Reversal of chronic stress-induced pain by transcranial direct current stimulation (tDCS) in an animal model.
Transcranial direct current stimulation (tDCS) has been suggested as a therapeutic tool for pain syndromes. Although initial results in human subjects are encouraging, it still remains unclear whether the effects of tDCS can reverse maladaptive plasticity associated with chronic pain. To investigate this question, we tested whether tDCS can reverse the specific behavioral effects of chronic stress in the pain system, and also those indexed by corticosterone and interleukin-1β levels in serum and TNFα levels in the hippocampus, in a well-controlled rat model of chronic restraint stress (CRS). Forty-one adult male Wistar rats were divided into two groups control and stress. The stress group was exposed to CRS for 11 weeks for the establishment of hyperalgesia and mechanical allodynia as shown by the hot plate and von Frey tests, respectively. Rats were then divided into four groups control, stress, stress+sham tDCS and stress+tDCS. Anodal or sham tDCS was applied for 20min/day over 8 days and the tests were repeated. Then, the animals were killed, blood collected and hippocampus removed for ELISA testing. This model of CRS proved effective to induce chronic pain, as the animals exhibited hyperalgesia and mechanical allodynia. The hot plate test showed an analgesic effect, and the von Frey test, an anti-allodynic effect after the last tDCS session, and there was a significant decrease in hippocampal TNFα levels. These results support the notion that tDCS reverses the detrimental effects of chronic stress on the pain system and decreases TNFα levels in the hippocampus.
Pain Pharmacology and Neuromodulation, Animals Models Laboratory, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS 90050-170, Brazil. lauren_adachi@hotmail.com
Lauren Naomi
LN
Spezia Adachi
Wolnei
W
Caumo
Gabriela
G
Laste
Liciane
L
Fernandes Medeiros
Joanna
J
Ripoll Rozisky
Andressa
A
de Souza
Felipe
F
Fregni
Iraci L S
IL
Torres
D000818:Animals; D059350:Chronic Pain / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D003345:Corticosterone / Q000097:blood; D004195:Disease Models, Animal; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D006930:Hyperalgesia / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D053583:Interleukin-1beta / Q000097:blood; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology; D059225:Nociception / Q000502:physiology; D010147:Pain Measurement / Q000379:methods; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical / Q000009:adverse effects; D013315:Stress, Psychological / Q000150:complications* / Q000503:physiopathology; D050781:Transcranial Magnetic Stimulation / Q000379:methods*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D003345:Corticosterone