Inflammation of peripheral tissues and injury to peripheral nerves induce diferring effects in the expression of the calcium-sensitive anandamide synthesising enzyme and related molecules in rat primary sensory neuron

Autor: Nagy, I, Suosa-Valente, J, Varga, A, Torres Perez, J, Jenes, A, Wahba, J, Mackie, K, Cravatt, B, Ueda, N, Tsuboi, K, Santha, P, Jancso, G, Tailor, H, Avelino, A
Přispěvatelé: Wellcome Trust, British Journal of Anaesthesia, Commission of the European Communities
Rok vydání: 2016
Předmět:
Popis: Elevation of intracellular Ca 2+ concentration induces the synthesis of N0 arachydonoylethanolamine (anandamide) in a sub0popu lation of primary sensory neurons. N0acylphosphatidylethanolamine phospholipa se D (NAPE0PLD) is the only known enzyme, which synthesises anandamide in a Ca 2+ 0dependent manner. NAPE0 PLD mRNA, as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1) and the inhibitory cannabinoid type 1 (CB1) receptor and the main anandamide0hydrolysing enzyme fatty acid amide hydrolase (FAAH) are all expressed by sub0populatio ns of nociceptive primary sensory neurons. Thus, NAPE0PLD, TRPV1, the CB1 rec eptor and FAAH could form an autocrine signalling system, which could shape t he activity of a major sub0 population of nociceptive primary sensory neurons, hence contribute to the development of pain. While the expression patterns of TRPV1, the CB1 receptor and FAAH have been comprehensively elucidated, little i s known about NAPE0PLD expression in primary sensory neurons under physiol ogical and pathological conditions. We report that NAPE0PLD is expressed by about a third of primary sensory neurons, the overwhelming majority of which also express nociceptive markers as well as the CB1 receptor, TRPV1 and FAAH . Inflammation of peripheral tissues and injury to peripheral nerves induce diff ering but concerted changes in the expression pattern of NAPE0PLD, the CB1 receptor, T RPV1 and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signalling system, in a major proportion of nociceptive primar y sensory neurons, and that alterations in that autocrine signalling by periphe ral pathologies could contribute to the development of both inflammatory and neuropathi c pain.
Databáze: OpenAIRE