuronal p75NTR contributes to the induction of a reactive state in SGCs. We found that reducing neuronal p75NTR protein expression in uninjured sensory neurons by intrathecal subarachnoid infusion of p75NTR‐selective anti‐sense oligodeoxynucleotides for one week was sufficient to induce a “reactive‐like” state in the perineuronal SGCs akin to that normally observed following peripheral nerve injury. This reactive state included significantly increased SGC p75NTR, GFAP and gap junction protein connexin‐43 protein expression, increased numbers of SGCs surrounding individual sensory neurons and decreased SGC K ir 4.1 channel expression. Collectively, this supports the tenet that reductions in target‐derived trophic support leading to, or as a consequence of, reduced neuronal p75NTR expression plays a critical role in switching the SGC to a reactive state. GLIA 2014;62:763–777