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Nociception And Pain Notes

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Lecture 14 & 15 Nociception and Pain

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Introduction o Pain is AWARENESS OF SUFFERING o NOCICEPTION= Detection of activity which damages tissues or has potential to cause tissue damage o Nociception does not always lead to pain o Exceptions
 Anaesthesia; Analgesia; Nerve block; Physical interruption of pathway; Genetic mutations (NaV1.7) o Definition
 Signal to alert organism of potentially injurious situations (acute &
 Signal encodes nature of painful stimulus and location
 Different types of pain perception

• Burning, stinging, itching, pricking, aching etc. o Incorrect to talk of "pain afferent", instead say NOCICEPTIVE AFFERENTS Types of clinical pain commonly referred to o Inflammatory pain; Cancer pain; Neuropathic pain; Visceral pain; Postoperative pain; Migraine/headache; Cutaneous pain Primary afferent nociceptors o Nociceptive primary afferent neurons
 Acute pain normally from activation of these
 Many are small sized, slow conducting, but not all o Nociceptive ending in skin mostly C- or A(delta) Few have A(alpha)/(beta) fibres
 Positions of endings largely speculative (very small)
 All have "free unmyelinated endings o Types
 High threshold Mechanical (C/A(delta)/A(beta))
 Thermal nociceptors (C/A(delta)/A(beta))
 Polymodal nociceptors (C/A(delta))- 50-90% in skin
 Silent nociceptors (C)- only active after damage o Fibres for different types of pain
 Sharp pricking= A-fibres
 Slow burning= C-fibre (often polymodal)
 Tickle and itch= C-fibres (histamine) o C-fibre polymodal nociceptors respond to more than one of the following
 Noxious mechanical
 Noxious heat
 Noxious chemical Demonstrate polymodal nature by recording from single afferents TRPV1 receptor: noxious heat and some noxious chemicals Found in plasma membrane of C-fibre terminals Forms an ion channel, activated by: Capsaicin & other pungent substances Noxious heat (e.g above ~42 C) Acid pH Channel=non-selective cation channel & depolarizes when active

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Activation by heat or capsaicin is enhanced by inflammatory agents TRPV1 antagonists block noxious heat detection in man Threshold to heat decreased by Low pH Inflammatory mediators (prostaglandins, bradykinins)
 So burns continues to burn after heat removed
 Other noxious chemicals act on specific receptors (e.g. Bradykinin)
 Noxious mechanical stimulation acts via molecular receptor whose identity is unclear Efferent (effector) functions of nociceptive afferents o Blood vessels
 Neurogenic inflammatory response (axon reflex)
 Responsible for flare and wheal of triple response (local reddening; flare; wheal=oedema)
 Does not require CNS to occur

Transmitters from central terminals of nociceptive primary afferent neurons o Released from primary afferent terminals onto 2nd order neurons o Not fully understood

o Above not only candidates, but known to play important roles Windup o Phenomenon in DORSAL HORN NEURONS (lamina V wide dynamic range neurons) o Response to C-fibre stimulation o Each stimulus leads to more and more evoked APs in WDR neurons o Specific receptor blockers of NMDA, and of NK1 each partially block windup o Phenomenon depends on both glutamate activation of glutamate NMDA receptors and of SP on NK1 receptors Spinal cord pathways for nociceptive info: ANTEROLATERAL TRACT/SPINOTHALAMIC TRACT o Nociception, temp, tickle, itch, sexual sensation, crude touch
 Not fully understood/some aspects still controversial
 More complex than dorsal column pathway:

• More diffuse effects on body physiology & emotional state than DC

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