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

Action Potential

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...

Ligand-gated Ion Channels

Ligand-gated Ion Channels

Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...

You might also read

Related Articles

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

Sort by

Same author

<i>In vitro</i> evaluation of monoamine oxidase and acetylcholinesterase enzyme activities of <i>Capparis cartilaginea</i> Decne.

Natural product research·2026

Same author

N-Lactoyl Phenylalanine Disrupts Insulin Signaling, Induces Inflammation, and Impairs Mitochondrial Respiration in Cell Models.

Cells·2025

Same author

Glycosyltransferases: glycoengineers in human milk oligosaccharide synthesis and manufacturing.

Frontiers in molecular biosciences·2025

Same author

Acetylcholinesterase and monoamine oxidase inhibitory activities of <i>Pistacia falcata</i> Becc. ex Martelli extract.

Natural product research·2025

Same author

Interactions of human milk oligosaccharides with the immune system.

Frontiers in immunology·2025

Same author

Exploring the Regulation of Cytochrome P450 in SH-SY5Y Cells: Implications for the Onset of Neurodegenerative Diseases.

International journal of molecular sciences·2024

Search research articles

Related Experiment Video

Updated: Jul 4, 2026

Conventional and Threshold-Tracking Transcranial Magnetic Stimulation Tests for Single-handed Operation

Conventional and Threshold-Tracking Transcranial Magnetic Stimulation Tests for Single-handed Operation

Published on: August 16, 2021

Complex I and energy thresholds in the brain.

Rashmi U Pathak¹, Gavin P Davey

¹School of Biochemistry and Immunology and Trinity College Institute of Neuroscience, Trinity College Dublin, Ireland.

Biochimica Et Biophysica Acta

|June 4, 2008

Summary

Mitochondrial electron transport chain (ETC) complex I deficiencies contribute to Parkinson's disease by disrupting brain energy metabolism. Research is ongoing to understand these complex I defects and their role in neurodegeneration.

More Related Videos

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Published on: March 31, 2016

Combining a Breath-Synchronized Olfactometer with Brain Simulation to Study the Impact of Odors on Corticospinal Excitability and Effective Connectivity

Combining a Breath-Synchronized Olfactometer with Brain Simulation to Study the Impact of Odors on Corticospinal Excitability and Effective Connectivity

Published on: January 19, 2024

Related Experiment Videos

Last Updated: Jul 4, 2026

Conventional and Threshold-Tracking Transcranial Magnetic Stimulation Tests for Single-handed Operation

Conventional and Threshold-Tracking Transcranial Magnetic Stimulation Tests for Single-handed Operation

Published on: August 16, 2021

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Published on: March 31, 2016

Combining a Breath-Synchronized Olfactometer with Brain Simulation to Study the Impact of Odors on Corticospinal Excitability and Effective Connectivity

Combining a Breath-Synchronized Olfactometer with Brain Simulation to Study the Impact of Odors on Corticospinal Excitability and Effective Connectivity

Published on: January 19, 2024

Area of Science:

Neuroscience
Biochemistry
Cell Biology

Background:

Mitochondrial electron transport chain (ETC) deficiencies are linked to impaired energy metabolism and neurodegeneration.
Reduced complex I activity in Parkinson's disease (PD) is hypothesized to cause bioenergetic dysfunction, leading to dopaminergic neuron loss.
Brain mitochondria heterogeneity complicates the assessment of ETC dysfunction, as synaptic and non-synaptic mitochondria exhibit different bioenergetic properties.

Purpose of the Study:

To explore the relationship between complex I activity and brain energy metabolism.
To investigate the nature of complex I defects in the context of Parkinson's disease.

Main Methods:

Review of existing literature on mitochondrial function, energy metabolism, and Parkinson's disease.
Analysis of studies investigating complex I activity in brain tissue.
Discussion of mitochondrial heterogeneity and its impact on bioenergetic assessments.

Main Results:

Complex I deficiencies are implicated in the bioenergetic dysfunction observed in Parkinson's disease.
Heterogeneity of brain mitochondria presents challenges in accurately measuring ETC function.
The precise molecular mechanisms driving complex I deficiencies in the parkinsonian brain remain largely unknown.

Conclusions:

Understanding complex I activity and its defects is crucial for elucidating the pathogenesis of Parkinson's disease.
Further research is needed to clarify the molecular underpinnings of complex I dysfunction in neurodegeneration.
Addressing mitochondrial dysfunction may offer therapeutic strategies for Parkinson's disease.