Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

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

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: 5-HT3 Receptor Antagonists

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,...

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

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: Cannabinoids

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,...

Cryptococcal Meningitis

Cryptococcal Meningitis

Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...

Combination Therapies and Personalized Medicine

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Neurological complications of current and emerging CAR-T cell therapies.

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics·2026

Same author

Cognitive dysfunction associated with cellular immunotherapy for cancer.

Neuro-oncology advances·2026

Same author

Non-ICANS Neurologic Events in Patients With Relapsed/Refractory Multiple Myeloma Treated With Ciltacabtagene Autoleucel: Clinical Presentation and Management in CARTITUDE Studies.

Clinical lymphoma, myeloma & leukemia·2026

Same author

Immunodeficiency-associated primary CNS lymphomas: an International Primary CNS Lymphoma Collaborative Group study.

Blood·2026

Same author

Clinical Manifestations of Primary CNS T-Cell Lymphoma: A Retrospective Study of Histopathologic, Molecular, and Neuroimaging Features.

Neurology·2026

Same author

Longitudinal changes of neurocognitive function and ALPS-index in patients with brain tumors receiving brain irradiation.

Journal of neuro-oncology·2026

Search research articles

Related Experiment Video

Updated: Jun 9, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Chemotherapy associated central nervous system damage.

Jörg Dietrich¹

¹Department of Neurology, MGH Cancer Center, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Yawkey 9E, Boston, Massachusetts 02114, USA. jdietrich1@partners.org

Advances in Experimental Medicine and Biology

|August 27, 2010

Summary

This summary is machine-generated.

Chemotherapy can harm the central nervous system (CNS), causing acute and delayed neurotoxicity in cancer survivors. Recent research is revealing the cell-biological mechanisms behind these neurological complications, like cognitive decline and brain atrophy.

More Related Videos

Assessment of Chimeric Antigen Receptor T Cell-Associated Toxicities Using an Acute Lymphoblastic Leukemia Patient-Derived Xenograft Mouse Model

Assessment of Chimeric Antigen Receptor T Cell-Associated Toxicities Using an Acute Lymphoblastic Leukemia Patient-Derived Xenograft Mouse Model

Published on: February 10, 2023

Related Experiment Videos

Last Updated: Jun 9, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Assessment of Chimeric Antigen Receptor T Cell-Associated Toxicities Using an Acute Lymphoblastic Leukemia Patient-Derived Xenograft Mouse Model

Assessment of Chimeric Antigen Receptor T Cell-Associated Toxicities Using an Acute Lymphoblastic Leukemia Patient-Derived Xenograft Mouse Model

Published on: February 10, 2023

Area of Science:

Neuroscience
Oncology
Toxicology

Background:

Chemotherapy frequently causes central nervous system (CNS) damage, leading to acute and delayed neurotoxicity.
This neurotoxicity is a significant concern for cancer survivors, manifesting as diverse neurological syndromes.
Increasing cancer survival rates and aggressive treatments correlate with a rising incidence of neurological complications.

Purpose of the Study:

To explore the underlying cell-biological mechanisms of chemotherapy-induced neurotoxicity.
To provide explanations for delayed neurological complications observed in cancer patients.

Main Methods:

Review of recent scientific literature on chemotherapy-induced neurotoxicity.
Analysis of cell-biological pathways implicated in neurological damage.

Main Results:

Chemotherapy's impact on the CNS includes neuro-vascular issues, focal deficits, and generalized decline.
Delayed effects such as cognitive impairment, cortical atrophy, and white matter abnormalities are increasingly recognized.
Emerging research is elucidating the cellular basis for these neurotoxic syndromes.

Conclusions:

Understanding the cell-biological mechanisms is crucial for managing chemotherapy-induced neurotoxicity.
This knowledge can inform strategies to mitigate long-term neurological effects in cancer survivors.
Further research into these mechanisms is vital for improving patient outcomes and quality of life.