Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

Local Anesthetics: Differential Sensitivity of Nerve Fibers

Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
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...
Local Anesthetics: Common Agents and Their Applications01:23

Local Anesthetics: Common Agents and Their Applications

Local anesthetics (LAs) are commonly used for various applications in medical and dental procedures. Some of the common agents used are cocaine, lidocaine, and bupivacaine.
Cocaine is an ester of benzoic acid and methylecgogine. It is used to anesthetize and vasoconstrict locally. Currently, it is used primarily for topical applications. It is beneficial for surgeries on the upper respiratory tract, providing anesthesia and shrinking the mucosa. Cocaine in the form of cocaine hydrochloride is...
Spasmolytic Agents: Chemical Classification01:29

Spasmolytic Agents: Chemical Classification

Spasmolytic agents are drugs used to alleviate muscle spasms and spasticity. They can be categorized into different chemical groups based on their mechanisms of action. Centrally acting spasmolytics primarily affect the spinal cord, while others directly target skeletal muscle cells.
A major class of centrally acting spasmolytics is the α2-agonist, such as tizanidine. These drugs bind to α2-adrenoceptors, inhibiting the release of the excitatory neurotransmitter glutamate. They also promote...

You might also read

Related Articles

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

Sort by
Same author

Therapy for acute nerve agent poisoning: An update.

Neurology. Clinical practice·2019
Same author

Sulfur mustard: a liquid, not a gas.

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America·2011
Same author

Case report: Long-term cognitive sequelae of sarin exposure.

Neurotoxicology·2009
Same author

Neurological problems of famous musicians: the classical genre.

Journal of child neurology·2009
Same author

Liquid sulfur mustard exposure.

Military medicine·2007
Same author

Vitamin D and Parkinson's disease--a hypothesis.

Movement disorders : official journal of the Movement Disorder Society·2007

Related Experiment Video

Updated: Jul 17, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Nerve agents.

Jonathan Newmark1

  • 1Deputy Joint Program Executive Officer for Medical Systems, Joint Program Executive Office for Chemical/Biological Defense, Falls Church, Virginia 22041-3203, USA. jonathan.newmark@us.army.mil

The Neurologist
|January 12, 2007
PubMed
Summary

Nerve agents cause severe poisoning by inhibiting acetylcholinesterase. Understanding nerve agent pathophysiology and treatment is vital for medical professionals to manage poisoning and prepare for chemical terrorism.

Area of Science:

  • Toxicology
  • Emergency Medicine
  • Neurology

Background:

  • Nerve agents are potent chemical warfare agents that inhibit acetylcholinesterase, leading to life-threatening cholinergic crisis.
  • Originally developed for military use, nerve agents pose a significant threat to civilian populations due to potential terrorist attacks.

Observation:

  • Acute nerve agent poisoning presents a complex clinical picture requiring prompt medical intervention.
  • Pyridostigmine bromide is approved for pretreatment against soman poisoning in military settings but has limited civilian application.

Findings:

  • Current civilian treatment protocols for acute nerve agent poisoning are largely adapted from military doctrine.
  • Effective management hinges on timely supportive care and appropriate antidotal administration.

More Related Videos

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

Related Experiment Videos

Last Updated: Jul 17, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

Implications:

  • Neurologists must be proficient in nerve agent toxicology and treatment to manage poisoned patients.
  • Medical communities need neurologists as resources for preparedness and response to chemical terrorism involving nerve agents.