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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

  1. Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA
  2. 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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