Neuroscience of Pain - Exam 1 Study Guide
Neuroscience of Pain - Exam 1 Study Guide NSC 4356
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This 7 page Study Guide was uploaded by Christine Thomas on Monday January 25, 2016. The Study Guide belongs to NSC 4356 at University of Texas at Dallas taught by Dr. Dussor in Fall 2015. Since its upload, it has received 188 views. For similar materials see Neurophysiology in Neuroscience at University of Texas at Dallas.
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Date Created: 01/25/16
Neuroscience of Pain Exam 1 Studv Guide WHAT IS PAIN 393 Pain gt Has many forms causes known and unknown purposes and can be either beneficial or unbeneficial to a person gt Tells us to avoid things that could hurt us survival I Teaches us to take care of ourselves survival gt Def unpleasant feeling and responsive experience that has to do with actual or possible tissue damage gt Can be caused by a trauma or a disease or a side effect of a treatment like chemo I Sometimes you can t find the reason behind the pain I And it can continue even after healing like phantom pain neuronal plasticity gt It s the number one reason people go and see the doctor for gt It can cause different kinds of reactions such as high heart rate blood pressure sweating activating the autonomic system muscle activity mood sleeping problems gt It can affect a person s life I Inefficient sleep interfering with intellectual work cause suicide allodynia light touch pain 393 Nociception gt Def encoding and processing of harmful stimuli in the nervous system I In other words your body is able to sense probable harm gt It starts in the high threshold sensory receptor of the peripheral somatosensory nervous system v Chronic Pain gt Is a disease of neuronal plasticity gt A third of pop suffers from some kind of chronic pain disorder gt Actoptic firing firing for no reason don t know why this is happening I For ten years Stan Cohen has been dealing with this pain of being stabbed in the arm and body telling him to get away like survival thus the painting gt Lasts about 36 months gt Know that Dr Phil Pizzo and his committee concluded I Pain represents a public health crisis I Treatment is a moral imperative I Pain s a medical concern that needs a cultural transformation gt There is no operational definition of chronic pain THE BASIC ANATOMY OF THE PERIPHERAL NERVOUS SYSTEM 393 Do nociceptors exist gt We need to be able to sense things that can injure us we need to have nociception gt There was a debate on if it did exist for about 60 70 years I They came up with two theories 0 Intensity theory there was no need for nociceptors 0 Specificity theory required nociceptors correct theory I Edward R Perl really important figure in the pain neuro field first president for the society of neuro studied nociception worked until he was 91 I You have neurons that are programed to respond to heat muscle tendon fibers noxious mechanical functions this is how the brain knows if something is just brushing your skin or pinching you skin intensely I Two kinds of fibers 0 A beta fibers heavily myelinated fibers 0 C fibers free nerve ending that go up into epidermis broken down into two different kinds 0 Peptidergic c fibers 0 Non peptidergic c fibers 393 Why do we need Nociceptors gt Need them to avoid things that can hurt us 393 Congenital insensitivity to pain really rare gt Three known mutations cause loss of development of nociceptors or nonfunctional nociceptors I NGF mutation I Mutation in trkA receptors for nerve growth 0 Don t develop nociceptors at all as well as sweat glands 0 They can t exercise vigorously 0 Lack acetylcholine also mentally retarded I Mutations in a voltage gated sodium channels called Nav 17 I Nociceptors develop but can t generate Loss of nociceptor function I Gain have pain all the time I Mutation that increases activity erythomyalgia burning man increase in skin temperature burning sensation skin turns red found mainly in hands and feet 9 Increased skin temperature skin appears to be read and they feel like their feet were on fire 393 Anatomy of peripheral nerve fibers gt Abeta large myelinated fasted conduction velocity gt Adelta small myelinated not quite as fast gt C fibers not myelinated still Schwan cells slow conduction gt Sensory neurons have no dendrites pseudo gt Referred pain branches terminated from dorsal Trigeminal ganglion face gt Sends projects throughout the brainstem Polymodal fiber or neuron can respond to multiple kind of stimuli which majority of C fibers are Physiologically defined nociceptor classes first and second pain gt First pain a delta gt Second pain c fibers slower speed takes time and lasts longer very poor adaptors continue to respond respond at high threshold gt Abeta respond at low threshold and rapidly adapting why you don t feel sitting in your seat Fast and slow pain are different gt Fast pain stinging I Well defined with regards to location I Its strength is defined I Can tell which toe you stubbed immediately gt Slow pain aching and burning Physiologically defined nociceptors classes in mouse skin gt Most nociceptors are polymodal most Respond to both heat and mechanical stimulation gt Only respond to noxious stimulation gt Don t not respond to low noxious stimulation but high Not all nociceptors are c fibers a beta fibers nociceptors gt Important for pain chronification gt Very active when pain becomes chronic I Evoke pricking pain more vigorous that C fiber responses I Type 1 deals with heat mechanical and chemical stimuli I Type 2 are A delta fibers All c fibers are nociceptors low threshold c fiber mechano receptors gt Respond to innocuous stimulation pleasant touch very little evidence that it is painful gt Some people have pain even with a gentle touch C fibers diversity gt Can respond to different kinds of stimuli polymodal