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1 inding C-nociceptors and limits pathological spontaneous pain.
2  reduces formalin-induced TRPA1 currents and spontaneous pain.
3 uggested that TREK2 knockdown might increase spontaneous pain.
4 ve to excite nociceptors acutely and produce spontaneous pain.
5 se characterized by mechanical allodynia and spontaneous pain.
6 doses (0.01-1 ng) prevented formalin-induced spontaneous pain.
7 mechanism via which bradykinin induces acute spontaneous pain.
8  these networks correlates with the level of spontaneous pain.
9 old allodynia, cold stress-induced pain, and spontaneous pain.
10                                              Spontaneous pain, a poorly understood aspect of human ne
11                   Therefore, both SA and SFL/spontaneous pain after nerve injury (mSNA) may result fr
12     Notably, blocking PD-L1 or PD-1 elicited spontaneous pain and allodynia in melanoma-bearing mice.
13     Moreover, i.t. BMSCs reduced CCI-induced spontaneous pain and axonal injury of dorsal root gangli
14 promoting and maintaining persistent ongoing spontaneous pain and evoked hyperalgesia pain in EAE.
15  correlating with the development of ongoing spontaneous pain and evoked hypersensitivity to mechanic
16 V2) of the trigeminal nerve in patients with spontaneous pain and evoked pain to brush (allodynia).
17     Intrathecal RvE1 injection also inhibits spontaneous pain and heat and mechanical hypersensitivit
18 n sensory neurons and provides evidence that spontaneous pain and hyperalgesia can have distinct unde
19               Inflammatory pain manifests as spontaneous pain and pain hypersensitivity.
20                     Conversely, the tonic or spontaneous pain and the anxiodepressive consequences of
21  the former correlating only to intensity of spontaneous pain and the latter correlating only to pain
22 n = 11), and contrast brain activity between spontaneous pain and thermal pain (CBP and healthy subje
23  allodynia and hyperalgesia, cold allodynia, spontaneous pain, and cold stress-induced pain.
24            Furthermore, greater intensity of spontaneous pain at the time of the FMRI scan correlated
25                                 There was no spontaneous pain, based on open field behavior.
26 1) Em and TREK2, (2) SF rate and Em, and (3) spontaneous pain behavior and C-nociceptor SF rate sugge
27                   TOW mice exhibited ongoing spontaneous pain behavior and increased sensitivity to e
28  finding, S1P-induced neuronal responses and spontaneous pain behavior in vivo were substantially red
29                                      Ongoing/spontaneous pain behavior is associated with ongoing/spo
30 showed a loss of enhanced pain responses and spontaneous pain behavior upon treatment with inflammato
31 jury to elicit faster onset of allodynia and spontaneous pain behavior.
32 nt heat source, and there was no evidence of spontaneous pain behavior.
33 nt, fibrosarcoma tumor-bearing mice produced spontaneous pain behaviors, suggesting that ET-1 activat
34     A3AR activation also relieved non-evoked spontaneous pain behaviours without promoting analgesic
35 in the mPFC were temporally synchronous with spontaneous pain changes in patients during a pain-ratin
36        Continuous ratings of fluctuations of spontaneous pain during functional magnetic resonance im
37 pathy characterized by temperature-dependent spontaneous pain, hyperalgesia/allodynia and signs of ne
38 N) to insula connectivity is associated with spontaneous pain in fibromyalgia patients.
39 gain of function mutations in NaV1.7 lead to spontaneous pain in humans whereas loss of function muta
40 clear whether PKC in other regions regulates spontaneous pain in PIPN.
41 etaII and PKCdelta, but not PKC, blocked the spontaneous pain induced by paclitaxel.
42     Tp1a proved to be analgesic by reversing spontaneous pain induced in mice by intraplantar injecti
43               Furthermore, capsaicin-induced spontaneous pain, inward currents in DRG neurons, and sy
44                                              Spontaneous pain levels were also analyzed for covarianc
45 ity to the DMN was associated with increased spontaneous pain levels.
46 increase in skin thickness and site-directed spontaneous pain-like (licking or wiping) and itch-like
47 on-specific silencing of PKCdelta attenuated spontaneous pain, mechanical allodynia, and heat hyperal
48                                      Neither spontaneous pain nor evoked pain was detected in the mic
49       These findings suggest that subjective spontaneous pain of CBP involves specific spatiotemporal
50                                         When spontaneous pain of CBP was contrasted to thermal stimul
51  Here, we identify brain regions involved in spontaneous pain of chronic back pain (CBP) in two separ
52 opathic pain, typified by the development of spontaneous pain or pain hypersensitivity following inju
53 ve pathway within the CNS, which may lead to spontaneous pain or pain hypersensitivity.
54 contrast, activation of LC(:PFC) exacerbated spontaneous pain, produced aversion and increased anxiet
55                  14b was able to inhibit the spontaneous pain reaction after rectal mustard oil appli
56                                              Spontaneous pain reflects direct activation of specific
57 , the animals treated with formalin showed a spontaneous pain response and mechanical allodynia that
58  animals treated with zymosan exhibited mild spontaneous pain responses during the first hour and mec
59 ly underlie the allodynia, hyperalgesia, and spontaneous pain seen in patients.
60 , but also for the first time to demonstrate spontaneous pain that is also experienced by patients.
61 traplantar injection of let-7b elicits rapid spontaneous pain via TLR7 and TRPA1.
62  using von Frey filaments, and the relief of spontaneous pain was determined by using place condition
63 tion, spontaneous foot lifting (a measure of spontaneous pain) was (1) greater in rats with naturally
64 ores, an absence of evoked pain, and ongoing spontaneous pain when compared with littermate wild-type

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