Effects of nitric oxide on spontaneous pain reaction and neuronal apoptosis in the spinal cord of rats induced by formalin inflammatory pain.
- Author:
Sai-chun CHU
1
;
Yu-yan HU
;
Qing-jun LI
;
Hui-na LI
;
Wen-bin LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Formaldehyde; Male; NG-Nitroarginine Methyl Ester; pharmacology; Neurons; pathology; Nitric Oxide; metabolism; physiology; Nitric Oxide Synthase; antagonists & inhibitors; Nociceptors; physiology; Pain; chemically induced; physiopathology; Rats; Rats, Sprague-Dawley; Spinal Cord; pathology; physiopathology
- From: Chinese Journal of Applied Physiology 2011;27(3):372-375
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe whether formalin inflammatory pain can induce neuron apoptosis in rats spinal cord or not and the effects of nitric oxide on the spontaneous pain reaction and neuron apoptosis in the spinal cord of rats with formalin inflammatory pain.
METHODSFormalin-induced paw licking time was used to reflect the degree of spontaneous pain of rats, and the flow cytometry was used to detecte neuron apoptosis rate of spinal cord.
RESULTSCompared with control group, the apoptosis ratio of spinal neuron was increased in the rats with formalin inflammatory pain, and peaked at 3d after formalin injection. Pre-intrathecal injection of NOS inhibitor L-NAME inhibited the nociceptive behavioural response in double phases induced by fonnrmalin injection and cut down the neuron apoptosis ratio of spinal cord of rats with formalin inflammatory pain. Nociceptive behavioural response and incraesed neuron apoptosis in the spinal cord were induced by intrathecal injection of L-Arg in normal rats.
CONCLUSIONThe results indicated that formalin inflammatory pain could induce the apoptosis of spinal neurons. The neurons apoptosis was the most significant on the third day after formalin injection. The increased pruduction of NO in spinal cord could promote the transmit of nociceptive information and participate the induction of neuronal apoptosis during the formalin inflammatory pain.