Segmental Axon Reflex Of The Spinal Cord

From the perspective of clinical practice, local physiologic responses merit emphasis. Knowledge about lesion-induced healing physiologic processes is continuously growing.

The lesion artificially created by needling mimics accidental injury but on a very small scale. When needling-induced lesions heal, no scarring is formed. Knowledge of the underlying mechanisms of these lesions enables clinicians to further understand the local axon reflex induced by needling.

After a needle is inserted into tissue, the surrounding area becomes reddened. Accompanying this flare is edema or swelling, as the tissue fills with fluid. The region surrounding the lesion becomes sensitive because of chemical reactions caused by the injury. An individual C fiber terminates over a wide area of skin, and so a needling-induced lesion probably affects only a fraction of a fiber's many branches directly. Action potential generated at the directly involved branches also affect the other peripheral branches, as well as the main or parent axon that conducts the signal to the CNS. At all the peripheral terminals of a C fiber, substance P and CGRP are released toward two principal targets: the smooth muscles surrounding peripheral blood vessels and histamine-rich mast cells. This causes the arterial smooth muscles to relax, thus increasing the flow of blood into the neighborhood of the damaged tissue. Thus water and electrolytes flow out of capillaries into extracellular space; this process is referred to as extravasation. Histamine released from mast cells leads to a pronounced inflammatory response. All of this is important for promoting the infiltration of damaged tissue with cellular elements that will protect against infection and promote repair. The local chemical changes resulting from the lesion cause greater sensitivity of the surrounding tissue. The chemical changes sensitize the protein receptors inserted into nocicep-tive axons (Fig. 6-10). This primary hyperalgesia is a direct result of the axon reflex.

The response of nociceptors is affected by the histamine released by mast cells and by the edema that results from extravasation. Histamine selectively interacts with only a subclass of the most slowly conducting C fibers in which histamine receptors are inserted into the membranes of their axon terminals.16 These histamine receptors and possibly other independent histamine receptors are related to itch, which may happen in some cases of injury.

Edema causes a general reduction in the pH of extracellular fluid from 7.4 to below 6.0. As outlined earlier, the protein receptors inserted into nocicep-tive axons are sensitive to the concentration of H+. Thus activation of one branch of a C fiber leads to increased sensitivity of all its branches, and all neighboring nociceptors, to noxious stimulation.

Injured tissue releases two powerful pain-inducing chemicals: prostaglandin and bradykinin. They are lipids of the prostaglandin family and the nonpeptide bradykinin. Prostaglandins are derivatives of arachidonic acid, a membrane fatty acid that is itself a major component of the lipid bilayer of cell membranes. Damage to tissue and the resulting disruption of cell membranes cause the release of arachidonic acid into extracellular fluid, in which it is broken down by the enzyme cyclooxygenase (COX) to form prostaglandin.

Na+ Ca2

Heat

ATP bradykinin

Na+ Ca2

Heat

ATP bradykinin

Figure 6-10 Polymodal nociceptor consists of a family of receptor channels referred to as transient receptor potential (TRP). The subfamily TRP-V1 channels respond to many different noxious stimuli, including heat and H+ produced in response to tissue swelling. The noxious stimuli open a nonspecific cation channel that, through an influx of Na+, depolarizes the nociceptor axon. Adenosine triphosphate (ATP) and bradykinin, the signals of tissue damage, bind to a G-protein coupled receptor (GPCR). Through a series of steps, the TPR-V1 is phosphorylated, which leads to a sensitization of the receptor. DAG, Diacylglycerol; Gq, a family of G proteins; PKC, protein kinase C; PLC, phospholipase C.

Figure 6-10 Polymodal nociceptor consists of a family of receptor channels referred to as transient receptor potential (TRP). The subfamily TRP-V1 channels respond to many different noxious stimuli, including heat and H+ produced in response to tissue swelling. The noxious stimuli open a nonspecific cation channel that, through an influx of Na+, depolarizes the nociceptor axon. Adenosine triphosphate (ATP) and bradykinin, the signals of tissue damage, bind to a G-protein coupled receptor (GPCR). Through a series of steps, the TPR-V1 is phosphorylated, which leads to a sensitization of the receptor. DAG, Diacylglycerol; Gq, a family of G proteins; PKC, protein kinase C; PLC, phospholipase C.

How To Reduce Acne Scarring

How To Reduce Acne Scarring

Acne is a name that is famous in its own right, but for all of the wrong reasons. Most teenagers know, and dread, the very word, as it so prevalently wrecks havoc on their faces throughout their adolescent years.

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