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Paw withdrawal latency

Fig. 5. CFA-induced heat hyperalgesia (evaluated as paw withdrawal latency) is significantly lower in PKR1- and PKR2-KO mice than in WT mice. Deletion of PKR1 but not of PKR2 gene strongly reduces the inflammation-induce PK2 upregulation. Fig. 5. CFA-induced heat hyperalgesia (evaluated as paw withdrawal latency) is significantly lower in PKR1- and PKR2-KO mice than in WT mice. Deletion of PKR1 but not of PKR2 gene strongly reduces the inflammation-induce PK2 upregulation.
Animal models of nociception can be divided according to the therapeutic indication Acute Pain, Migraine Pain, Inflammatory Pain, Visceral Pain, Neuropathic Pain. Different degrees of chronification (up to weeks in neuropathic pain models) and different stimuli (mechanical, thermal, chemical, electrical) are used depending on the experimental question. In most cases a nociceptive threshold (e g. withdrawal latency of a paw) is determined. Sometimes, nociceptive intensities are determined e.g. in order to quantify hyperalgesia. [Pg.578]

Adult, male Sprague-Dawley rats were assessed for analgesic activity using the rat paw-hot plate assay. The latency hot plate paw withdrawal was measured by a Hot Plate Analgesia Meter. The temperature of the hot plate was set and calibrated at 52°C and the rats were removed from the heat stimulus by 36 seconds after placement. [Pg.98]


See other pages where Paw withdrawal latency is mentioned: [Pg.226]    [Pg.90]    [Pg.528]    [Pg.144]    [Pg.146]    [Pg.226]    [Pg.90]    [Pg.528]    [Pg.144]    [Pg.146]    [Pg.224]    [Pg.222]    [Pg.453]    [Pg.146]    [Pg.288]    [Pg.441]   
See also in sourсe #XX -- [ Pg.144 , Pg.145 ]




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