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Related Concept Videos

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

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

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

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

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.
Phenothiazines, such as prochlorperazine...
Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

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,...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

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.
Two synthetic agonists of THC,...
Diphtheria01:28

Diphtheria

Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...

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Updated: Jun 6, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Chemotherapy-induced peripheral neurotoxicity.

Guido Cavaletti1, Paola Marmiroli

  • 1Department of Neuroscience and Biomedical Technologies, University of Milano-Bicocca, Via Cadore 48, Monza, Italy. guido.cavaletti@unimib.it

Nature Reviews. Neurology
|November 10, 2010
PubMed
Summary

Chemotherapy-induced peripheral neurotoxicity (CIPN) significantly impacts cancer patients

Area of Science:

  • Oncology
  • Neuroscience
  • Pharmacology

Background:

  • Chemotherapy-induced peripheral neurotoxicity (CIPN) is a frequent, severe adverse effect of cancer treatment, impacting daily life.
  • CIPN arises from various chemotherapy agents used for solid and hematological malignancies.
  • Mechanisms of CIPN are not fully understood, with drug structure potentially influencing pathogenesis.

Purpose of the Study:

  • To review the mechanistic and clinical aspects of chemotherapy-induced peripheral neurotoxicity.
  • To discuss controversial issues including onset mechanisms, patient assessment, and current treatment strategies.

Main Methods:

  • Comprehensive literature review of mechanistic and clinical studies on CIPN.
  • Analysis of neurotoxic compound properties and their relation to neurotoxicity variations.

Related Experiment Videos

Last Updated: Jun 6, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

  • Evaluation of current neuroprotection and treatment options for CIPN.

    • Main Results:

    • CIPN presents significant challenges, with limited preventive or ameliorative pharmacological options.
    • Chemotherapy schedule modifications are often necessary, potentially compromising optimal cancer treatment.
    • Symptomatic therapies for CIPN are frequently ineffective.

    Conclusions:

    • Understanding CIPN mechanisms and clinical impact is crucial for patient management.
    • Current neuroprotection and treatment strategies for CIPN are insufficient.
    • Further research is needed to develop effective interventions for CIPN.