Electroconvulsive stimulation (ECS) increases the expression of neuropeptide Y (NPY) in rat brains in a model of neuropathic pain: a quantitative real-time polymerase chain reaction (RT-PCR) study.
OBJECTIVE
Electroconvulsive shock therapy (ECT) has been widely used as an effective and established treatment for refractory depression and schizophrenia. Some reports have shown that ECT is also effective for treating refractory neuropathic pain.


METHODS
In a rat model of neuropathic pain produced by chronic constrictive injury (CCI) of the sciatic nerve, thermal hyperalgesia, and mechanical allodynia were observed from day 2 after surgery. An electroconvulsive shock (ECS) was administered to rodents once daily for 6 days on days 7-12 after CCI operation using a pulse generator. Thermal and mechanical stimulation tests were performed to assess pain thresholds. Real-time polymerase chain reaction was used to measure the gene expression levels for 5HT(1A)R, 5HT(2A)R, neuropeptide Y (NPY), and GABAA(alpha1)R in the brain.


RESULTS
After ECS, the latency to withdrawal from thermal stimulation was significantly increased; however, pain withdrawal thresholds in response to mechanical stimulation were not significantly changed. Expression ratios of NPY were significantly greater after ECS.


CONCLUSIONS
Symptoms of neuropathic pain improved and expression of NPY in the brain was increased in CCI model rats after ECS, suggesting that changes in the expression of NPY in the brain may be related to the mechanism of action of ECT in treating neuropathic pain.
Okabe
Tadashi
T
Department of Anesthesiology, Nippon Medical School, Tokyo, Japan. t-okabe@msj.biglobe.ne.jp
Sato
Chiyo
C
Matsumoto
Keisuke
K
Ozawa
Hitoshi
H
Sakamoto
Atsuhiro
A
D000818:Animals; D001921:Brain / Q000378:metabolism; D001923:Brain Chemistry / Q000235:genetics*; D004195:Disease Models, Animal; D004565:Electroconvulsive Therapy; D005786:Gene Expression Regulation / Q000502:physiology; D008297:Male; D009478:Neuropeptide Y / Q000235:genetics* / Q000378:metabolism; D010147:Pain Measurement; D017288:Pain Threshold / Q000502:physiology; D010148:Intractable Pain / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D010523:Peripheral Nervous System Diseases / Q000235:genetics* / Q000378:metabolism / Q000628:therapy*; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000235:genetics; D044282:Receptor, Serotonin, 5-HT1A / Q000235:genetics; D044402:Receptor, Serotonin, 5-HT2A / Q000235:genetics; D011963:Receptors, GABA-A / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020426:Sciatic Neuropathy / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D012701:Serotonin / Q000378:metabolism; D009435:Synaptic Transmission / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
C546242:Gabra1 protein, rat; D009478:Neuropeptide Y; D012333:RNA, Messenger; D044402:Receptor, Serotonin, 5-HT2A; D011963:Receptors, GABA-A; D044282:Receptor, Serotonin, 5-HT1A; D012701:Serotonin; D005680:gamma-Aminobutyric Acid