| Term 
 | Definition 
 
        | Perception of pain.  Depends on specific receptors & pathways.  Brain needs to know about noxious stimuli faster! |  | 
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        | Term 
 | Definition 
 
        | Unspecialized nerve cell endings that start sensation of pain.  Transduce many stimuli into receptor potentials which trigger afferent AP's.  From cell bodies in dorsal root ganglia/trigeminal ganglion (facee), one axon to periphery & one to spinal cord/brain stem. |  | 
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        | Term 
 
        | Peripheral nociceptive axons |  | Definition 
 
        | End in unspecialized free endings.  Categorized by axon properties.  Either Adelta (myelinated, 5-30m/s) or C (unmyelinated, <2m/s).  Usually unmyelinated or lightly myelinated.  Much slower velocities than other somatics. |  | 
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        | Term 
 | Definition 
 
        | Fast pain pathway.  Responds to dangerously intense mechanical (pressure) or both intense mechanical AND thermal (pressure & heat) stimuli.  Called Adelta mechanosensitive nociceptors or Adelta mechanothermal nociceptors. |  | 
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        | Term 
 | Definition 
 
        | Slow pain pathway.  Respond to thermal, mechanical, and chemical stimuli (so polymodal). Called polymodal nociceptors. |  | 
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        | Term 
 | Definition 
 
        | Called first pain, Adelta responsible. |  | 
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        | Term 
 | Definition 
 
        | Called second pain.  C axons responsible. |  | 
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        | Term 
 
        | Aalpha and Abeta give pain? |  | Definition 
 
        | No, but if stimulus is enough to activate nearby Adelta nociceptors, will get tingling or if stimulus is super powerful will still get sharp pain!  If stimulus goes even farther, C axons will activate and have duller, longer-lasting pain. |  | 
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        | Term 
 | Definition 
 
        | Sensitive to heat at least 45C and capsaicin.  Also called VR-1 or TRPV1. [image] [image] [image] |  | 
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        | Term 
 | Definition 
 
        | Higher threshold for heat, 52C.  Not sensitive to capsaicin.  Only in Adelta receptors.  Also called VRL-1 or TRPV2. |  | 
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        | Term 
 
        | Transient receptor potential channels |  | Definition 
 
        | TRPs.  Family of receptors, including VR-1 and VRL-1.  Like voltage-gated K+ channels w/ 6 transmembrane domains, pore between 5&6.  Resting, closed pore.  Activated & open, influx of Na+ and Ca2+ to make AP's in nociceptive fibers. [image] |  | 
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        | Term 
 
        | Central Pain Pathway (body): dorsolateral, first-order |  | Definition 
 
        | Originate with other sensory neurons in dorsal root ganglia.  Branch into ascending and descending collaterals at dorsal horn to make dorsolateral tract of Lissauer.  Run up and down for on/two spinal segments, penetrate gray matter of dorsal horn.  Give branches that contact second-order neurons in Rexed's laminae 1 and 5. [image] |  | 
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        | Term 
 
        | Central Pain Pathway (body): dorsolateral, second-order |  | Definition 
 
        | Cross midline and ascend to brainstem and thalamus in anterolateral quadrant of contralateral half of spinal cord.  Past this is anterolateral system. [image] |  | 
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        | Term 
 
        | Central Pain Pathways (body): anterolateral system |  | Definition 
 
        | Conveying of pain and temp info to higher centers. [image] |  | 
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        | Term 
 
        | Central Pain Pathways: anterolateral, first-order & second-order |  | Definition 
 
        | First-orders terminate in dorsal horn (from dorsolateral), second-order from dorsal horn send axons across midline and ascend on contralateral side of cord (anterolateral column) to thalamus and brainstem.  Second-orders go to many structures in brainstem and forebrain. |  | 
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        | Term 
 
        | Dorsal column pain symptoms |  | Definition 
 
        | Touch, pressure, vibration, proprioception.  Ipsilateral. |  | 
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        | Term 
 | Definition 
 
        | Pain and temperature.  Contralateral side. |  | 
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        | Term 
 | Definition 
 
        | When you have area after dorsal horn injured, lose cutaneous info on ipsilateral side and lose pain & temp on contralateral side because of how the tracts are set up. |  | 
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        | Term 
 
        | Sensory discriminative aspects of pain |  | Definition 
 
        | Location, intensity, quality of noxious stimuli.  Depend on info from VPL to SI and SII.  Small, localized receptive fields.  Slide 12 |  | 
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        | Term 
 
        | Affective-motivational aspects |  | Definition 
 
        | Unpleasant feeling, fear, anxiety, autonomic activation of fight-or-flight.  From VPL to subdivisions of reticular formation, deep layers of superior colluculus, central gray, hypothalamus, amygdala, midline thalamic nuclei )important for transmitting nociceptive signals to anterior cingulate cortex and insula). Slide 16.   |  | 
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        | Term 
 
