Amylin- a peptide expressed by nociceptors- modulates chronic neuropathic pain

Authors
LS Almeida, JM Castro_Lopes, FL Neto, CS Potes

Lab
Universidade do Porto, Alameda Prof Hernâni Monteiro, Porto, Portugal

Journal
European Journal of Pain

Abstract
Continuous subcutaneous amylin administration aggravated cold allodynia in SNI_animals, possibly via amylin_receptors (AmyR) in supraspinal areas. Acute intrathecal administration of amylin attenuated mechanical hyperalgesia, whereas AC187 reduced mechanical allodynia, suggesting distinct roles of endogenous amylin and of pharmacological amylin doses when targeting spinal cord amylin_receptors. Chronic amylin administration promoted c_Fos activation only in the dorsal horn neurons of SHAM_animals, suggesting a distinctive role of amylin in the activation of the spinal neuronal circuitry under neuropathic and physiological conditions. ERK1/2 phosphorylation increased in the dorsal horn neurons of SNI_rats chronically treated with amylin. This ERK1/2 cascade activation may be related with amylin's effect on the aggravation of cold allodynia in SNI_rats. Amylin's nociceptive effects seem to depend on the treatment duration and route of administration by acting at different levels of the nervous system.

BIOSEB Instruments Used:
Cold Hot Plate Test (BIO-CHP)