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

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...

You might also read

Related Articles

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

Sort by
Same author

A systematic review of the potential neurotoxicity of micro-and nanoplastics: the known and unknown.

Particle and fibre toxicology·2025
Same author

Deubiquitinating Enzyme UCH-L1 Regulates Neuronal Ca<sup>2+</sup> Signaling.

ACS chemical neuroscience·2025
Same author

Extracellular ATP regulates phagocytic activity, mitochondrial respiration, and cytokine secretion of human astrocytic cells.

Purinergic signalling·2025
Same author

Extracellular mixed histones are neurotoxic and modulate select neuroimmune responses of glial cells.

PloS one·2024
Same author

ROS-dependent degeneration of human neurons induced by environmentally relevant levels of micro- and nanoplastics of diverse shapes and forms.

Journal of hazardous materials·2024
Same author

Acetylcholine synergizes with netrin-1 to drive persistent firing in the entorhinal cortex.

Cell reports·2024

Related Experiment Video

Updated: May 30, 2026

Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain
09:50

Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain

Published on: October 29, 2017

Hyperforin changes the zinc-storage capacities of brain cells.

Julien Gibon1, Pierre Richaud, Alexandre Bouron

  • 1UMR CNRS 5249, Grenoble, France.

Neuropharmacology
|August 23, 2011
PubMed
Summary

Hyperforin, a plant extract, alters brain cell zinc and calcium stores and influences metallothionein expression. Chronic exposure impacts brain sulfur content and thiol status, suggesting changes in zinc storage capacity.

More Related Videos

Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay
07:55

Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay

Published on: June 2, 2023

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining
07:32

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining

Published on: May 23, 2025

Related Experiment Videos

Last Updated: May 30, 2026

Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain
09:50

Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain

Published on: October 29, 2017

Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay
07:55

Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay

Published on: June 2, 2023

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining
07:32

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining

Published on: May 23, 2025

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Hyperforin is a plant extract known to affect mitochondrial function.
  • It is recognized for its ability to release zinc (Zn2+) and calcium (Ca2+) from organelles.
  • Understanding its impact on brain cells is crucial for potential therapeutic applications.

Purpose of the Study:

  • To investigate the effects of chronic hyperforin treatment on brain cells.
  • To examine changes in intracellular ion pools (Ca2+, Zn2+) and metallothionein (MT) expression.
  • To assess the impact on brain sulfur content and thiol status.

Main Methods:

  • In vitro studies using dissociated cortical neurons treated with hyperforin.
  • Live-cell imaging with fluorescent probes (FluoZin-3, Fluo-4) to monitor ion dynamics.
  • Quantitative PCR to analyze metallothionein mRNA expression.
  • In vivo studies involving chronic hyperforin administration to mice.

Main Results:

  • Hyperforin treatment reduced sensitive Ca2+ and Zn2+ pools but increased a specific Zn2+ pool.
  • Metallothionein (MT) mRNA levels increased in neurons, dependent on zinc availability.
  • Chronic hyperforin administration in mice elevated brain sulfur content and MT gene expression.
  • Long-term treatment did not alter overall brain calcium or zinc levels.

Conclusions:

  • Hyperforin influences the size of intracellular Zn2+ pools and MT expression in a zinc-dependent manner.
  • Chronic hyperforin exposure alters brain cellular sulfur content and thiol status.
  • The findings suggest hyperforin modifies brain cell Zn-storage capacity and interferes with cellular thiol balance.