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

Autor: Jose V. Torres-Perez, Hiren Tailor, Angelika Varga, Ken Mackie, Natsuo Ueda, Kazuhito Tsuboi, Agnes Jenes, João Sousa-Valente, John Wahba, Gábor Jancsó, António Avelino, Péter Sántha, Benjamin F. Cravatt, István Nagy
Rok vydání: 2017
Předmět:
Male
Nociception
0301 basic medicine
Cannabinoid receptor
medicine.medical_treatment
Nociceptive Pain
Mice
chemistry.chemical_compound
Transient receptor potential channel
0302 clinical medicine
Dorsal root ganglion
Fatty acid amide hydrolase
Image Processing
Computer-Assisted
Elméleti orvostudományok
In Situ Hybridization
Fluorescence
Microscopy
Confocal
Reverse Transcriptase Polymerase Chain Reaction
General Neuroscience
Axotomy
Orvostudományok
Anandamide
Immunohistochemistry
medicine.anatomical_structure
lipids (amino acids
peptides
and proteins)
psychological phenomena and processes
Signal Transduction
Sensory Receptor Cells
Polyunsaturated Alkamides
Blotting
Western
TRPV1
Arachidonic Acids
Biology
03 medical and health sciences
Phospholipase D
medicine
Animals
Rats
Wistar
Autocrine signalling
Inflammation
Rats
Mice
Inbred C57BL
Disease Models
Animal
Spinal Nerves
030104 developmental biology
nervous system
chemistry
Cannabinoid
Neuroscience
030217 neurology & neurosurgery
Endocannabinoids
Zdroj: Journal of Comparative Neurology. 525:1778-1796
ISSN: 0021-9967
DOI: 10.1002/cne.24154
Popis: Elevation of intracellular Ca2+ 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 Ca2+ -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.
Databáze: OpenAIRE
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