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1 l learning and observation influence placebo hypoalgesia.
2 ffects in reinforcement learning and placebo hypoalgesia.
3 s to noxious stimuli and produces behavioral hypoalgesia.
4 ectations and experience can lead to placebo hypoalgesia.
5 e known to influence the strength of placebo hypoalgesia.
6 pioid-mediated, but not non-opioid-mediated, hypoalgesia.
7 luid) ingestion does not, by itself, produce hypoalgesia.
8 ve as a predictor of observationally-induced hypoalgesia.
9 a and attenuates mu-opioid-receptor-mediated hypoalgesia.
10 V1 phosphorylation, resulting in significant hypoalgesia.
11 llodynia with a simultaneous unilateral heat hypoalgesia.
12 specificity of the PAG's role in conditional hypoalgesia.
13 MDL28170 prevented capsaicin-induced thermal hypoalgesia.
14 diabetic nerves and NGF deprivation produces hypoalgesia.
15 lic link, Polg(D257A) mice exhibited thermal hypoalgesia.
16 Mice fed the HFHFD developed persistent heat hypoalgesia after 3 months, but a reduction in epidermal
17 d power) and sex, where males showed greater hypoalgesia after HI exercise with increasing fitness le
18                             However, placebo hypoalgesia, although mediated by associative learning,
19  at 8 mo of age exhibited loss of sensation, hypoalgesia (an increase in mechanical threshold), and d
20 CCR2 signalling resulted in more severe heat hypoalgesia and accelerated skin denervation, as did del
21 es delta- and kappa-opioid-receptor-mediated hypoalgesia and attenuates mu-opioid-receptor-mediated h
22 hypoxia marker (IGFBP-1) was associated with hypoalgesia and increased potency to opioid analgesia; o
23 mal MNCV and SNCV and alleviation of thermal hypoalgesia and intraepidermal nerve fiber loss but not
24 AMP resulted in a similar pattern, with heat hypoalgesia and mechanical allodynia occurring simultane
25  B2 activation contributed to the mechanical hypoalgesia and MNCV deficits in both diabetic genotypes
26 rspective reviews recent findings in placebo hypoalgesia and provides a conceptual account of how exp
27  allodynia and essentially corrected thermal hypoalgesia and sensory nerve conduction deficit without
28 crease in nerve conduction velocity, thermal hypoalgesia, and a reduction in intraepidermal nerve fib
29 crease in nerve conduction velocity, thermal hypoalgesia, and intraepidermal nerve fiber profiles.
30 epletion of sensory nerve terminals, thermal hypoalgesia, and nerve conduction slowing in diverse rod
31 te and the high-intensity tail flick assays (hypoalgesia), but there was no difference in the low-int
32  treatment expectancy effects (e.g., placebo hypoalgesia) can be explained by a Bayesian integration
33       These results suggest that conditional hypoalgesia (CHA) is subserved by mu but not kappa opioi
34 longer-lasting mechanical allodynia and heat hypoalgesia compared with injection of capsaicin into sk
35         Our results indicate that in placebo hypoalgesia contextual treatment information engages pre
36 tion velocity (MNCV), mechanical and thermal hypoalgesia, Erb B2 phosphorylation (pErb B2), and epide
37 uring milk letdown, cause varying degrees of hypoalgesia in 10-day-old rats.
38 otor activity, increased ring catalepsy, and hypoalgesia in hotplate and formalin tests.
39 s applied to the PAG block the expression of hypoalgesia in rats exposed to a Pavlovian signal for sh
40 onduction slowing and thermal and mechanical hypoalgesia in the absence of any reduction of hyperglyc
41 ent to decrease MNCV and induce a mechanical hypoalgesia in the absence of diabetes.
42 ion deficits, tactile allodynia, and thermal hypoalgesia in the absence of intraepidermal nerve fiber
43 ction velocity, prevented the development of hypoalgesia in the hind paw, and reduced superoxide and
44  hedgehog-IgG fusion protein, as was thermal hypoalgesia in the paw.
45 sible for the expression of several forms of hypoalgesia in the rat.
46 in a secondary mechanical allodynia and heat hypoalgesia lasting approximately 3 hr.
47 suggest that observationally-induced placebo hypoalgesia may be driven by anticipatory mechanisms tha
48 titers showed significant (P < 0.05) thermal hypoalgesia measured using the hot plate test (52 degree
49 e and pain, we investigated exercise-induced hypoalgesia (N = 39, 21 female).
50 est that selective visceral hyperalgesia and hypoalgesia of peripheral or central origin may be prese
51 rning has been central in explaining placebo hypoalgesia, placebo hypoalgesic effects show little ext
52          These results support the idea that hypoalgesia produced by aversive auditory stimuli uses a
53                  This form of stress-induced hypoalgesia represents a response to unconditional fear
54 ies, resulting in less extinction of placebo hypoalgesia.SIGNIFICANCE STATEMENT In aversive and appet
55 conduction velocity (SNCV) deficits, thermal hypoalgesia, tactile allodynia, and a remarkable ( appro
56 ented or alleviated diabetes-induced thermal hypoalgesia, tactile allodynia, motor and sensory nerve
57                       Hyperextension-induced hypoalgesia terminated immediately with stretch cessatio
58                                         Heat hypoalgesia that occurs after injection into deep tissue
59  a stimulus-bound, partially opioid-mediated hypoalgesia that previous research has shown to be poten
60 n modulation through treatment cues (placebo hypoalgesia, treatment context) with pain modulation thr
61  in electrodes C3, Cz, and C4 indicated that hypoalgesia was positively correlated with resting state
62          High doses of chemotherapy produced hypoalgesia whereas lower doses produced hyperalgesia.
63 activation after a bout of VCS that produced hypoalgesia, with and without co-administration of AF.