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

Chemical Synapses01:26

Chemical Synapses

10.9K
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
10.9K
Chemical Synapses01:26

Chemical Synapses

9.5K
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
9.5K
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

5.9K
The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
5.9K
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

53
The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
53
The Neuromuscular Junction01:19

The Neuromuscular Junction

17.6K
The nervous system consists of complex motor neuron circuits, including upper motor neurons originating from the cerebral cortex and lower motor neurons starting in the spinal cord, coordinating both voluntary and involuntary movements. Among these, somatic motor neurons activate skeletal muscles and are classified into alpha, beta, and gamma types. Alpha neurons are vital for voluntary movement coordination, while gamma neurons adjust muscle spindle sensitivity, and the function of beta...
17.6K
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

3.5K
Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
3.5K

You might also read

Related Articles

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

Sort by
Same author

Challenges and Design Strategies for Stable Zinc Anodes in Rechargeable Zinc Batteries.

Small (Weinheim an der Bergstrasse, Germany)·2025
Same author

Incorporating the International Council of Nurses' Competencies Into the Nursing Program Curriculum.

The Journal of nursing education·2025
Same author

Special Issue: Creating Competent Disaster Nurses.

The Journal of nursing education·2025
Same author

Stabilizing Dye-Sensitized Upconversion Hybrids by Cyclooctatetraene.

Nano letters·2024
Same author

Aggregation-Induced Emission of Naphthalene Diimides: Effect of Chain Length on Liquid and Solid-Phase Emissive Properties.

Chemistry, an Asian journal·2024
Same author

Retraction of "A Core-Substituted Naphthalene Diimide Fluoride Sensor".

Organic letters·2024

Related Experiment Video

Updated: May 1, 2026

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration
06:35

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration

Published on: June 15, 2018

22.7K

Motor neuron disease: a chemical perspective.

Laura K Wood1, Steven J Langford

  • 1School of Chemistry, Monash University , Clayton, Victoria 3800, Australia.

Journal of Medicinal Chemistry
|April 4, 2014
PubMed
Summary

This perspective explores the causes of neurodegenerative diseases, focusing on amyotrophic lateral sclerosis (ALS). It details pathways leading to neuron death and discusses strategies to halt these processes.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathogenesis

Background:

  • Neurodegenerative diseases involve neuron dysfunction and death.
  • Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder.
  • Apoptotic pathways play a critical role in neuron loss.

Purpose of the Study:

  • To provide a background on neurodegenerative disease pathogenesis.
  • To specifically detail the pathogenesis of amyotrophic lateral sclerosis (ALS).
  • To overview pathways leading to premature neuronal apoptosis and discuss intervention strategies.

Main Methods:

  • Literature review and synthesis of existing research.
  • Analysis of genetic and sporadic pathways in neurodegeneration.
  • Review of current and proposed therapeutic approaches.

More Related Videos

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons
07:43

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons

Published on: January 7, 2019

6.4K
Electrophysiological Motor Unit Number Estimation MUNE Measuring Compound Muscle Action Potential CMAP in Mouse Hindlimb Muscles
09:07

Electrophysiological Motor Unit Number Estimation MUNE Measuring Compound Muscle Action Potential CMAP in Mouse Hindlimb Muscles

Published on: September 25, 2015

23.9K

Related Experiment Videos

Last Updated: May 1, 2026

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration
06:35

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration

Published on: June 15, 2018

22.7K
Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons
07:43

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons

Published on: January 7, 2019

6.4K
Electrophysiological Motor Unit Number Estimation MUNE Measuring Compound Muscle Action Potential CMAP in Mouse Hindlimb Muscles
09:07

Electrophysiological Motor Unit Number Estimation MUNE Measuring Compound Muscle Action Potential CMAP in Mouse Hindlimb Muscles

Published on: September 25, 2015

23.9K

Main Results:

  • Identified multiple genetic and sporadic pathways contributing to neurodegeneration.
  • Highlighted the role of premature apoptotic pathway activation in neurons.
  • Summarized diverse therapeutic strategies targeting neuronal apoptosis.

Conclusions:

  • Understanding disease pathways is crucial for developing effective treatments.
  • Targeting apoptotic pathways offers potential therapeutic avenues for ALS.
  • Further research is needed to translate these approaches into clinical practice.