By Charles William Isenberg, Johann Ludwig Krapf
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75, 105–119. This page intentionally left blank CHAPTER 2 History of Ion Channels in the Pain Sensory System J. Szolcsa´nyi and G. Petho¨ Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pe´cs, H‐7602 Pe´cs, Szigeti u. 12 Hungary I. Introduction II. The TRPV1/VR1 Capsaicin Receptor A. Discovery of Capsaicin Desensitization B. Prediction of the Capsaicin Receptor on C‐Polymodal Nociceptors C. Mechanism of Sensory Blockade Induced by TRPV1 Agonists D. Discovery of the Capsaicin‐Gated Cation Channel III.
The second stage is the sensory neuron blockade characterized by a decreased function of the nerve terminals, which manifests itself as an attenuation of their responsiveness to physical and chemical stimuli, and as a decreased sensory‐eVerent function due to a diminished neuropeptide release. At this stage ultrastructural changes are present without degeneration. The third stage is characterized by degeneration of the terminal axon and mitochondrial damage in the somata of nociceptive and preoptic neurons.
On one hand topical application of irritants to unbroken skin or onto the blister base (Foster and Ramage, 1981) supported the selective chemical excitability of cutaneous C‐polymodal nociceptors. , 1996). , 1990) activated also nonnociceptive types of cutaneous aVerents, raising the possibility that in the skin the superficial position of C‐polymodal nociceptors and not their unique excitability spectrum is responsible for their chemonociceptive nature. 2 mg) given intra‐ arterially into the ear artery of the rabbit elicited discharges exclusively in 2.
An Imperfect Outline of the Elements of the Galla Language by Charles William Isenberg, Johann Ludwig Krapf