The TRPV1, which can also be stimulated with heat, protons and physical abrasion, permits cations to pass through the cell membrane when activated. The resulting depolarisation of the neuron stimulates it to signal to the brain. By binding to the TRPV1 receptor, the capsaicin molecule produces similar sensations to those of excessive heat
The result appears to be that the nerves are overwhelmed from the burning sensation and are unable to report pain for an extended period of time. With chronic exposure to capsaicin, neurons are depleted of neurotransmitters and it leads to reduction in sensation of pain and blockade of neurogenic inflammation.
The mechanism of action of capsaicin is complex and involves a cascade of events that results in nociceptive fiber dysfunction. Capsaicin affects the transient receptor potential vanilloid 1 (TRPV1) receptor, which is involved in sensing heat, warmth, and pain, as well as substance P, which transmits pain and itch sensations from the peripheral to the central nervous system. When stimulated by capsaicin, the TRPV1 receptor releases sensory neuropeptides and blocks axonal transport of substance P in
sensory neurons. Continued application of capsaicin results in further depletion of substance P from peripheral sensory neurons, as well as decreased synthesis and transport of substance P within the neuron. The net effect is a temporary and modest diminution of pain perception that occurs over a period of 2-4 weeks and persists with repeated application.
With high capsaicin content pharmaceutical grade.
Apply using gloves use sparingly a very little goes a long long way. Allow 60 minutes to start to work.