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Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
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5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Mechanosensory encoding dysfunction emerges from cancer-chemotherapy interaction.

Stephen N Housley1,2, Paul Nardelli1, Travis M Rotterman1

  • 1School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, United States.

Frontiers in Molecular Biosciences
|December 12, 2022
PubMed
Summary

Cancer and chemotherapy worsen nerve damage, leading to more severe chemotherapy-induced neural disorders (CIND). This study reveals that cancer amplifies chemotherapy

Keywords:
cancer treatmentchemotherapycutaneousneurotoxicityproprioceptionsensorimotor abnormalitiessensory encoding

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Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Chemotherapy-induced neural disorders (CIND) cause persistent sensory, motor, and cognitive disabilities in cancer survivors.
  • Existing treatments offer limited relief for CIND, highlighting the need for understanding underlying mechanisms.
  • Preclinical studies suggest cancer itself may exacerbate chemotherapy's neurotoxic effects.

Purpose of the Study:

  • To investigate whether cancer amplifies chemotherapy-induced sensory defects across various low threshold mechanosensory receptor (LTMR) submodalities.
  • To compare the independent and combined effects of cancer and chemotherapy on neural encoding of sensory stimuli.
  • To identify potential therapeutic targets for mitigating CIND severity.

Main Methods:

  • Electrophysiological recordings in rats to measure action potential firing patterns in multiple LTMR types.
  • Comparison of neural responses in healthy rats, cancer-bearing rats, and rats treated with oxaliplatin (chemotherapy).
  • Analysis of encoding defects under independent and combined conditions of cancer and chemotherapy.

Main Results:

  • Chemotherapy alone caused aberrant encoding in LTMRs.
  • Cancer alone also induced sensory encoding defects in some LTMRs.
  • The combination of cancer and chemotherapy significantly worsened encoding aberrations, particularly in slowly adapting LTMRs.

Conclusions:

  • The severity of CIND is modulated by a codependent interaction between chemotherapy side effects and cancer's systemic processes.
  • Cancer amplifies chemotherapy-induced neural encoding defects across multiple mechanosensory pathways.
  • Targeting cancer-mediated amplification of neurotoxicity may offer a novel therapeutic strategy for reducing CIND.