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

Regulation of Metabolism

Regulation of Metabolism

Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...

Mitochondrial Membranes

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...

Mitochondria

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

You might also read

Related Articles

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

Sort by

Same author

Both Nuclear and Membrane Estrogen Receptor Alpha Impact the Expression of Estrogen Receptors and Plasticity Markers in the Mouse Hypothalamus and Hippocampus.

Biology·2023

Same author

Sleep Deprivation and Circadian Disruption Stress, Allostasis, and Allostatic Load.

Sleep medicine clinics·2022

Same author

Sex and chronic stress alter the distribution of glutamate receptors within rat hippocampal CA3 pyramidal cells following oxycodone conditioned place preference.

Neurobiology of stress·2022

Same author

Corticosterone induces discrete epigenetic signatures in the dorsal and ventral hippocampus that depend upon sex and genotype: focus on methylated Nr3c1 gene.

Translational psychiatry·2022

Same author

Genomic modules and intramodular network concordance in susceptible and resilient male mice across models of stress.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology·2021

Same author

Acute Delta 9-tetrahydrocannabinol administration differentially alters the hippocampal opioid system in adult female and male rats.

Synapse (New York, N.Y.)·2021

Search research articles

Related Experiment Video

Updated: Jun 25, 2026

Mitochondrial Preparation from Microglia for Glycan Analysis

Mitochondrial Preparation from Microglia for Glycan Analysis

Published on: May 30, 2025

Dynamic regulation of mitochondrial function by glucocorticoids.

Jing Du¹, Yun Wang, Richard Hunter

¹Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.

Proceedings of the National Academy of Sciences of the United States of America

|February 10, 2009

Summary

Glucocorticoids exhibit a biphasic effect on neural plasticity and mitochondrial function. Low doses are neuroprotective, while high doses increase neuronal toxicity, impacting cellular resilience.

More Related Videos

High-Resolution Fluorespirometry to Assess Dynamic Changes in Mitochondrial Membrane Potential in Human Immune Cells

High-Resolution Fluorespirometry to Assess Dynamic Changes in Mitochondrial Membrane Potential in Human Immune Cells

Published on: May 24, 2024

Related Experiment Videos

Last Updated: Jun 25, 2026

Mitochondrial Preparation from Microglia for Glycan Analysis

Mitochondrial Preparation from Microglia for Glycan Analysis

Published on: May 30, 2025

High-Resolution Fluorespirometry to Assess Dynamic Changes in Mitochondrial Membrane Potential in Human Immune Cells

High-Resolution Fluorespirometry to Assess Dynamic Changes in Mitochondrial Membrane Potential in Human Immune Cells

Published on: May 24, 2024

Area of Science:

Neuroscience
Cell Biology
Endocrinology

Background:

Glucocorticoids modulate neural plasticity and memory in a dose-dependent manner.
Chronic stress and elevated glucocorticoid levels are linked to cognitive deficits and neuronal damage.
Mitochondrial function is crucial for neuronal health and plasticity.

Purpose of the Study:

To investigate the biphasic effects of corticosterone (CORT) on mitochondrial function and neuroprotection.
To elucidate the molecular mechanisms underlying CORT's effects on neuronal resilience.
To examine the role of glucocorticoid receptors (GRs) and Bcl-2 in mediating these effects.

Main Methods:

Primary cortical neurons and in vivo rodent models were used.
Mitochondrial function was assessed by measuring oxidation, membrane potential, and calcium holding capacity.
Western blotting and immunofluorescence were employed to analyze GR and Bcl-2 levels and localization.

Main Results:

CORT exhibited an inverted "U"-shaped regulation of mitochondrial function.
Low CORT doses were neuroprotective against kainic acid-induced toxicity, while high doses enhanced it.
CORT treatment led to GR-Bcl-2 complex formation and mitochondrial translocation, but chronic high-dose CORT decreased their mitochondrial levels.

Conclusions:

Glucocorticoids exert biphasic effects on neuronal plasticity and mitochondrial function.
The GR-Bcl-2 interaction in mitochondria is a key mechanism mediating these effects.
Findings offer insights into stress-related cognitive impairments and potential therapeutic strategies.