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1 diovascular responses during an experimental noxious stimulus.
2        Off food, animals reverse away from a noxious stimulus.
3 ance learning in the absence of a peripheral noxious stimulus.
4  conditioning blocked learning elicited by a noxious stimulus.
5 ous stimulus on the reaction to a subsequent noxious stimulus.
6 oxious stimulus that closely follows another noxious stimulus.
7 cal threat to an individual is exposure to a noxious stimulus.
8  spinal cord and in the brainstem to a tonic noxious stimulus.
9 the response measure, test time, and type of noxious stimulus.
10 er reported the interaction between task and noxious stimulus.
11 ividual learns to successfully avoid a truly noxious stimulus.
12 oral adaptations and the unpleasantness of a noxious stimulus.
13 rsion to formalin injection, an inflammatory noxious stimulus.
14 eral to pain stimulation within 200 ms after noxious stimulus; (2) pre-stimulus alpha activity was si
15 ee hind limb withdrawal reflexes of an acute noxious stimulus (20 % mustard oil) applied to a number
16 atory, we identified and selectively labeled noxious-stimulus-activated PBL neurons and performed com
17 ify neurons according to their response to a noxious stimulus and map their location based on stainin
18 nctional ASICs, are insensitive to acid as a noxious stimulus and show diminished avoidance of acidic
19 n can be unmasked by the administration of a noxious stimulus and that it is manifested as increased
20 he cortical activity immediately preceding a noxious stimulus and the capacity of such a stimulus to
21 ve examined the variables of gender, type of noxious stimulus, and the origin of nociceptive input as
22 ed to the onset of allodynia, in which a non-noxious stimulus becomes painful.
23  reflects the susceptibility to a subsequent noxious stimulus being perceived as painful.
24  however, possible diverse responses to this noxious stimulus between brain areas were not reported i
25 utes an anatomical substrate through which a noxious stimulus can activate 5HT neurons of the NRM and
26 log of a form of arousal induced by a mildly noxious stimulus can promote two antagonistic responses,
27          To determine if administration of a noxious stimulus can unmask a sensitization of dorsal ho
28  cingulate cortex (ACC) corresponding to the noxious stimulus condition.
29 t reprogram mouse and human fibroblasts into noxious stimulus-detecting (nociceptor) neurons.
30                               Transcripts of noxious stimulus-detecting TrpA1 channels are alternativ
31 ns to prevent central sensitization when the noxious stimulus does not produce inflammation and it is
32                               Interestingly, noxious stimulus evoked spinal neuronal firing was decre
33                        Here, we observe that noxious-stimulus evoked brain activity in healthy neonat
34  investigate inter-individual variability in noxious-stimulus evoked brain activity.
35 tify negative associations between predicted noxious-stimulus evoked responses and white matter mean
36 625, 0.125, and 0.25 mg/kg, i.v.) suppressed noxious stimulus-evoked activity of VPL neurons in a dos
37        Before morphine, the magnitude of the noxious stimulus-evoked burst in ON cells correlated wit
38                                              Noxious stimulus-evoked firing was affected more than sp
39  we found that morphine had little effect on noxious stimulus-evoked internalization of the NK-1 rece
40  nerve injury and inflammation and prevented noxious stimulus-evoked neuronal activation in spinal co
41 udied how the nervous system selects between noxious stimulus-evoked withdrawals and micturition, mov
42 between a neutral stimulus (tone [CS]) and a noxious stimulus (foot shock [US]).
43 , spinal, and cortical responses to a single noxious stimulus; however, it is not known whether the d
44                       When re-exposed to the noxious stimulus in a familiar environment, both male an
45 ic sensory dysfunction following a transient noxious stimulus in the neonatal period and a potentiall
46 ect of chronic administration of morphine on noxious stimulus-induced antinociception (NSIA) produced
47       GBR-12935 also produced a reduction in noxious stimulus-induced c-fos expression in nociceptive
48 ciceptive neurons was obtained by monitoring noxious stimulus-induced c-fos expression in rats having
49 induced by activation of an opioid-mediated, noxious stimulus-induced endogenous pain control circuit
50               Morphine significantly reduced noxious stimulus-induced Fos expression in lamina I, but
51 viously observed sites of ADX enhancement of noxious stimulus-induced Fos-like immunoreactivity.
52 endent (BOLD) signal to small differences in noxious stimulus intensities within individuals.
53 f the magnitude and duration of decreases in noxious stimulus intensity.
54          Additionally, we show that, after a noxious stimulus (intradermal capsaicin injection), thes
55 ere examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute la
56 ggests that movement of the limb away from a noxious stimulus is a sensitive indication of nociceptiv
57 ancement of an unhabituated response after a noxious stimulus is applied outside of the reflex recept
58 ty.SIGNIFICANCE STATEMENT The intensity of a noxious stimulus is encoded by the frequency of action p
59 ned stimulus that was previously paired to a noxious stimulus leads to the gradual disappearance of c
60 ively, such neurons may signal itch, whereas noxious stimulus levels recruit these and a larger popul
61 n of ipsilateral brain targets and defective noxious stimulus localization or topognosis, we generate
62 erareal communication immediately before the noxious stimulus may determine the responsiveness to inc
63                To fulfill these functions, a noxious stimulus might induce a percept which, in turn,
64 sts that the brain can distinguish different noxious stimulus modalities from the earliest stages of
65 ors are polymodal (i.e., respond to multiple noxious stimulus modalities, such as mechanical and ther
66 g, rostral CeA Calcrl+ neurons stably encode noxious stimulus occurrence, while caudal CeA Calcrl+ ne
67 movement is a defensive strike targeted to a noxious stimulus on the abdomen.
68  predictive of the modulatory effects of one noxious stimulus on the reaction to a subsequent noxious
69 hieved optogenetically, without any external noxious stimulus or injury.
70 active change of the retina in response to a noxious stimulus or to RGC death.
71 nockout larvae, whereas responses to another noxious stimulus or touch were not affected.
72 nonassociative learning in which a strong or noxious stimulus persistently enhances the response prod
73 g primary afferents and their responses to a noxious stimulus (subcutaneous formalin injection).
74  prolonged (up to 48 h) stress response to a noxious stimulus such as UVB.
75 a Drosophila melanogaster larva encounters a noxious stimulus, such as the focal pressure a parasitic
76                          Prior exposure to a noxious stimulus (tailshock) has selective effects on th
77 on and off cells in enhancing reactions to a noxious stimulus that closely follows another noxious st
78 re we show that the probability for a phasic noxious stimulus to entail an arousal is modulated by th
79 open question is whether the property of the noxious stimulus underlying the genetic correlation is h
80                        Five minutes later, a noxious stimulus was delivered to the paw.
81  reported significantly higher pain when the noxious stimulus was preceded by the high-intensity visu
82 inates from visceral organs in response to a noxious stimulus which, if prolonged, may lead to chroni
83 lects the sensorimotor transformation of the noxious stimulus, with some neurons encoding sensory inf