NGF Enhances CGRP Release Evoked by Capsaicin from Rat Trigeminal Neurons: Differential Inhibition by SNAP-25-Cleaving Proteases

Autor:	Mariia Belinskaia, Tomas Zurawski, Seshu Kumar Kaza, Caren Antoniazzi, J. Oliver Dolly, Gary W. Lawrence
Rok vydání:	2022
Předmět:	Sensory Receptor Cells Synaptosomal-Associated Protein 25 QH301-705.5 chimeric neurotoxin trigeminal ganglion neurons capsaicin calcitonin gene-related peptide Article Exocytosis nerve growth factor Catalysis Inorganic Chemistry nociceptor sensitisation Animals botulinum neurotoxins Calcium Signaling Botulinum Toxins Type A Biology (General) Physical and Theoretical Chemistry QD1-999 TRPV1 Molecular Biology Spectroscopy Dose-Response Relationship Drug Organic Chemistry General Medicine Rats Computer Science Applications Chemistry Trigeminal Ganglion nervous system Proteolysis Calcium
Zdroj:	International Journal of Molecular Sciences; Volume 23; Issue 2; Pages: 892 International Journal of Molecular Sciences, Vol 23, Iss 892, p 892 (2022) International Journal of Molecular Sciences
ISSN:	1422-0067
DOI:	10.3390/ijms23020892
Popis:	Nerve growth factor (NGF) is known to intensify pain in various ways, so perturbing pertinent effects without negating its essential influences on neuronal functions could help the search for much-needed analgesics. Towards this goal, cultured neurons from neonatal rat trigeminal ganglia—a locus for craniofacial sensory nerves—were used to examine how NGF affects the Ca2+-dependent release of a pain mediator, calcitonin gene-related peptide (CGRP), that is triggered by activating a key signal transducer, transient receptor potential vanilloid 1 (TRPV1) with capsaicin (CAP). Measurements utilised neurons fed with or deprived of NGF for 2 days. Acute re-introduction of NGF induced Ca2+-dependent CGRP exocytosis that was inhibited by botulinum neurotoxin type A (BoNT/A) or a chimera of/E and/A (/EA), which truncated SNAP-25 (synaptosomal-associated protein with Mr = 25 k) at distinct sites. NGF additionally caused a Ca2+-independent enhancement of the neuropeptide release evoked by low concentrations (2+-dependent exocytosis at different intensities of stimulation.
Databáze:	OpenAIRE
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