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

8.9K
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...
8.9K
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

353
Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
353
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

1.6K
Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
1.6K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

2.3K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
2.3K
Skeletal Muscle Relaxants: Adverse Effects01:21

Skeletal Muscle Relaxants: Adverse Effects

401
Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
Unlike...
401
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

10.1K
When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
10.1K

You might also read

Related Articles

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

Sort by
Same author

Cancer-derived extracellular succinate: a driver of cancer metastasis.

Journal of biomedical science·2022
Same author

Association of Tumor Hydroxyindole O-Methyltransferase and Serum 5-Methoxytryptophan with Long-Term Survival of Hepatocellular Carcinoma.

Cancers·2021
Same author

Cytoguardin: A Tryptophan Metabolite against Cancer Growth and Metastasis.

International journal of molecular sciences·2021
Same author

Control of Mesenchymal Stromal Cell Senescence by Tryptophan Metabolites.

International journal of molecular sciences·2021
Same author

5-methoxytryptophan: an arsenal against vascular injury and inflammation.

Journal of biomedical science·2020
Same author

Restoration of hydroxyindole <i>O</i>-methyltransferase levels in human cancer cells induces a tryptophan-metabolic switch and attenuates cancer progression.

The Journal of biological chemistry·2018

Related Experiment Video

Updated: Jul 23, 2025

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function
11:47

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function

Published on: January 22, 2017

10.6K

Extracellular Succinate: A Physiological Messenger and a Pathological Trigger.

Kenneth K Wu1,2,3

  • 1Institute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli County 35053, Taiwan.

International Journal of Molecular Sciences
|July 14, 2023
PubMed
Summary
This summary is machine-generated.

Extracellular succinate plays dual roles in health and disease. This review explores how succinate signaling via succinate receptor-1 (SUCNR-1) impacts tissue adaptation and pathology, guiding therapeutic strategies.

Keywords:
extracellular succinatefibrosisinflammationmyocardial infarctionsuccinate dehydrogenasesuccinate receptor-1

More Related Videos

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
11:12

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Published on: September 13, 2024

449
Inner Mitochondrial Membrane Sensitivity to Na+ Reveals Partially Segmented Functional CoQ Pools
05:27

Inner Mitochondrial Membrane Sensitivity to Na+ Reveals Partially Segmented Functional CoQ Pools

Published on: July 20, 2022

1.9K

Related Experiment Videos

Last Updated: Jul 23, 2025

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function
11:47

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function

Published on: January 22, 2017

10.6K
Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
11:12

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Published on: September 13, 2024

449
Inner Mitochondrial Membrane Sensitivity to Na+ Reveals Partially Segmented Functional CoQ Pools
05:27

Inner Mitochondrial Membrane Sensitivity to Na+ Reveals Partially Segmented Functional CoQ Pools

Published on: July 20, 2022

1.9K

Area of Science:

  • Biochemistry and Molecular Biology
  • Cellular Physiology
  • Immunology and Inflammation

Background:

  • Skeletal muscle cells release succinate into extracellular space during physiological stress like exercise and cold exposure.
  • Conversely, toxins and injury promote succinate secretion, leading to tissue damage, inflammation, and fibrosis.
  • Extracellular succinate acts through cell surface succinate receptor-1 (SUCNR-1), influencing cellular signaling and gene expression.

Purpose of the Study:

  • To review the current understanding of extracellular succinate's role in both physiological and pathological conditions.
  • To elucidate the mechanisms by which succinate signaling impacts cellular function and tissue outcomes.
  • To discuss the therapeutic implications of targeting the succinate-SUCNR-1 axis.

Main Methods:

  • Literature review of studies investigating extracellular succinate.
  • Analysis of research on SUCNR-1 signaling pathways.
  • Synthesis of findings related to succinate's effects in health and disease models.

Main Results:

  • Succinate mediates adaptive responses in skeletal muscle under physiological stress.
  • Succinate contributes to tissue injury, inflammation, and fibrosis induced by external insults.
  • SUCNR-1 activation is central to both beneficial and detrimental succinate actions.

Conclusions:

  • The dual role of SUCNR-1 in physiological adaptation and pathological processes presents challenges for drug development.
  • Further research is needed to differentiate the specific actions of succinate in various contexts.
  • Targeting the succinate-SUCNR-1 pathway holds potential for novel therapeutic interventions in diseases involving inflammation and fibrosis.