Sandbox Reserved 1652: Difference between revisions

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====Desensitization====
====Desensitization====


A repeated exposure of TRPV1 to capsaicin fails to activate the receptor. It occurs by a CA2+-dependent mechanism that leads to a '''desphosphorylation''' by the '''calcineurin''' [https://en.wikipedia.org/wiki/Phosphatase phosphatase] of the serine and threonine residues which have been previously phosphorylated by PKA (<scene name='86/868185/S502_t370/2'>S502 and T370</scene>). Thus, the decrease in TRPV1 phosphorylation diminish the sensitivity of the capsaicin channel and leads to a decrease in capsaicin's response by '''negative feedback'''.
A repeated exposure of TRPV1 to capsaicin fails to activate the receptor. It occurs by a Ca2+-dependent mechanism that leads to a '''desphosphorylation''' by the '''calcineurin''' [https://en.wikipedia.org/wiki/Phosphatase phosphatase] of the serine and threonine residues which have been previously phosphorylated by PKA (<scene name='86/868185/S502_t370/2'>S502 and T370</scene>). Thus, the decrease in TRPV1 phosphorylation diminish the sensitivity of the capsaicin channel and leads to a decrease in capsaicin's response by '''negative feedback'''.
The '''over-stimulation''' of TRPV1 is followed by the nerve endings' death due to calcium overload, causing analgesia. <ref name="Integrating TRPV1 Receptor Function with Capsaicin Psychophysics">G. Smutzer et R. K. Devassy, « Integrating TRPV1 Receptor Function with Capsaicin Psychophysics », Advances in Pharmacological Sciences, janv. 14, 2016</ref>
The '''over-stimulation''' of TRPV1 is followed by the nerve endings' death due to calcium overload, causing analgesia. <ref name="Integrating TRPV1 Receptor Function with Capsaicin Psychophysics">G. Smutzer et R. K. Devassy, « Integrating TRPV1 Receptor Function with Capsaicin Psychophysics », Advances in Pharmacological Sciences, janv. 14, 2016</ref>