Yu.M. USACHEV, Yu.V. MEDVEDEVA (2020) 'TRPV1-MEDIATED PRESYNAPTIC SIGNALING IN SENSORY NEURONS' in O.A. Krishtal, E.A. Lukyanetz (Eds.), ESSAYS ON NEUROPHYSIOLOGY BY PLATON KOSTYUK AND HIS STUDENTS, AKADEMPERIODYKA, pp. 190-197
TRPV1-MEDIATED PRESYNAPTIC SIGNALING IN SENSORY NEURONS
Yu.M. USACHEV1, Yu.V. MEDVEDEVA2
- Department of Pharmacology, University of Iowa Carver
College of Medicine, Iowa City, Iowa 52242, USA
- Department of Neurology, University of California, Irvine, CA 92697, USA
DOI: https://doi.org/10.15407/biph.books.EssNeur.190

Abstract
Transient receptor potential vanilloid 1 (TRPV1) is a key molecular sensor for noxious stimuli in primary sensory neurons. Activation of TRPV1 by capsaicin or endogenous agonists induces a robust and prolonged elevation of presynaptic intracellular calcium
[Ca2+]i, leading to sustained synaptic activity. Using patch-clamp recordings and calcium imaging in dorsal root ganglion (DRG) and spinal cord (SC) co-cultures, we demonstrated that TRPV1-mediated calcium entry primarily drives synaptic facilitation, independent of voltage-gated calcium channels. Mitochondria play a crucial role in shaping this response by buffering and gradually releasing calcium, thus extending synaptic activity beyond the initial stimulus. Blocking mitochondrial calcium uptake or release significantly altered TRPV1-induced neurotransmission, highlighting the role of intracellular calcium cycling in prolonged synaptic facilitation. These findings provide insights into TRPV1-mediated presynaptic signaling mechanisms and their implications for pain processing.
Keywords:
TRPV1, presynaptic calcium, synaptic activity, mitochondria, glutamate release, capsaicin, dorsal root ganglion, spinal cord, neurotransmission, pain signaling
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