Peripheral inflammation induces p38 MAPK activation in the soma of C fiber nociceptors in
the dorsal root ganglion (DRG) after 24 hr. Inflammation also increases protein, but not …

The transient receptor potential ion channel, TRPV1 plays an essential role in the
development of inflammatory thermal hyperalgesia. We investigated the dependence of …

Alterations in the intracellular signal transduction pathway in primary afferents may
contribute to pain hypersensitivity. We demonstrated that very rapid phosphorylation of p38 …

Nociceptors, or pain‐sensitive receptors, are unique among sensory receptors in that their
sensitivity is increased by noxious stimulation. This process, called sensitization or …

Injury or inflammation release a range of inflammatory mediators that increase the sensitivity
of sensory neurons to noxious thermal or mechanical stimuli. The heat-and capsaicin-gated …

Cold hyperalgesia is a well-documented symptom of inflammatory and neuropathic pain;
however, the underlying mechanisms of this enhanced sensitivity to cold are poorly …

Although the PI3K (phosphatidylinositol 3-kinase) pathway typically regulates cell growth
and survival, increasing evidence indicates the involvement of this pathway in neural …

The neuropeptide substance P (SP) is expressed in unmyelinated primary sensory neurons
and represents the best known “pain” neurotransmitter. It is generally believed that SP …

Sensitization of the pain-transducing ion channel TRPV1 underlies thermal hyperalgesia by
proalgesic agents such as nerve growth factor (NGF). The currently accepted model is that …

TNFα is involved in the generation of hyperalgesia in pathological states such as
neuropathy and inflammation. The pronociceptive action of TNFα may be mediated at least …