Galanin over-expression decreases the development of neuropathic pain-like behaviors in mice after partial sciatic nerve injury

Karin Hygge-Blakeman, Pablo Brumovsky, Jing Xia Hao, Xiao Jun Xu, Tomas Hökfelt, Jacqueline Crawley, Zsuzsanna Wiesenfeld-Hallin

Research output: Contribution to journalArticle

34 Scopus citations


The neuropeptide galanin may have a role in modulation of nociception, particularly after peripheral nerve injury. Here we assessed the development of neuropathic pain-like behaviors in mice overexpressing galanin under the dopamine β-hydroxylase promoter. Unoperated galanin over-expressing mice exhibited a moderately reduced sensitivity to noxious heat. Both galanin over-expressing mice and wild-type controls developed mechanical and heat hypersensitivity after photochemically induced partial sciatic nerve ischemic injury. The magnitude and persistence of such pain-like behaviors were significantly less, and recovery was faster in galanin over-expressing mice compared to wild types. However, the recovery from toe-spread deficits did not differ between galanin over-expressing and wild-type mice after a crush injury to the sciatic nerve. Thus, early recovery in pain-like response is unlikely to result from accelerated regeneration in the galanin over-expressing mice. Immunohistochemical analysis showed that galanin is over-expressed both in small and large dorsal root ganglion cells in the transgene mouse, whereas large galanin-positive neurons were never seen in wild-type mice. The present results in general support an inhibitory role of galanin in nociception and indicate that increased availability of galanin in spinal dorsal horn at the time or shortly after nerve injury may reduce the development of pain-like behaviors in mice.

Original languageEnglish (US)
Pages (from-to)152-158
Number of pages7
JournalBrain Research
Issue number1-2
StatePublished - Oct 29 2004
Externally publishedYes



  • Galanin over-expression
  • Neuropathy
  • Nociception
  • Spinal cord

ASJC Scopus subject areas

  • Neuroscience(all)

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