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Smad‐interacting protein 1 affects acute and tonic, but not chronic pain
Author(s) -
Pradier B.,
Jeub M.,
Markert A.,
Mauer D.,
Tolksdorf K.,
Van de Putte T.,
Seuntjens E.,
GailusDurner V.,
Fuchs H.,
Hrabě de Angelis M.,
Huylebroeck D.,
Beck H.,
Zimmer A.,
Rácz I.
Publication year - 2014
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2013.00366.x
Subject(s) - nociception , sciatic nerve , neuropathic pain , medicine , nociceptor , anesthesia , neuroscience , biology , receptor
Background Smad‐interacting protein 1 (also named Z eb2 and Z fhx1b ) is a transcription factor that plays an important role in neuronal development and, when mutated, causes M owat– W ilson syndrome ( MWS ). A corresponding mouse model carrying a heterozygous Z eb2 deletion was comprehensively analysed in the G erman M ouse Clinic. The most prominent phenotype was the reduced pain sensitivity. In this study, we investigated the role of Z eb2 in inflammatory and neuropathic pain. Methods For this, we tested mutant Z eb2 animals in different models of inflammatory pain like abdominal constriction, formalin and carrageenan test. Furthermore, we studied the pain reactivity of the mice after peripheral nerve ligation. To examine the nociceptive transmission of primary sensory dorsal root ganglia ( DRG ) neurons, we determined the neuronal activity in the spinal dorsal horn after the formalin test using staining of c‐ F os. Next, we characterized the neuronal cell population in the DRGs and in the sciatic nerve to study the effect of the Z eb2 mutation on peripheral nerve morphology. Results The present data show that Z eb2 is involved in the development of primary sensory DRG neurons, especially of C ‐ and A δ fibres. These alterations contribute to a hypoalgesic phenotype in inflammatory but not in neuropathic pain in these Z eb2 +/ − mice. Conclusion Our data suggest that the under‐reaction to pain observed in MWS patients results from a reduced responsivity to nociceptive stimulation rather than an inability to communicate discomfort.