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Inflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium‐sensitive N‐arachydonoylethanolamine‐synthesizing enzyme and related molecules in rat primary sensory neurons

Elevation of intracellular Ca concentration induces the synthesis of N‐arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N‐acylphosphatidylethanolamine phospholipase D (NAPE‐PLD) is the only known enzyme that synthesizes anandamide in a Ca‐dependent manner. NAPE‐PL... Full description

Journal Title: Journal of Comparative Neurology 01 June 2017, Vol.525(8), pp.1778-1796
Main Author: Sousa‐Valente, João
Other Authors: Varga, Angelika , Torres‐Perez, Jose Vicente , Jenes, Agnes , Wahba, John , Mackie, Ken , Cravatt, Benjamin , Ueda, Natsuo , Tsuboi, Kazuhito , Santha, Peter , Jancso, Gabor , Tailor, Hiren , Avelino, António , Nagy, Istvan
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ID: ISSN: 0021-9967 ; E-ISSN: 1096-9861 ; DOI: 10.1002/cne.24154
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title: Inflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium‐sensitive N‐arachydonoylethanolamine‐synthesizing enzyme and related molecules in rat primary sensory neurons
format: Article
creator:
  • Sousa‐Valente, João
  • Varga, Angelika
  • Torres‐Perez, Jose Vicente
  • Jenes, Agnes
  • Wahba, John
  • Mackie, Ken
  • Cravatt, Benjamin
  • Ueda, Natsuo
  • Tsuboi, Kazuhito
  • Santha, Peter
  • Jancso, Gabor
  • Tailor, Hiren
  • Avelino, António
  • Nagy, Istvan
subjects:
  • Cannabinoid Type 1 Receptor
  • Fatty Acid Amide Hydrolase
  • Inflammation
  • Neuropathy
  • Pain
  • Transient Receptor Potential Vanilloid Type 1 Ion Channel
ispartof: Journal of Comparative Neurology, 01 June 2017, Vol.525(8), pp.1778-1796
description: Elevation of intracellular Ca concentration induces the synthesis of N‐arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N‐acylphosphatidylethanolamine phospholipase D (NAPE‐PLD) is the only known enzyme that synthesizes anandamide in a Ca‐dependent manner. NAPE‐PLD mRNA as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1), the inhibitory cannabinoid type 1 (CB1) receptor, and the main anandamide‐hydrolyzing enzyme fatty acid amide hydrolase (FAAH), are all expressed by subpopulations of nociceptive primary sensory neurons. Thus, NAPE‐PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain. Although the expression patterns of TRPV1, the CB1 receptor, and FAAH have been comprehensively elucidated, little is known about NAPE‐PLD expression in primary sensory neurons under physiological and pathological conditions. This study shows that NAPE‐PLD is expressed by about one‐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 differing but concerted changes in the expression pattern of NAPE‐PLD, the CB1 receptor, TRPV1, and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signaling system in a major proportion of nociceptive primary sensory neurons and that alterations in that autocrine signaling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain. The anandamide‐synthesising NAPE‐PLD, together with the anandamide‐responding CB1 receptor and TRPV1, and the anandamide‐hydrolysing FAAH, forms a signalling system, which responds to peripheral pathological processes and regulates the activity of a sub‐population of nociceptive primary sensory neurons. Hence, NAPE‐PLD could be the target for the development of novel analgesics.
language:
source:
identifier: ISSN: 0021-9967 ; E-ISSN: 1096-9861 ; DOI: 10.1002/cne.24154
fulltext: fulltext
issn:
  • 0021-9967
  • 00219967
  • 1096-9861
  • 10969861
url: Link