        | Pain & Temp Pathways from Face: first-order |  | Definition 
 
        | Neurons in trigeminal ganglion and from ganglia associated w/ cranial nerves VII, IX and X. [image]  Descend to medulla and make spinal trigeminal tract.  Terminate into two subdivisions, pars interpolaris and pars caudalis. [image] |  | 
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        | Term 
 
        | Pain and Temp from Face: second-order |  | Definition 
 
        | Neurons cross midline and terminate in many targets of brainstem and thalamus.  Targets grouped into mediating affective/motivational aspects and that mediate discriminative aspects (like body). Discriminative: projections to contralateral VPM, from VPM, SI, and SII. Affective: to targets in reticular formation and midbrain, midline nuclei of thalamus which supply cingulate and insular regions of cortex. [image]  [image] |  | 
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        | Term 
 
        | Other reasons for anterolateral system |  | Definition 
 
        | Important for transmitting innocuous info to higher centers.  W/o dorsal column system, can mediate nondiscriminative touch.  Mediates innocuous temp sensation, to higher centers by secondary neurons in lamina 1. [image]   [image] [image] |  | 
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        | Term 
 
        | Innocuous temp fibers & channels |  | Definition 
 
        | Warm fibers respond w/ increasing spike discharge rates to increases in temp. Cold fibers respond w/ increasing spike discharge rates to decreases in temp. TRP channels respond: TRPV3 and TRPV4 respond to warm, TRPM8 responds to cold. |  | 
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        | Term 
 | Definition 
 
        | Many distinct classes of selective neurons for noxious & innocuous types of info from anterolateral.  Sensitive to first pain, second pain, innocuous warmth, innocuous cold, histamine (mediating itch), slow mechanical stimulation (sensual touch), class that senses lactic acid & metabolites released by muscle contraction. |  | 
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        | Term 
 
        | Class that senses lactic acid & metabolites |  | Definition 
 
        | Maybe responsible for representing physiological condition of body (interoception). |  | 
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        | Term 
 
        | Interoception vs. exteroception |  | Definition 
 
        | Intero: drives mechanisms for homeostasis. Extero: touch and pressure. |  | 
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        | Term 
 | Definition 
 
        | After painful stimulus w/ tissue damage, stimuli in & around injury feel much more painful. |  | 
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        | Term 
 
        | Peripheral sensitization (hyperalgesia) |  | Definition 
 
        | Interaction of nociceptors w/ substances released when tissue damaged.  Interact with receptors or ion channels of nociceptive fibers and change responses. Slide 23 & 22 |  | 
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        | Term 
 
        | Central sensitization (allodynia) |  | Definition 
 
        | Immediate-onset, activity-dependent increase in excitability or neurons in dorsal horn after high activity of nociceptive receptors.  Nerves that couldn't make AP's now make AP's and increase pain sensitivity.  From transcription-dependent and transcription-independent processes. Slide 24 |  | 
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        | Term 
 
        | Transcription-independent allodynia |  | Definition 
 
        | "Windup" - progressive increase in discharge rate of dorsal horn neurons from low-frequency activation of nociceptors.  Stimulation constant amount, but feeling of intensity increases with each stimulation.  Only during period of stimulation.  Depolarization from activation of voltage-dependent calcium channels and removal of Mg in NMDA receptors, increasing sensitivity of dorsal horn to glutamate. Slide 24 |  | 
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        | Term 
 | Definition 
 
        | Thought to involve LTP-like enhancements of postsynaptic potentials.  Longest-lasting from transcription-dependent processes or from changes in neuronal activity (at site of injury)/humoral signals (more widespread changes). |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | From afferent fibers or central pathways themselves being damaged.  Persistent sensitizations. |  | 
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        | Term 
 | Definition 
 
        | From internal organs.  Balloon-intestine experiment. |  | 
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        | Term 
 | Definition 
 
        | Feel pain in some other part than where the pain is actually sensed (arm pain during heart attack).  Currents activate arm/shoulder nerves which are very close to heart nerves and cause pain. |  | 
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        | Term 
 
        | Descending pain-modulating pathways |  | Definition 
 
        | Start in somatosensory cortex (to thalamus) and hypothalamus, thalamus to midbrain where thalmic neurons synapse with ascending pathways in medulla and spinal cord and get pain relief.  Somewhat from opioid neurotrans.  http://static.howstuffworks.com/gif/pain-1.gif |  | 
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        | Term 
 | Definition 
 
        | Physiological response after receiving treatment w/o drug (but thinking there is a drug in the treatment).  Less response of pain receptors, and if opioid receptors blocked still have pain!   Mostly from central modulation. |  | 
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        | Term 
 
        | Other places where pain-modulating pathways start |  | Definition 
 
        | Many brainstem sites like parabrachial nucleus, dorsal raphe, locus coeruleus, and medullary reticular formation.  Fig. 10.8 |  | 
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