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This mechanical hypersensitivity is not modified by oxaliplatin.
Mechanical hypersensitivity is also elicited by downregulation of 4E-BP1 in the spinal cord dorsal horn.
Preclinical studies suggest that this so-called extracranial cephalic mechanical hypersensitivity is mediated by sensitization of central trigeminovascular neurons in the spinal trigeminal nucleus (42).
Nevertheless, the role of IB4 neurons in mechanical hypersensitivity is demonstrated by a large body of evidence [ 5, 22, 39, 44, 47- 49].
The initial data showed that TRPV1-deficient mice exhibit normal responses to noxious mechanical stimuli and that inflammation-evoked mechanical hypersensitivity is not reduced [ 31].
In two different models of HIV-1 associated neuropathy, Bhangoo et al. [ 85, 91] demonstrate that antiretroviral drug- or viral coat protein-, gp120-, induced mechanical hypersensitivity is attenuated by acute, systemic treatment with CCR2 or CXCR4 antagonists.
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Basal and nitroglycerin-evoked mechanical hypersensitivity was evaluated using manual von Frey hair stimulation of the hindpaw.
Development of significant mechanical hypersensitivity was observed in CCI rats after postoperative day 4 (P < 0.05 vs. sham) and heat hypersensitivity developed after postoperative day 2 (P < 0.05 vs. sham).
The tests of the developmental time window of mechanical hypersensitivity were evaluated at 2, 4, 8 h, and then at 1, 2, 3, 5, 7, and 10 days after injection of BmK I.
Mechanical hypersensitivity was determined as response frequency to 10 presentations of a 0.4g von Frey filament.
For this, mechanical hypersensitivity was evaluated from day 1 to day 15 after an intraplantar injection of CFA in mice.
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