Abstract
Injurious mechanical, thermal, or chemical stimuli acting on somatic and visceral tissues are encoded into a discharge of nerve impulses by peripheral endings of Aδ and C nociceptor neurons located at sensory ganglia. Nociceptors are functionally classified as mechano-, polymodal, and silent nociceptors. Noxious stimuli are transduced by membrane receptor/channel proteins at nociceptor endings into depolarizing currents that evoke propagated nerve impulses into their parent axon. Inflammatory mediators, released by tissue injury, act on membrane receptors through second messenger cascades, causing decreased threshold and enhanced spontaneous and stimulus-evoked impulse activity (sensitization). Damage to peripheral nociceptor neurons also changes membrane protein expression and causes long-lasting disturbances in excitability and impulse firing.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
