Navigation überspringen
Universitätsbibliothek Heidelberg
Status: Bibliographieeintrag

Verfügbarkeit
Standort: ---
Exemplare: ---
heiBIB
 Online-Ressource
Verfasst von:Wang, Dan [VerfasserIn]   i
 Gao, Qi [VerfasserIn]   i
 Schäfer, Ina [VerfasserIn]   i
 Mörz, Handan [VerfasserIn]   i
 Hoheisel, Ulrich [VerfasserIn]   i
 Rohr, Karl [VerfasserIn]   i
 Greffrath, Wolfgang [VerfasserIn]   i
 Treede, Rolf-Detlef [VerfasserIn]   i
Titel:TRPM3-mediated dynamic mitochondrial activity in nerve growth factor-induced latent sensitization of chronic low back pain
Verf.angabe:Dan Wang, Qi Gao, Ina Schaefer, Handan Moerz, Ulrich Hoheisel, Karl Rohr, Wolfgang Greffrath, Rolf-Detlef Treede
E-Jahr:2022
Jahr:4 April 2022
Umfang:14 S.
Fussnoten:Gesehen am 19.12.2022
Titel Quelle:Enthalten in: Pain
Ort Quelle:New York, NY [u.a.] : Lippincott Williams and Wilkins, 1975
Jahr Quelle:2022
Band/Heft Quelle:163(2022), 11, Seite e1115-e1127
ISSN Quelle:1872-6623
Abstract:The transient receptor potential ion channel TRPM3 is highly prevalent on nociceptive dorsal root ganglion (DRG) neurons, but its functions in neuronal plasticity of chronic pain remain obscure. In an animal model of nonspecific low back pain (LBP), latent spinal sensitization known as nociceptive priming is induced by nerve growth factor (NGF) injection. Here, we address the TRPM3-associated molecular basis of NGF-induced latent spinal sensitization at presynaptic level by studying TRPM3-mediated calcium transients in DRG neurons. By investigating TRPM3-expressing HEK cells, we further show the dynamic mitochondrial activity downstream of TRPM3 activation. NGF enhances TRPM3 function, attenuates TRPM3 tachyphylaxis, and slows intracellular calcium clearance; TRPM3 activation triggers more mitochondrial calcium loading than depolarization does, causing a steady-state mitochondrial calcium elevation and a delayed recovery of cytosolic calcium; mitochondrial calcium buffering accounts for approximately 40% of calcium influx subsequent to TRPM3 activation. TRPM3 activation provokes an outbreak of pulsatile superoxide production (mitoflash) that comes in the form of a surge in frequency being tunable. We suggest that mitoflash pulsations downstream of TRPM3 activation might be an early signaling event initiating pain sensitization. Tuning of mitoflash activity would be a novel bottom-up therapeutic strategy for chronic pain conditions such as LBP and beyond.
DOI:doi:10.1097/j.pain.0000000000002642
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1097/j.pain.0000000000002642
 Volltext: https://journals.lww.com/pain/Fulltext/2022/11000/TRPM3_mediated_dynamic_mitochondrial_activity_in.21.aspx
 DOI: https://doi.org/10.1097/j.pain.0000000000002642
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1827888555
Verknüpfungen:→ Zeitschrift

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/68999352   QR-Code
zum Seitenanfang