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Neuroscience of Pain - Exam 4 Study Guide

by: Christine Thomas

Neuroscience of Pain - Exam 4 Study Guide NSC 4358

Marketplace > University of Texas at Dallas > Neuroscience > NSC 4358 > Neuroscience of Pain Exam 4 Study Guide
Christine Thomas

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Make sure to go over his review ppt
Neuroscience of Pain
Dr. Price
Study Guide
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This 6 page Study Guide was uploaded by Christine Thomas on Monday April 25, 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 45 views. For similar materials see Neuroscience of Pain in Neuroscience at University of Texas at Dallas.

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Date Created: 04/25/16
Neuroscience of Pain Exam 4 Study Giude  Existing neuropathic pain therapeutics are ineffective  Number needed to treat – NNT  Used in clinical trials  1 out of 7 patients are going to get efficacy  Pharmacological Treatments on the horizon  Have drugs that are in phase 3 clinical trails or have a lot of genetic evidence  TRPV1  Work for inflammatory pain  Most of the ones that are made cause hypothermia – cause fever  Trying to find TRPV1 that are slightly different  Or trying to combines things to reduce the hypothermia  P2X3  Nociceptors  activated by ATP  causeing them to fire AP  causes pain  Cough (activating nociceptors that are innervating your air way – can block that with this aganoist)  Intractable cough (coughing 1 every 10 mins) found that  Orphan disease  Efficacy in ostio arthritis  TRPM  Cold receptor  Not sure if it gives a gain of function or loss of function  Used for neuropathic pain – cold  Watched in the migraine area  Nav blockers  Biologics for Pain  Molecules that are usually oral available – 300-400lbs – labiskies rule of 5 (rules that drugs must obey)  Anti NGF therapies  Antibodies – they bind to their targets – humanized so that they wont activate their own immune system  Stay in your system for at least a month  Take away things that are promoting pain  Stopped trials until recently – for cox 2 inhibitors  ANTI CGRP therapies  Successful for migraine  IL10  Shuts down immune system?  Disease Modifying therapies  System when you have an injury that sysnthesizes you nociceptors  If you take it away long enough it causes plasticity  Trying to resolve something to do with plasticity  Central Dogma of Molecular Biology  Three steps  Initation  Eongation  Termination  Can change gene expression RAPIDLY  Its REVERSIBLE – can be turned on and off  In the cause of neurons – can give you fine SPATIAL CONTROL  1981 – ozzie stuart  Looked at hippocampal neuron  If you look at the base of the dentritic spine (you normally done see ribosomes except at the base of spine – these guys are involved in spinal plasticity  Local translation controls postsynaptic plasticity  Have to have local sysnthesize to have plasticity  AMP Kinase activators decrease mTOR and ERK activity  Took a rat and injected – gave them pain  Activated by a drug called metphormine – used for diabeties (type 2 diabetes)  most wildly used drug on earth  Mice given higher doses then in humans  Blood levels are higher than given in a human  Metformin treatment reverses nerve injury-induced microglial activation  Reverses activation of microglia in the spina cord  The Optogenetics Revolution in Neuroscience  Hope is to create very specific pain therapeutics  Minipulation of neurogenesis with light  A CL pump can move in one direction  hyperpolarization  Peripheral nervous system  Channelrhodopsin: an algae light operated ion channel that has been engineered to control neuronal activity  Modified that it is activated by blue light and sodium ions  Halorhodopsin: a light activated chloride pump found in archaea that hyperpolarizes cells  Halo – activated by yellow light – depolarization  Migraine  Tension types headaches  Migrane – number three  common  neurological disorder  low back brain cause more disability than any of these diseases  but migraine is in the top ten  A bunch of ppl have migraine  Definition of Migraine  Definition: last 4-72 hours  They don’t like to be in the light or sound  Comes from greek word – hemicranias  Pain on one side of the head  Later called micrania  Migraine Epidemiology  Prodominately effects female – around the age of puberty – peaks at 30 years old and then decreases with ages  Relativily low in you mid teens – can affect 30% of female pop btwn 20-30 years old  Triggers  Well known to have trigger – common trigger being stress  Can be triggered by food too…  MSG is common reason  Some ppl even respond to drugs  Nirtoglycerin – basal dilator  Usually gives you a migrane  Aura  Most ppl have migrane without aura  With aura  They know a migrane is coming  Something emerges in their visual field  Migraine headache comes right after that – good cue to take medication before an attack – taking medication early allows them not to have pain  They see sharp edges that start to move – differ from person to person  Characteristics of Migraine  before attack  two days before attack  Durng an attack  4-72 ours  change in temp  sensitivity to sound/ light  they have allodynia in their face or other parts of their body  Pain isolated to one area of head but allodynia can be all over the body  After an attack  Feels like a hung over  Can last hours to days after attack  Phases of migraine: aura  Cortical spreading compression – moving across area of brain that is producing depression  Visual cortex  Cortical-spreading depression  Moving through area you are seeing  Usually has a focus – where it starts  bands of changes of excitability – and then stops  Causes a depolarization and chronic allu  Above is the recording of the soma  Extracellar concentration goes up  can raise the extracellar to go crazy  almost like you are inverting the ions inside the brain  lots of glutamate release  Comes back to normal when in moves back  Meninges  Activatiors of nociceptors found in meninges  Dura matter. Arachnoid, pia mater – where pain comes from – pain feel like its behind their eyes  What is the Mechanism of Migraine Pain?  