The Neural Mechanisms Underlying The Effects Of Acute Restraint Stress On Bee Venom-induced Nociception And Inflammation

Background and purpose: Inflammation caused by peripheral tissue injury produces pain-related behavior (persistent spontaneous nociception and hyperalgesia) and inflammatory reaction such as redness and edema. Inflammation can be divided into neurogenic and histogenic process. Inflammation triggered by substances released from sensory nerve terminals is referred to as"neurogenic inflammation."Nociceptive impulses also can be antidromically transmitted into the peripheral nerve terminals when they are sent to the spinal cord from the injury site. The process is generally attributed to the release of substance P(SP) and calcitonin gene-related peptide(CGRP) mediated by axon reflex and/or dorsal root reflex. These inflammatory mediators then induce or promote the dilation of peripheral blood vessels and the inflammation processes. Histogenic inflammation refers to the process that local insults cause the release of a lot of inflammatory mediators such as bradykinin,prostaglandin E2,5-HT,histamine and cytokinin which promote the development of inflammation. Clinical inflammatory pain is characterized as persistent spontaneous pain, thermal and mechanical hyperalgesia. Inflammatory pain is generally resulted from the sensitization of peripheral nociceptors and central neurons.Acute stress alone can induce analgesia and cause an inflammatory response. Stress is closely linked to our most primitive biological pathways,...