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Lecture

Pain II

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Department
Biological Sciences
Course Code
55-101
Professor
Habetler

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Description
Outline of Lecture 30 (02-27 B; Caterina) Pain II I. There are many types of noxious stimuli - Pain can be caused by mechanical, chemical, thermalndor electrical stimuli - Basic pathway is DRG synapses in dorsal horn to 2 order neuron, which projects to thalamus via STT, where it synapses to 3 order neuron to cortex - Endogenous chemical stimuli include pH, ATP, K, histamine, and inflammatory products - There are exogenous compounds that can also cause pain - Prostaglandins and leukotrienes mediate hyperalgesia - NSAIDs mediate their affects by inhibiting cycloxygenase (part of prost. pathway) - COX I is expr in a wide variety of tissues, including gut, mediates GI protection - COX II has restricted expr, excluding gut, and mediates inflammation - COX II selective drugs ought to be anti-inflammatory w/o irritating gut - COX III mediates CNS effects on pain and fever - Some C fibers release CGRP and substance P, causes neurogenic inflammation and further pain stimulation (positive feedback) II. Transduction of noxious stimuli to action potential - Transduction of stimulus to action potential relies on ionotropic and metabotropic receptors - Modulation of nociception relies on GPCRs and neurotrophin receptors - Nociceptive neurons exhibit considerable molecular and functional heterogeneity A) ION CHANNELS - Ligand: ATP, serotonin, etc. can activate specific ligand gated ion channels - pH: Acid-sensing ion channels (ASICs) are Na channels sensitive to drops in pH - Heat: TRPV1 is stimulated at 43°C, but is also sensitive to capsaicin and H+ - Mechanical: ASIC a
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