Ocipital part of the meninges – is innervated by the C2 dorsal room ganglia  Ideas  Nocicptors innervated by meninges –  CSD – create large change in  Sterile inflammation inside the skull  Migraine is basal dilation –  Migrane feels like a throbbing – throbbing coming from blooding when you heart beats  Movements of blood cause of heart beat can cause throbbing  Vaso contriction  Don’t know how these works are working – cause they are vasoconstrictors  Vaso dilation – not the cause of migraine pain  Pharmacotherapy of migraine  They take medication all the time to prevent migrane – prophylactic  Opioids  Opioid- easily addictable  To decrease this is by using them less frequently for pain  Acute pain – injury might be awful – treated over two days  Chronic pain – may arise from acute pain but can last for their entire life  Opioids will help them – but there is evidence that they can cause harm and maybe no affect at all (most definitely effects acute pain)  Asprin  First commercialized by bayer  Comes from willow leaves  Active ingredient was found in 1838  Opium  Used by samerians and greek (Chinese was using something else)  First synthesized by bayer and sold in a form of heroin  Heroin is very dangerous cause its potent  Can cause resptitory represent  Analgesics for Acute Pain  Caine – block voltage gated Na channels – give them locally they can block pain  Nerve block – helps preventing chronic pain  Stops the nociceptor signal from getting the signal at all  Physicians in the military have learned this the most  They try to put in the nerve block as soon as possible  And found that these work very very well  Ppl with severe injuries = opioids are bad for them  Cause pain makes the situation worse  Analgesics for Acute-Chronic Pain  Morphine  Oldest synthetic out there  Fentanyl  Have a short half life  They don’t have an onset that is very very quick  Methadone  Used for treating addiction (sometimes used for cancer pain)  Used cause it has a low efficacy  Also lasts for a long time – gives you a short stimulation for a long period of time  Side effects  Respitory depression (most important cause this is what kills them)  Vomiting  Almost everyone who takes opioid will have constipation  Hard time concentrating  Substance abuse issue  Analgesics for Acute Pain  Acetaminophen – Tylenol –not an NSAID (ppl think that they are) does not inhibit cox 1 or 2  is a fever reducer but not an anti inflammatory  does reduce pain  in acute setting – good to use with another drug – a syntergetic action  Actual _______ act on Cox1 and 2  Cox1  lost = GI tract irritation  Cox 2  Inducable – not expressed in tissue until some kind of injury  NSAIDs goal is to reduce COX 2  NSAID  Asprin – binds covalently – shuts of enzymes forever (need to produces new ones)  They bind in the enzyme pocket but can removed by precursers or by drug being metabolized  More severe side effect  Asprin really not used for pain any more but rather for ppl who can have strokes or (low platelet)  Cox 2 required for maintence of cardio vascular ________  Side effects  Ulcers (important one)  STEROIDS  Rarely used but also used for pain over a long term but for diseases  Sone – steroids  Inhibit PA2 and alters transcription and decreases inflammation  Have very bad side effects after used for a long time  If you take them over and over again = destroy cartilage  Analgesics  They bind to three different receptors  Mu (most important)  Delta  Kappa  When activate new opioid receptors  Pre -  Block Ca2+ Influx  Opens K+ Channels – K+ efflux  Decreases excitatory neurotransmitter release  Post –  Open K+ Channels  Hyperpolarize 2O-order neuron  Inhibit Action Potential Generation  Activation of GI decreses _________  Opioids act at μ, δ, and κ GPCRs (G coipled)  Super spinal areas – periacidutal grey  RVM – resp depression found here  Die cause they have acute resp dep = stop breathing = brain dead  Have opioid receptors in your GI tract = constipation  Contraction of smooth muscle goes down and things stop moving  Centrally-acting Analgesics  Clonadine – alpha 2  Very effective  Binds to alpha 2 receptors everywhere in body and cardio vascular system = cause neg cardio effects  Used as a locally acting analgesics  TOLERANCE  Mediated by a receptor mediated _________  What happens when a receptor binds to ligand  Changes shape  GI created  Binds to beta resta____ = gets internalized  When you take a drug – you swamp system with an artificial transmitter – pushing hemostats with internalized receptor 


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