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Postnatal expression of the homeobox gene Prrxl1 ( Drg11 ) is increased in inflammatory but not neuropathic pain
Author(s) -
Monteirol Clara,
Rebelol Sandra,
Galhardol Vasco,
Reguengal Carlos,
Limal Deolinda
Publication year - 2011
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 - 10.1016/j.ejpain.2010.10.007
Subject(s) - neuropathic pain , nociception , dorsal root ganglion , medicine , homeobox , sni , chronic pain , endocrinology , neuroscience , anesthesia , gene expression , dorsum , anatomy , biology , gene , receptor , biochemistry , hydrolysis , acid hydrolysis
The paired‐type homeodomain transcription factor Prrxl1 (also known as Drg11) is a key regulator of the differentiation and survival of dorsal root ganglia (DRG) and spinal nociceptive neurons in pre‐ and perinatal stages. Prrxl1 −/− mice exhibit abnormalities in DRG‐spinal projections, defects in superficial dorsal horn structure and neurochemistry, and reduced nociceptive behaviour in several pain tests. Although a low expression of Prrxl1 persists in dorsal root ganglia beyond embryonic development, no data exist on its role in adult life. In this paper we evaluate whether DRG expression of Prrxl1 is affected both in inflammatory and neuropathic models of pain in adult mice. Ipsilateral versus contralateral relative expression of Prrxl1 in the DRG was compared in control and pain animals. The expression of Prrxl1 mRNA in mice with zymosan‐induced peripheral inflammation presented a 3.06±0.71‐fold‐increase in ipsilateral ganglia, which was significantly different from the value observed in control animals. In contrast, a slight, non‐statistically significant decrease was detected in the SNI model of neuropathy. Interestingly, the expression of the mRNA splice variant Prrxl1b was unchanged in both pain conditions. Immunohistochemical studies showed an increase in the number of Prrxl1‐positive neurons in the inflammatory pain model, which belonged both in the peptidergic and non‐peptidergic categories. Our present results point to a role for Prrxl1 in sensitization of nociceptive neurons upon inflammatory pain.