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1 ning, fear behaviors, neurodegeneration, and pain sensation.
2 pivotal for TRPV1 activation and subsequent pain sensation.
3 performance of PANs with significantly less pain sensation.
4 d subsequent neuronal activation, leading to pain sensation.
5 TRPA1 and TRPV1 are ion channels crucial for pain sensation.
6 ical variables, including blood pressure and pain sensation.
7 t mechanical stimuli that generate touch and pain sensation.
8 r paddle of NaV1.7, the subtype critical for pain sensation.
9 he complex molecular processes that underlie pain sensation.
10 crobiota is required for the normal visceral pain sensation.
11 therapy in CP to attenuate both fibrosis and pain sensation.
12 V1) channels, membrane receptors involved in pain sensation.
13 neurodegeneration after ischemic stroke, and pain sensation.
14 pathetic neurons underlies distinct types of pain sensation.
15 for probing molecular mechanisms underlying pain sensation.
16 proton-gated channels that are important for pain sensation.
17 contrast retain normal touch and mechanical pain sensation.
18 r loss of function as the basis for impaired pain sensation.
19 ctively participate in acute temperature and pain sensation.
20 ands such as capsaicin, leading to a burning pain sensation.
21 e role voltage-gated sodium channels play in pain sensation.
22 n the nociceptive system, leading to reduced pain sensation.
23 ved in processing the affective component of pain sensation.
24 nsory neurons, mediates inflammatory thermal pain sensation.
25 hat described in somatic pathways regulating pain sensation.
26 uli or to low pH to mediate normal touch and pain sensation.
27 ed in modulating moderate- to high-intensity pain sensation.
28 led to VR1 being considered as important for pain sensation.
29 n regulate spinal nociceptive processing and pain sensation.
30 iving increasing attention as a modulator of pain sensation.
31 hannels mediate temperature transduction and pain sensation.
32 olecules are important for modality specific pain sensations.
33 ations versus those with predominantly acute pain sensations.
34 oupings of scans associated with deqi versus pain sensations.
35 sential first step for eliciting thermal and pain sensations.
36 on channel that plays a key role in enhanced pain sensation after inflammation, but directly blocking
37 VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyp
38 chomotor behaviors, anxiety, depression, and pain sensation and in the rewarding effects of alcohol a
39 All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von
40 a nonselective cation channel that mediates pain sensations and is commonly activated by a wide vari
41 into contact with the body, evoking touch or pain sensations and possibly triggering an approach or e
42 sory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotyp
44 ss of VGLUT3 specifically impairs mechanical pain sensation, and in particular the mechanical hyperse
45 heat-sensitive ion channel also involved in pain sensation, and is the receptor for capsaicin, the a
48 confirms the involvement of this channel in pain sensation, as well as in hypersensitivity to noxiou
49 1.7 is believed to be a critical mediator of pain sensation based on clinical genetic studies and pha
50 ot appear to play a major role in mechanical pain sensation, because the stimulus-response function o
54 0 as a critical regulator of nociception and pain sensation by modulating TRP channels expression in
58 nately deqi sensation grouping and the acute pain sensation grouping (deqi>pain contrast), only negat
59 physiological processes, including touch and pain sensation, hearing, and blood pressure regulation.
60 rimental focal neuritis produces neuropathic pain sensations (heat- and mechano-hyperalgesia, and col
61 fic antagonist, TAK-242, attenuated visceral pain sensation in animals with functional TLR4 when admi
62 gated sodium channel, Nav1.7, is critical to pain sensation in mammals, pharmacological inhibitors of
63 ociceptive responses are used as measures of pain sensation in newborn humans, as they are in animals
64 the cardiovascular and immune systems and in pain sensation in peripheral systems through their inter
65 ciceptors showed a defect in nociception and pain sensation in response to thermal, mechanical and in
66 acetylation of genes that regulate visceral pain sensation in the peripheral nervous system of rats.
67 better match the psychophysics of mechanical pain sensations in humans than the discharge of the HPC
68 imulus intensity and alters the magnitude of pain sensations in the direction of the trend of increas
69 e mammalian capsaicin receptor implicated in pain sensation; in AWC olfactory neurons, ODR-3 may inte
70 cal studies show serial interactions between pain sensation intensity, pain unpleasantness, and secon
72 uli are applied to primate hairy skin, first pain sensation is mediated by type-II A-fibre nociceptor
73 sociated with physiological and pathological pain sensation, making presynaptic P2X receptors a possi
74 ains unresolved whether changes in one's own pain sensation may affect empathic responding to others'
79 trahydrocannabinol (delta-9-THC), may reduce pain sensation, studies of humans have produced inconsis
80 ain levels of anandamide and display reduced pain sensation that is reversed by the CB(1) antagonist
81 amygdala in the processing and modulation of pain sensation, the experience of which involves a consi
84 viously known as VR1, has been implicated in pain sensation under both physiological and pathological
85 efore, may give rise to acute post-traumatic pain sensation via a yet elusive molecular mechanism.
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