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1 iators without affecting baseline mechanical nociceptive threshold.
2 ed the enhancement without altering baseline nociceptive threshold.
3 the spinal cord leads to a chronic decreased nociceptive threshold.
4 on velocity, resting membrane potential, and nociceptive threshold.
5 but had no significant effect on the normal nociceptive threshold.
6 and SNAP significantly increased mechanical nociceptive thresholds.
7 ough it had no effect on baseline mechanical nociceptive thresholds.
8 than 2 h) increase in mechanical and thermal nociceptive thresholds.
9 eurons and partial restoration of behavioral nociceptive thresholds.
10 -term removal of NA afferents did not affect nociceptive thresholds.
11 with opioid-mediated elevations in maternal nociceptive thresholds.
12 pioid receptor OPRM1, resulting in increased nociceptive thresholds.
13 restored thermal and ameliorated mechanical nociceptive thresholds.
15 high-dose morphine (HDM, 3 mg/kg) increased nociceptive threshold (analgesia) and induced priming, n
16 ptor primary cilium in control of mechanical nociceptive threshold and inflammatory and neuropathic p
17 Restoring central NA normalized both the nociceptive threshold and morphine efficacy, which is co
18 contributes only modestly to determining the nociceptive threshold and that its antinociceptive effec
19 Behavioural measures included mechanical nociceptive thresholds and distances run on exercise whe
20 t, the (beta)arr2-KO mice have greater basal nociceptive thresholds and markedly enhanced sensitivity
21 e gestation or its hormonal simulation, when nociceptive thresholds are elevated by approximately 70%
23 vioral data showed that minocycline restored nociceptive thresholds, at which time spinal microglial
24 of duloxetine, which alone had no effect on nociceptive threshold, both prevented and reversed mecha
25 und stress exhibited no change in mechanical nociceptive threshold, but showed a marked increase in h
26 idence for tonic modulation of basal thermal nociceptive thresholds by the spinal cannabinoid system.
27 ey and Brown Norway rats, SS rats have lower nociceptive thresholds due to increased inflammatory med
29 n, characterized by a decrease in mechanical nociceptive threshold (hyperalgesia), arises through act
30 ind paw induced a decrease in the mechanical nociceptive threshold (hypernociception), which was asso
31 mal morphine, at a dose that does not affect nociceptive threshold in controls, exacerbates mechanica
33 as associated with an increase in mechanical nociceptive threshold in vivo and decrease in nociceptor
35 y, engaging the A3AR mechanism did not alter nociceptive thresholds in non-neuropathy animals and the
36 igated the mechanisms responsible for higher nociceptive thresholds in red-haired mice resulting from
37 he absence of injury, thermal and mechanical nociceptive thresholds increased 2 weeks post-treatment
39 d to surgical tail resections and mechanical nociceptive thresholds (MNT) were measured in the acute
40 and heterozygous (+/-) counterparts; thermal nociceptive thresholds obtained in +/+ and +/- mice did
41 TX) or naltriben (NTB) substantially reduces nociceptive thresholds of gestation (day 20) and HSP (da
42 -Arg-Thr-Pen-Thr-NH2 (CTAP) has no effect on nociceptive thresholds of gestational day 20, as was pre
43 ain in the absence of a stimulus and reduced nociceptive thresholds so that normally innocuous stimul
44 If endogenous cannabinoids modulate basal nociceptive thresholds, then alterations in this system
45 s became hyperresponsive and when behavioral nociceptive thresholds to mechanical and thermal stimuli
47 e P-mediated chronic hyperalgesia (decreased nociceptive threshold) to thermal, but not mechanical, s
49 s became hyperresponsive and when behavioral nociceptive thresholds were decreased to both mechanical