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titleInflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium‐sensitive N‐arachydonoylethanolamine‐synthesizing enzyme and related molecules in rat primary sensory neurons
creatorSousa‐Valente, João ; Varga, Angelika ; Torres‐Perez, Jose Vicente ; Jenes, Agnes ; Wahba, John ; Mackie, Ken ; Cravatt, Benjamin ; Ueda, Natsuo ; Tsuboi, Kazuhito ; Santha, Peter ; Jancso, Gabor ; Tailor, Hiren ; Avelino, António ; Nagy, Istvan
ispartofJournal of Comparative Neurology, 01 June 2017, Vol.525(8), pp.1778-1796
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subjectCannabinoid Type 1 Receptor ; Fatty Acid Amide Hydrolase ; Inflammation ; Neuropathy ; Pain ; Transient Receptor Potential Vanilloid Type 1 Ion Channel
descriptionElevation of intracellular Ca concentration induces the synthesis of N‐arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N‐acylphosphatidylethanolamine phospholipase D (NAPE‐PLD) is the only known enzyme that synthesizes anandamide in a Ca‐dependent manner. NAPE‐PLD mRNA as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1), the inhibitory cannabinoid type 1 (CB1) receptor, and the main anandamide‐hydrolyzing enzyme fatty acid amide hydrolase (FAAH), are all expressed by subpopulations of nociceptive primary sensory neurons. Thus, NAPE‐PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain. Although the expression patterns of TRPV1, the CB1 receptor, and FAAH have been comprehensively elucidated, little is known about NAPE‐PLD expression in primary sensory neurons under physiological and pathological conditions. This study shows that NAPE‐PLD is expressed by about one‐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 differing but concerted changes in the expression pattern of NAPE‐PLD, the CB1 receptor, TRPV1, and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signaling system in a major proportion of nociceptive primary sensory neurons and that alterations in that autocrine signaling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain. The anandamide‐synthesising NAPE‐PLD, together with the anandamide‐responding CB1 receptor and TRPV1, and the anandamide‐hydrolysing FAAH, forms a signalling system, which responds to peripheral pathological processes and regulates the activity of a sub‐population of nociceptive primary sensory neurons. Hence, NAPE‐PLD could be the target for the development of novel analgesics.
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titleInflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium‐sensitive N‐arachydonoylethanolamine‐synthesizing enzyme and related molecules in rat primary sensory neurons
descriptionElevation of intracellular Ca concentration induces the synthesis of N‐arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N‐acylphosphatidylethanolamine phospholipase D (NAPE‐PLD) is the only known enzyme that synthesizes anandamide in a Ca‐dependent manner. NAPE‐PLD mRNA as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1), the inhibitory cannabinoid type 1 (CB1) receptor, and the main anandamide‐hydrolyzing enzyme fatty acid amide hydrolase (FAAH), are all expressed by subpopulations of nociceptive primary sensory neurons. Thus, NAPE‐PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain. Although the expression patterns of TRPV1, the CB1 receptor, and FAAH have been comprehensively elucidated, little is known about NAPE‐PLD expression in primary sensory neurons under physiological and pathological conditions. This study shows that NAPE‐PLD is expressed by about one‐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 differing but concerted changes in the expression pattern of NAPE‐PLD, the CB1 receptor, TRPV1, and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signaling system in a major proportion of nociceptive primary sensory neurons and that alterations in that autocrine signaling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain. The anandamide‐synthesising NAPE‐PLD, together with the anandamide‐responding CB1 receptor and TRPV1, and the anandamide‐hydrolysing FAAH, forms a signalling system, which responds to peripheral pathological processes and regulates the activity of a sub‐population of nociceptive primary sensory neurons. Hence, NAPE‐PLD could be the target for the development of novel analgesics.
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titleInflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium‐sensitive N‐arachydonoylethanolamine‐synthesizing enzyme and related molecules in rat primary sensory neurons
authorSousa‐Valente, João ; Varga, Angelika ; Torres‐Perez, Jose Vicente ; Jenes, Agnes ; Wahba, John ; Mackie, Ken ; Cravatt, Benjamin ; Ueda, Natsuo ; Tsuboi, Kazuhito ; Santha, Peter ; Jancso, Gabor ; Tailor, Hiren ; Avelino, António ; Nagy, Istvan
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abstractElevation of intracellular Ca concentration induces the synthesis of N‐arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N‐acylphosphatidylethanolamine phospholipase D (NAPE‐PLD) is the only known enzyme that synthesizes anandamide in a Ca‐dependent manner. NAPE‐PLD mRNA as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1), the inhibitory cannabinoid type 1 (CB1) receptor, and the main anandamide‐hydrolyzing enzyme fatty acid amide hydrolase (FAAH), are all expressed by subpopulations of nociceptive primary sensory neurons. Thus, NAPE‐PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain. Although the expression patterns of TRPV1, the CB1 receptor, and FAAH have been comprehensively elucidated, little is known about NAPE‐PLD expression in primary sensory neurons under physiological and pathological conditions. This study shows that NAPE‐PLD is expressed by about one‐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 differing but concerted changes in the expression pattern of NAPE‐PLD, the CB1 receptor, TRPV1, and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signaling system in a major proportion of nociceptive primary sensory neurons and that alterations in that autocrine signaling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain. The anandamide‐synthesising NAPE‐PLD, together with the anandamide‐responding CB1 receptor and TRPV1, and the anandamide‐hydrolysing FAAH, forms a signalling system, which responds to peripheral pathological processes and regulates the activity of a sub‐population of nociceptive primary sensory neurons. Hence, NAPE‐PLD could be the target for the development of novel analgesics.
doi10.1002/cne.24154
pages1778-1796
date2017-06-01