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  1. Article ; Online: Postsurgical Latent Pain Sensitization Is Driven by Descending Serotonergic Facilitation and Masked by µ-Opioid Receptor Constitutive Activity in the Rostral Ventromedial Medulla.

    Cooper, Andrew H / Hedden, Naomi S / Prasoon, Pranav / Qi, Yanmei / Taylor, Bradley K

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2022  Volume 42, Issue 30, Page(s) 5870–5881

    Abstract: Following tissue injury, latent sensitization (LS) of nociceptive signaling can persist indefinitely, kept in remission by compensatory µ-opioid receptor constitutive activity ( ... ...

    Abstract Following tissue injury, latent sensitization (LS) of nociceptive signaling can persist indefinitely, kept in remission by compensatory µ-opioid receptor constitutive activity (MOR
    MeSH term(s) Analgesics, Opioid ; Animals ; Female ; Hyperalgesia/metabolism ; Male ; Medulla Oblongata/physiology ; Mice ; Narcotic Antagonists/pharmacology ; Pain, Postoperative/metabolism ; Receptors, Opioid, mu/metabolism ; Serotonin/metabolism
    Chemical Substances Analgesics, Opioid ; Narcotic Antagonists ; Receptors, Opioid, mu ; Serotonin (333DO1RDJY)
    Language English
    Publishing date 2022-06-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.2038-21.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The left central nucleus of the amygdala contributes to mechanical allodynia and hyperalgesia following right-sided peripheral nerve injury.

    Cooper, Andrew H / Brightwell, Jennifer J / Hedden, Naomi S / Taylor, Bradley K

    Neuroscience letters

    2018  Volume 684, Page(s) 187–192

    Abstract: The left and right central nucleus of the amygdala (CeA) exert asymmetric pronociceptive functions. In the setting of a transient noxious stimulus or persistent inflammatory pain, neuronal activity increases in the right but not left CeA, regardless of ... ...

    Abstract The left and right central nucleus of the amygdala (CeA) exert asymmetric pronociceptive functions. In the setting of a transient noxious stimulus or persistent inflammatory pain, neuronal activity increases in the right but not left CeA, regardless of side of injury. Much less is known regarding this lateralization with respect to the behavioral manifestations of persistent neuropathic pain. To address this question, we conducted spared nerve injury (SNI) to the left or right hindlimb and then inactivated the left and/or right CeA with local microinjection of lidocaine. We evaluated injury-induced hypersensitivity with von Frey hairs (mechanical allodynia), a blunt pin (mechanical hyperalgesia), and acetone application (cold allodynia). Following left-sided SNI, inactivation of the right or bilateral CeA attenuated mechanical allodynia and hyperalgesia as well as cold hypersensitivity, while inactivation of the left CeA had no effect. Following right-sided SNI, we observed a modality-dependent effect: mechanical allodynia was attenuated by inactivation of the left but neither the right nor bilateral CeA, mechanical hyperalgesia was attenuated by left, right and bilateral intra-CeA lidocaine, and cold allodynia was unaffected. These data suggest that CeA-mediated control of neuropathic pain is not strictly limited to the right CeA as previously assumed. We conclude that functional lateralization depends on the type of pain, side of injury and the sensory modality, and that the left CeA contributes to mechanical allodynia and hyperalgesia after peripheral nerve injury to the right side of the body.
    MeSH term(s) Anesthetics, Local/administration & dosage ; Animals ; Central Amygdaloid Nucleus/drug effects ; Central Amygdaloid Nucleus/physiology ; Functional Laterality/physiology ; Hyperalgesia/drug therapy ; Hyperalgesia/physiopathology ; Lidocaine/administration & dosage ; Male ; Microinjections/methods ; Peripheral Nerve Injuries/drug therapy ; Peripheral Nerve Injuries/physiopathology ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Anesthetics, Local ; Lidocaine (98PI200987)
    Language English
    Publishing date 2018-08-13
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2018.08.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Endogenous µ-opioid receptor activity in the lateral and capsular subdivisions of the right central nucleus of the amygdala prevents chronic postoperative pain.

    Cooper, Andrew H / Hedden, Naomi S / Corder, Gregory / Lamerand, Sydney R / Donahue, Renee R / Morales-Medina, Julio C / Selan, Lindsay / Prasoon, Pranav / Taylor, Bradley K

    Journal of neuroscience research

    2021  Volume 100, Issue 1, Page(s) 48–65

    Abstract: Tissue injury induces a long-lasting latent sensitization (LS) of spinal nociceptive signaling that is kept in remission by an opposing µ-opioid receptor (MOR) constitutive activity. To test the hypothesis that supraspinal sites become engaged, we ... ...

    Abstract Tissue injury induces a long-lasting latent sensitization (LS) of spinal nociceptive signaling that is kept in remission by an opposing µ-opioid receptor (MOR) constitutive activity. To test the hypothesis that supraspinal sites become engaged, we induced hindpaw inflammation, waited 3 weeks for mechanical hypersensitivity to resolve, and then injected the opioid receptor inhibitors naltrexone, CTOP or β-funaltrexamine subcutaneously, and/or into the cerebral ventricles. Intracerebroventricular injection of each inhibitor reinstated hypersensitivity and produced somatic signs of withdrawal, indicative of LS and endogenous opioid dependence, respectively. In naïve or sham controls, systemic naloxone (3 mg/kg) produced conditioned place aversion, and systemic naltrexone (3 mg/kg) increased Fos expression in the central nucleus of the amygdala (CeA). In LS animals tested 3 weeks after plantar incision, systemic naltrexone reinstated mechanical hypersensitivity and produced an even greater increase in Fos than in sham controls, particularly in the capsular subdivision of the right CeA. One third of Fos+ profiles co-expressed protein kinase C delta (PKCδ), and 35% of PKCδ neurons co-expressed tdTomato+ in Oprm1
    MeSH term(s) Animals ; Central Amygdaloid Nucleus/metabolism ; Female ; Hyperalgesia/drug therapy ; Hyperalgesia/metabolism ; Hyperalgesia/prevention & control ; Male ; Mice ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Pain, Postoperative/drug therapy ; Pain, Postoperative/prevention & control ; Receptors, Opioid ; Receptors, Opioid, mu
    Chemical Substances Narcotic Antagonists ; Receptors, Opioid ; Receptors, Opioid, mu ; Naloxone (36B82AMQ7N)
    Language English
    Publishing date 2021-05-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 195324-2
    ISSN 1097-4547 ; 0360-4012
    ISSN (online) 1097-4547
    ISSN 0360-4012
    DOI 10.1002/jnr.24846
    Database MEDical Literature Analysis and Retrieval System OnLINE

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