Neuroscience of Pain Exam 3 Study Guide part 1
Neuroscience of Pain Exam 3 Study Guide part 1 NSC 4358
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This 3 page Study Guide was uploaded by Christine Thomas on Thursday March 31, 2016. The Study Guide belongs to NSC 4358 at University of Texas at Dallas taught by Dr. Price in Spring 2016. Since its upload, it has received 22 views. For similar materials see Neuroscience of Pain in Neuroscience at University of Texas at Dallas.
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Date Created: 03/31/16
Neuroscience of Pain – Study Guide Exam 3 Sensitization There are these sensitizers – act on receptors called etbotrobic recotor which are found on the cell surface that is non ionic (g-protein / kinases) Nuclear receptors also play a role but don’t mucha bout them Acitivators are almost always ion channels – sensitizers found out side of cells activation of receptor that send signals that changes how the ion channel performs cause it can’t do it itself Forforlation changes how receptor works There is a ion channel that has an metobotropic affect – calcium (has a specialized role – some sensitizers are ion channels that don’t allow calcium through) Ck2 Peripheral sensitization Singaling changes = (inflammation) ion channels that act as acitvators and metabotropic Changes the ionization of the channel And IB4 always nonpeptaergic receptors ? Nope Once injured they show CGRP You would have convertded your DRG through injury to have completely different phenotype Targets in A Extracellular factors that are involved in inflammation These are targets most commeonly used to treat pain And phenotypic switches Some types of peripheral sensitization Sympathetic nervous system can sanitize or even activate under some certain circumstance in the nociceptive system Prostaglandin E2 mediate nociceptor sensitization. Signaling PGE2 – produced Acts on G protein receptors (EP receotor) Causes intracellular kinases that can signal through a variy of differet mechanisms. Major downstream target Phosphorlation of volatege gated sodium chainless VGSC – drops threshold at which it opens Depolarization (not much?) Peripheral sensitization and changes in response to the sympathetic nervous system Calsagia – original name for disease – surgeon found soldiers were developing neuropathic pain after injury and after healing (earliest description of phantom limp pain) changed to be called reflex sympatheic Shut of sympathic nerivous sytem in the patients – part of pathology When you activated the SNS – pain would get worse Sympathic chain be removed – sysmethically maintain pain Now called complex regional pain system If you look at affected limb – clear changes in sympathic tone – change in temp (change in blood flow) and limb sweating all the time or at all Nerve injury can make polymodal C fibers responsive to the sympathetic nervous system There is something to the disease Found – Took rats – did a nerve injury In controlled animals there is no access from the SNS to nociceptor s If you do a nerve injury and come back later – some part of SNS is activated – repsonds to NE Sympthetically can maintain pain How stress can exaberate pain Heat – nerve injury increases how nociceptors repond to pain Mediated by NE coing for Symthetic chain Many of the ion channels involved in nociception and expressed by primary afferent nociceptors can be sensitized: Ion channels involved in thermo- sensation There are cold activated channels as well Not commonly observed TRM8 – major sensor for cold – does reduce ability to tell what is cold It becomes sensitized you can shift from having a activation at 18 but can move it to 26 deg C Up-regulation of TRPV1 (capsaicin and vanilloid receptor type 1) after inflammation sensitize nociceptors to heat: Intracellular signaling promotes sensitization through a variety of mechanisms Get a bigger response what ever temp it is Occurs through changes in expression Any cells that expresses TRPV 1 If two and normal is 220 – hyperagllesia Nerve injury can drive a down-regulation of voltage-gated K channels causing enhanced excitability If you have a lot of K and less of Na = modulates their excitability Nerve injury downregulates Kv9.1 expression (right) and knockdown of Kv9.1 expression makes DRG neurons hyperexcitable (left) Lots of expression of KB9.1 – when there is no injurey AFTER INJURY ITS COMPLETELY GONE Looked at ectopic activity (either with an injury and put it into a dish) in this cause they used small inhibityory RNA Peripheral nerve block targeting the DRG innervating the affected dermatome was nearly 100% successful in immediately reversing neuropathic pain Glial 5 main functions- 1. surround neurons/ hold them in place - (Astrocytes) 2. supply nutrients and trophic factors - (Astrocytes) 3. form myelin - (Oligodendrocytes) 4. destroy pathogens/ remove dead neurons - (Microglia) 5. modulate neurotransmission by regulating transmitter availability and/or uptake - (Astrocytes) Many kinds of glia in nervous system Main 3 glial cells in CNS (one also in PNS) Astrocytes – found in blood – recycling neurotransmitter Communicate with active neurons Blood oxygenation level control by them Detect change in neuronal activity Oligodendrocytes Myelinated cells – schwann cells – single cells Microglia – immune cells for the brain What are the exact things that can turn on Microglia (microglia normally come from bone marrow – they populate your brain from very young) Pathogen – virus or bacteria (primary function to take a ambaic form) Ischemia – stroke Neurogeneration Activated astrocytes Microglia Able to produce immune factors - cytokines and aminokines Take on both inflammatory and non inflammatory M1 polarization – moving toward pro inflammatory - TNF M2 – moving toward anti inflammatory - IL10 In periphery – promoting immune cells into a tissue DRG – activated by them too Many CNS can be modulated by cytokines as well What does this microglial activation look like? Happens throughout ipsilateral spinal cord Interestingly microglia seem to only be activated in the spinal dorsal horn by nerve injury
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