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Neuroscience of Pain – Exam 2 Study Guide [Part1]

by: Christine Thomas

Neuroscience of Pain – Exam 2 Study Guide [Part1] NSC 4358

Marketplace > University of Texas at Dallas > Neuroscience > NSC 4358 > Neuroscience of Pain Exam 2 Study Guide Part1
Christine Thomas

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Ok so make sure to go over the powerpoints! I will put up another full blown Study Guide after the lecture on Monday! Best of Luck studying!
Neuroscience of Pain
Dr. Price
Study Guide
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This 3 page Study Guide was uploaded by Christine Thomas on Friday February 19, 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 48 views. For similar materials see Neuroscience of Pain in Neuroscience at University of Texas at Dallas.


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Date Created: 02/19/16
Neuroscience of Pain – Exam 1 Study Guide  Ascending projections of the anterior portion of the STT from neurons in lamina IV-V of the spinal horn.  Shown here are two parts of the same pathway  Projections coming out of Lamna 5 and Lamna 1  Second order neuron – synapses here  Where part of pain – is fast cause its coming from a delta fibers – they tell you that you hand is on the stop and not your foot – action that comes after you move your hand is when your brain starts to work  This pathway is specific – through thalamus  pimary somatosensory cortex  Projections of the lateral portion of the spinothalamic tract from cells in lamina I of the dorsal horn  The lamna 1 neurons – they have a polysynaptic imput from a beta fibers  Second order neuron is also found here  Goes from later protion – brainstem – reticular formation – thalamus – primary sensory cortex and other areas  Signulet cortex – what is the pain doing to me  Not pain specific  ACC  Insula  Every part of brain can be modulated by pain  They can come up into the limbic system – like insula  Spinomesencephalic tract  You can by pass thalamus to get to other pain areas of the brain (straight into amygdala and hypothalamus)  Neurons are actually separate  How you feel about your self any given moment of time (feeling of dying)  Integration of Touch and Pain Tracts From the Body  They are separate lines of info – one coming from abeta fibers and  What part is not associated with the fine touch part  Showing the WHAT part  Asending system – integrates with decending system that modulates with  “WHERE” AND “WHAT” PATHWAYS FOR ACUTE PAIN  What – mostly coming from c fibers / lamina 1  Part of this path way uses the non classical pathway – difference how they are projecting into the thalamus  Dorsal – more emotion  TWO DIFFERENT ASCENDING SENSORY PATHWAYS HAVE BEEN IDENTIFIED:  Fast – meaning there are fewer connection to get to the limbic system  THE NON-CLASSICAL PATHWAYS  Taste system uses this but not used as widly as pain system  Dorsal thalamus straight into the amygdala and ACC  Let’s head back to the spinal dorsal horn and look more closely at how these pathways originate  The pain gate  Came up with this theory – gate control theory with the diagram shown above  This whole this is actually completely wrong  Build a model that can be broken down into parts and do different hypothesis  What do these dorsal horn interneuron cells look like?  Many dorsal horn neurons that receive C- or Adelta-fiber inputs are interneurons that do not project out of the spinal cord (only about 5% are projection neurons!!)  What do these dorsal horn interneuron cells look like?  Many dorsal horn neurons that receive C- or Adelta-fiber inputs are interneurons that do not project out of the spinal cord (only about 5% are projection neurons!!)  So which afferent fiber types contribute to these limbic connections?  Conclusion of paper : pep and non pep class give rise to two independent pathways- distribute to same brain areas but in different ways  If you infect a cell with one of these traces – it will distribute across cell and  Exclusively found in the IB4 neurons – happy accident  Cells are yellow – means transfer is pretty selective to IB4 pos class  IB4 – more for pos neurons  Lamina 5 – getting mostly c delta inputs  These are actually post synaptic to some of the lamina 1 neurons  Projections to limbic areas arise from both fiber types but take different routes to get there and do not converge once they are there!  Polysynaptic – lamina 2-5  Globus pallidus – motor control  Ib4 – non -pep  Substance P-Saporin selectively lesions cells that express NK1 receptors  Lamina 1 neurons  Receive direct input from C fiber s  Classic WHAT part of the pain pathway  Took saprin – ribosomal toxin – it shuts down protein synthesis – it doesn’t get into cells very well  If you can ge tthem in then you can lesion the cells very well  Substance P  Approach shown above  Substance P-Saporin selectively lesions the small number of dorsal horn neurons that express NK1  They gave an intra thecal injection – humans get this injections commonly – given to pain patients – it injects neurons  Started as an experiemental tool to send drugs to spinal cord  Asking what kind of lesion it would make in the spinal cord  They didn’t see a major loss of neurons  They saw that there was a reduction in NK1 (which is in orange)  What is the consequence of loss of these lamina I neurons that express the substance P receptor?  Doesn’t cause a lost of pain sensation all together – all pain perfectly intact  Blocks pain amplification  In animals with inflammation – only develop a small mechanical and thermal  Nerve injured – reduces neuropathic pain  Lamina 1 – important for post  Substance p and MK1  Hyperalgesic Priming as a Model of Transition to Chronic Pain  Inflammatory stimulus  PGE2 – advil reduces this  If you take a low dose of PGE2 into a non primed mouse – not much change  In a prime animal – will have pain for at least two weeks  Plasticity may be “masked” via endogenous analgesic mechanisms  Evidence that recovery from pain may not really happen  They took rats and cause inflammation  Animal get hypersensitivity  This suggested even when pain resolves the plasticity doesn’t dissolve  Lesion of NK1 neurons blocks hyperalgesic priming  Trying to figure out if pain is persistant or not  If you lesion those nk1 – you should remove the primate – shouldn’t be able to prime the animal  Transi-effect really early  21 days after injury – challenge with PG2 response  Required for long lasting pain induced plasticity  NK1 failed in humans – outcome is that its not gonna work 


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