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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

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Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
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Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

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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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Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

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Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
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Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

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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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Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...
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Factors Influencing Drug Absorption: Disease States and Pharmacology01:25

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Multiple disease states can significantly influence the oral drug absorption process by affecting blood flow and the functionality of the gastrointestinal (GI) system. Various GI diseases, including conditions that alter GI motility, such as diarrhea, decreased acid secretions (achlorhydria), and infections, have been associated with reduced drug absorption.
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Chemotherapy-Induced Neuropathy Affecting the Gastrointestinal Tract.

Gema Vera1,2,3, Kulmira Nurgali4,5,6, Raquel Abalo1,2,3,7,8

  • 1Department of Basic Health Sciences, University Rey Juan Carlos (URJC), Alcorcón, Spain.

Neurogastroenterology and Motility
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Summary

Cancer treatments like chemotherapy can cause nerve damage in the gut, leading to long-term gastrointestinal problems. This chemotherapy-induced enteric neuropathy affects gut function and the brain-gut axis.

Keywords:
brain–gut axiscancerchemotherapyentericgastrointestinalneurotoxicity

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Area of Science:

  • Neuroscience
  • Gastroenterology
  • Oncology

Background:

  • Cancer survivorship is increasing, presenting new challenges.
  • Cancer treatments cause significant gastrointestinal (GI) side effects, both acute and chronic.
  • These side effects impact patient quality of life and survivorship.

Purpose of the Study:

  • To review the neurotoxic effects of chemotherapy on the enteric nervous system (ENS) and gut extrinsic innervation.
  • To explore how these neurotoxic effects contribute to long-term GI dysfunctions.
  • To highlight the impact on the brain-gut axis (BGA) and identify research gaps.

Main Methods:

  • Literature review focusing on animal models and human studies.
  • Analysis of research on chemotherapy-induced enteric neuropathy (CIEN).
  • Examination of studies on chemotherapy's effects on visceral sensitivity and gut innervation.

Main Results:

  • Chemotherapy can induce enteric neuropathy (CIEN), characterized by reduced nerve cell/fiber density and altered neuronal subpopulations in the ENS.
  • CIEN affects both the myenteric and submucosal plexuses, impacting GI motor function.
  • Emerging evidence suggests chemotherapy also affects extrinsic gut innervation, potentially leading to BGA disorders.

Conclusions:

  • Cancer therapies, particularly chemotherapy, induce neuropathic effects on intrinsic and extrinsic GI innervation.
  • These neurotoxic effects significantly impact GI function and the brain-gut axis.
  • This is an under-investigated area requiring further research.