To examine changes in sensitivity, non-noxious mechanical, noxious thermal and non-noxious cold stimuli were applied to the mid-plantar surface (Fig. 1b) of the right (ipsilateral) and left (contralateral) hindpaws.
On the other hand, secondary hyperalgesia and allodynia results in increased sensitivity to noxious and non-noxious stimuli outside of the area of tissue injury and involves the central sensitization of spinothalamic tract neurons via a mechanism that depends on the activation of several second messenger cascades (PKC, PKA, NO/PKG, etc).
Furthermore, infusion of hypertonic saline into the tibialis anterior muscle in people with knee OA results in greater areas of referred pain and longer lasting sensitivity to noxious stimuli [ 35], and there are widespread increases in sensitivity to noxious stimuli (secondary hyperalgesia) among people with OA [ 36].
Sensitivity to noxious heat of homozygous σ1R knockout mice did not differ from wild-type mice.
Our main finding was that elimination of TRPV2 from adult PSNs resulted in loss of behavioural sensitivity to noxious mechanical stimuli, but not to heat and gentle touch.
Numerous pathophysiological conditions result in the chronic dysregulation of mechanosensory signaling, leading to pain triggered by light touch (allodynia), as well as enhanced sensitivity to noxious mechanical stimuli.
Experimental pain models inducing hyperalgesia, i.e. an increased sensitivity to noxious stimuli often present in clinical pain, are important tools for studying antinociceptive drug profiles.
Numerous animal studies suggest that acute and chronic exposure to opioids can be associated with the development of hyperalgesia, i.e. an increased sensitivity to noxious stimuli.
Due to the large between-individual variability in the sensitivity to noxious signals, standardized TS and CPM tests may not yield any meaningful data in up to 50% of the population due to floor or ceiling effects.
We demonstrate that sleep loss, but not sleep fragmentation, in healthy mice increases sensitivity to noxious stimuli (referred to as 'pain') without general sensory hyper-responsiveness. Moderate daily repeated sleep loss leads to a progressive accumulation of sleep debt and also to exaggerated pain responses, both of which are rescued after restoration of normal sleep.
