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Amygdaloid administration of tetrapentylammonium attenuates development of pain and anxiety-like behavior following peripheral nerve injury
Author(s) -
Zuyue Chen,
Hong Wei,
Boriss Sagalajev,
Ari Koivisto,
Antti Pertovaara
Publication year - 2018
Publication title -
pharmacological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.706
H-Index - 83
eISSN - 2299-5684
pISSN - 1734-1140
DOI - 10.1016/j.pharep.2018.08.005
Subject(s) - neuropathic pain , medicine , sni , anesthesia , nerve injury , perioperative , chronic pain , minocycline , allodynia , pharmacology , hyperalgesia , nociception , receptor , physical therapy , biochemistry , chemistry , microbiology and biotechnology , hydrolysis , acid hydrolysis , biology , antibiotics
The central amygdaloid nucleus (CeA) is involved in processing and descending regulation of pain. Amygdaloid mechanisms underlying pain processing and control are poorly known. Here we tested the hypothesis that perioperative CeA administration of tetrapentylammonium (TPA), a non-selective THIK-1 channel blocker and thereby inhibitor of microglia, attenuates development of chronic neuropathic pain and comorbid anxiety-like behavior.

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