gt Have different phenotypes and use different kinds of peptides nonpeptide neurotransmitters gt Grossly grouped into two categories I C nociceptors 0 Peptidergic I Nonpeptidergic I Proprioceptor Sensitized nociceptors gt Thermal allodynia gt Synthesized 393 Make sure to look over the squid experiment they added MgCl and notice what happened to squid when it was uninjured controlled injured injured with MgCL and notice out of which of the categories did the squid survive more in VOLTAGE GATED CHANNELS IN NOCICEPTORS O O 90 90 Phases of the Action Potential gt Rest potential gt Threshold membrane potential where channels begin to open When you reach adulthood it is gone but when you injure it then it will reexpress again It produces really large ramp currents generated potential currents I Has a really long open time I Persistent currents amplifies small depolarization I They are involved in letting you get to threshold excitability I Expressed after nerve injury I excited Like Nav17 Nav 19 mutations are associated with altered human pain phenotypes Nav 19 There are many mutations that do the same thing in Nav 17 Really good target Behind Nav 17 Ttx resistant channels Amplifies small depolarizations and stays open for a really long time I Can move action potential closer to threshold makes it more excitable VVVVV TRANSDUCTION OF PAIN SIGNALS ION CHANNELS AND GPCR O 90 Two types of Receptors gt Ionotropic I It s going to bind to the extra site I Channels are going to open and there will be a ow of ions gt Metabotropic I G protein opens the channels 393 Ionotropic Receptors gt Mediate Rapid Postsynaptic effect happens really fast gt They are on a millisecond time scale gt There are different kind of ionotropic receptors I Well known glutamate receptors I Nicotinic acetylcholine 393 General features of ionotropic receptors gt Cys loop I its btwn the second and thirds transmembrane gt NMDA has two major sub units I NR1 only has one subtype I NR2 has 4 different kinds of subtypes abcd gt You re going to need two P2X Family Receptors gt They are ATP sensitive activated gt ATP produced in the mitochondria I IMPORTANT TO as a neurotransmitter There are 7 sub units P2X7 IS homomeric P2X6 IS NOT HOMOMERIC ASIC channels are activated by protons we have a lot of protons in acidic VVVV circumstances Activation of ATPgated P2X3 channels initiates nociceptive signaling P2X3 channels are primary ATPgated channels expressed by nociceptors gt ATP will actiated P2X3 IMPORTANT highly expressive nociceptor Acid Sensing Ion Channel ASIC families pH sensors in nociceptors gt ASIC I Sensitive to pH I If you have an increase in protons then there will be activation of the ASIC channel I Depending on the izophorm dire range of acidic Transient Receptor Potential TRP Channels gt There are 28 TRP channels gt They share a lot of similarities in they look like each other gt But they have different families 5 major ones actually gt They are all are thermal sensitive meaning they are activated through temperature TRP Channels are thermosensors in nociceptors and other sensory neurons TRPA 1 has a lot of Ankyrin TRP 1 activated by heat below 18 degrees C They can also be activated by natural products garlic cinnamon TRPM 8 Cold temp also activated by mint TRPV 4 activated by heat temp above 25 degrees do not know natural activation VVVVV V stand for Vanilloid TRPV 3 3039 degrees activated TRPV 1 activated by capsaicin spicy food activate by camphor used in cream that VV actually burns the skin Vicks TRP channels are critical for pain sensing TRPVl agonists gt Capsaicin is Agonist of TRPVl channels TRPVl channel antagonists as novel analgesics While they quite effectively block noxious heat pain they cause an increase in core body temperature that has so far precluded their use in the clinic gt Why would you have an increase in this I tonically activated if you block it your body doesn t know if it should cool it Heterotrimeric large Gproteins gt Exchange from the GTP to the GDP the beta gamma units are going to stay together but the alpha are going to effect to protein gt When they are on when bound to GTP and off when bound to GDP Depending on receptor activated you can also activate the guanylyl cyclase same as the adenylyl cyclase gt Activated by Galpha proteins gt Phosphodiesterase Responsible for termination of the signal Phospholipase C PLC and IP3DAG signaling gt Galphaq activated by PLC gt PIP2 are all over the plasma membrane inositol 145triphosphate I 1P3 can bind to certain Calcium channels and produce a release of calcium in the cytoplasm I DAG also active activates PKC Recorded CMH off a rats skin they are sensitive to heat gt Decreases cause it is desenthesization Opioids gt There are peptides gt All are Galpha I the three group of endogenous opioid receptor ligands gt KNOW endorphins enkephalins dynorphins gt Morphine you take in the hospital they activate the Mu receptors I That s why you can only take certain doses Endo cannabinoids gt Endocannabinoids tetrahydrocannabinol I Active component of marijuana gt Two different ligands I 2 AG I Anandamide gt Two different receptors I CB2 peripheral nervous system Trk Receptors autophosphorylation gt IMPORTANT MUST KNOW gt You have two monomers gt Growth factors that binds the receptor not activated yet gt You have 4 phosphate gt Adapter proteins able to activate all the proteins inside 393 Differences between sensitization and activation gt Activation Whether stimuli can produce action potential I Stimuli that act on ion channels activators gt Sensitization Whether stimuli alters the function of ion channels I Stimuli that act on GPCTs or Trks sensitizers I May still cause nociceptors to activate 0 Cause B2Rs changes threshold for P2X3 I activated at very to ATP concentrations ambient concentration
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