Open AccessInhibition of the Cyclic Adenosine Monophosphate Pathway Attenuates Neuropathic Pain and Reduces Phosphorylation of Cyclic Adenosine Monophosphate Response Element-Binding in the Spinal Cord After Partial Sciatic Nerve Ligation in Rats
Author(s) -
Jiin-Tarng Liou,
Fu-Chao Liu,
Shi-Tai Hsin,
Ching-Yue Yang,
Ping-Wing Lui
Publication year - 2007
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/01.ane.0000287652.42309.5c
Subject(s) - creb , medicine , neuropathic pain , sciatic nerve , cyclic adenosine monophosphate , cyclic amp response element binding protein , endocrinology , protein kinase a , nociception , hyperalgesia , adenosine , allodynia , spinal cord , pharmacology , anesthesia , kinase , chemistry , receptor , transcription factor , biochemistry , psychiatry , gene
Recent reports have identified a role for cyclic adenosine monophosphate (cAMP) transduction in nociceptive processing. Spinal activation of the cAMP induced gene transcription through the activation of protein kinase A and cAMP response element-binding protein (CREB). Intrathecal injection of protein kinase A inhibitor reversed the mechanical hyperalgesia, whereas injection of CREB antisense attenuated tactile allodynia caused by partial sciatic nerve ligation (PSNL) in rats. In the present study, we aimed to assess the effects of spinal cAMP transduction on the nociceptive processing in a chronic neuropathic pain model.