Hyperalgesia and increased neuropathic pain-like response in mice lacking galanin receptor 1 receptors

  title={Hyperalgesia and increased neuropathic pain-like response in mice lacking galanin receptor 1 receptors},
  author={Karin Hygge Blakeman and Jingxia Hao and X‐J. Xu and Arie S. Jacoby and J. Shine and Jacqueline N. Crawley and Tiina P. Iismaa and Zsuzsanna Wiesenfeld‐Hallin},

A Role of Supraspinal Galanin in Behavioural Hyperalgesia in the Rat

Exogenous GAL in the DMH had a pronociceptive effect that is mediated by GALR1 in healthy and arthritic animals and is associated with alterations of c-Fos expression in RVM and DRN that are serotonergic brainstem nuclei known to be involved in the regulation of pain.

Activation of the galanin receptor 2 in the periphery reverses nerve injury-induced allodynia

These findings are consistent with the hypothesis that the high level of endogenous galanin in injured primary afferents activates peripheral GalR2, which leads to an increase in C-fibre mechanical activation thresholds and a marked reduction in evoked and ongoing nociceptive responses.

Differential roles of galanin on mechanical and cooling responses at the primary afferent nociceptor

A novel galaninergic mechanism that inhibits cooling evoked neuronal activity and nociceptive behaviours via a putative GalR1 mode of action that would also be consistent with a TRP channel-dependent mechanism is identified.



Intrathecal galanin alleviates allodynia‐like behaviour in rats after partial peripheral nerve injury

  • J. HaoT. Shi Zsuzsanna Wiesenfeld‐Hallin
  • Biology
    The European journal of neuroscience
  • 1999
Galanin significantly alleviated the mechanical‐ and cold‐allodynia‐like behaviours in nerve injured rats, and was not associated with motor impairment or sedation, and GMAP relieved mechanical allodynia much less than galanin.

Galanin knockout mice reveal nociceptive deficits following peripheral nerve injury

Results show that galanin may play a role in nociceptive processing in the spinal cord, with interrelated inhibitory and excitatory effects, and demonstrate that a relationship exists between the degree of nerve injury‐induced Galanin expression and the level of behavioural hypersensitivity.

Receptor subtype-specific pronociceptive and analgesic actions of galanin in the spinal cord: Selective actions via GalR1 and GalR2 receptors

Data indicate that a low dose of galanin has a nociceptive role at the spinal cord level mediated by GalR2 receptors, whereas the antiallodynic effect of high-dose galan in on neuropathic pain is mediated by the GalR1 receptors.

Galanin in sensory neurons in the spinal cord.

It is concluded that GAL may have an important role in the control of nervous impulses that underlie pain states that can occur after peripheral nerve injury.

Galanin and spinal nociceptive mechanisms: recent advances and therapeutic implications

Peripheral nerve injury and inflammation, conditions associated with chronic pain, upregulate the synthesis of galanin in sensory neurons and spinal cord neurons, respectively, raising the possibility that modulation of the activity of the Galanin system may produce antinociception.

Development of a Mouse Model of Neuropathic Pain Following Photochemically Induced Ischemia in the Sciatic Nerve

It is concluded that an intravascular photochemical reaction leading to ischemia results in graded damage to the sciatic nerve in mice, and the nerve injury is associated with the development of abnormal pain-related behaviors.

Primary afferent-evoked release of immunoreactive galanin in the spinal cord of the neuropathic rat.

Release of ir-galanin at stimulus strengths sufficient to activate C fibres, in an area of the spinal cord thought to be concerned with nociceptive transmission, indicates a possible role for this peptide in the spinal modulation of pain after peripheral nerve injury.