A central mechanism of analgesia in mice and humans lacking the sodium channel NaV1.7
Donald Iain MacDonald, Shafaq Sikandar, Jan Weiss, Martina Pyrski, Ana Paula Luiz, Queensta Millet, Edward C. Emery, Flavia Mancini, Gian Domenico Iannetti, Sascha R.A. Alles, Manuel Arcangeletti, Jing Zhao, James J. Cox, Robert M. Brownstone, Frank Zufall, John N. Wood
Abstract
1.7-null mutations show naloxone-reversible analgesia. Thus, inhibition of neurotransmitter release is the principal mechanism of anosmia and analgesia in mouse and human Nav1.7-null mutants.
Topics & Concepts
NociceptorNeuroscienceSodium channelNeurotransmitterNociceptionOpioidKnockout mouseChemistryCentral nervous systemMedicineInternal medicineBiologyReceptorSodiumOrganic chemistryPain Mechanisms and TreatmentsIon channel regulation and functionNeuroscience and Neuropharmacology Research