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

Acid-Base Balance01:25

Acid-Base Balance

2.3K
The human body maintains a narrow pH range regulated through acid-base balance. This balance is crucial as changes in the hydrogen ion concentration can disrupt cell membrane stability, alter protein structures, and change enzyme activities. The normal pH of arterial blood is 7.4, venous blood and interstitial fluid is 7.35, and intracellular fluid averages 7.0.
When the pH of arterial blood rises above 7.45, it results in a condition called alkalosis. Conversely, a drop below 7.35 leads to...
2.3K
Balancing Redox Equations02:58

Balancing Redox Equations

61.7K
Electrochemistry is the science involved in the interconversion of electrical and chemical reactions. Such reactions are called reduction-oxidation, or redox reactions. These important reactions are defined by changes in oxidation states for one or more reactant elements and include a subset of reactions involving the transfer of electrons between reactant species. Electrochemistry as a field has evolved to yield sufficient insights on the fundamental principles of redox chemistry and multiple...
61.7K
Disorders of Acid-Base Balance01:29

Disorders of Acid-Base Balance

1.9K
The human body maintains a precise pH range of arterial blood between 7.35 and 7.45. Deviations result in either acidosis (pH < 7.35) or alkalosis (pH > 7.45). These conditions are further classified as respiratory or metabolic disorders based on their underlying cause.
Respiratory Acidosis and Alkalosis
Respiratory acidosis occurs due to an increase in the partial pressure of carbon dioxide PCO2 in the blood. It often arises from shallow breathing or impaired gas exchange caused by...
1.9K
Respiratory Regulation of Acid-Base Balance01:18

Respiratory Regulation of Acid-Base Balance

1.7K
Respiratory compensation is a vital physiological process that stabilizes blood plasma pH by regulating the partial pressure of carbon dioxide (PCO2), a key determinant of pH levels. Most carbon dioxide in the blood dissolves and converts into carbonic acid (H2CO3). It dissociates into hydrogen ions (H+) and bicarbonate ions (HCO3⁻). There is also an inverse relationship between PCO2​​ and pH.
When carbon dioxide levels increase in the blood, more H+ and HCO3⁻ are...
1.7K
Overview of Fatty Acid Metabolism01:28

Overview of Fatty Acid Metabolism

36.8K
Lipids also are sources of energy that power cellular processes. Like carbohydrates, lipids are composed of carbon, hydrogen, and oxygen, but these atoms are arranged differently. Most lipids are nonpolar and hydrophobic. Major types include fats and oils, waxes, phospholipids, and steroids.
Fatty acids are catabolized in a process called beta-oxidation, which takes place in the matrix of the mitochondria and converts their fatty acid chains into two-carbon units of acetyl groups. The acetyl...
36.8K
Renal Regulation of Acid-Base Balance01:29

Renal Regulation of Acid-Base Balance

1.6K
Metabolic reactions in the body produce nonvolatile acids, such as sulfuric acid, which generate an acid load of approximately 1 mEq of H+ per kilogram of body weight daily. Excreting H+ in the urine is essential to balance this acid load.
In the kidneys, cells within the proximal convoluted tubules (PCT) and the collecting ducts secrete hydrogen ions (H+) into the tubular fluid. Specifically, in the PCT, Na+/H+ antiporters secrete H+ while reabsorbing Na+.
However, the intercalated cells in...
1.6K

You might also read

Related Articles

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

Sort by
Same author

FMR1 gene therapy restores translationally relevant phenotypes in a mouse model for fragile X syndrome.

Gene therapy·2026
Same author

Cell-Intrinsic Regulation of Epilepsy-Associated Pathology by mTORC1 and mTORC2.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026
Same author

Scientific Symposium: Biological Sex as a Factor in Epilepsy Research and Treatment.

Epilepsy currents·2026
Same author

Age dependent impairment of home cage behavior and reactivity in <i>Cntnap2</i> knock out mouse model.

bioRxiv : the preprint server for biology·2026
Same author

Correction: A sensitive and reproducible qRT-PCR assay detects physiological relevant trace levels of FMR1 mRNA in individuals with Fragile X syndrome.

Scientific reports·2025
Same author

Altered PI3K/mTOR Signaling within the Forebrain Leads to Respiratory Deficits in a Mouse Model of Epilepsy.

eNeuro·2025

Related Experiment Video

Updated: Jan 26, 2026

Preparation, Purification, and Use of Fatty Acid-containing Liposomes
10:43

Preparation, Purification, and Use of Fatty Acid-containing Liposomes

Published on: February 9, 2018

83.1K

Losing Balance Over a Fatty Acid.

Christina Gross

    Epilepsy Currents
    |April 9, 2019
    PubMed
    Summary

    Deficiency in AMPA receptor (AMPAR) palmitoylation increases seizure susceptibility in mice. This study identifies AMPAR palmitoylation as critical for maintaining brain network stability and preventing epilepsy.

    Area of Science:

    • Neuroscience
    • Molecular Biology
    • Epilepsy Research

    Background:

    • Synaptic AMPA receptor (AMPAR) expression is crucial for excitatory transmission and plasticity.
    • Dysregulation of AMPARs can lead to epilepsy, but underlying mechanisms are not fully understood.
    • AMPAR trafficking is regulated by reversible S-palmitoylation at C-termini.

    Purpose of the Study:

    • To investigate the in vivo role of AMPAR palmitoylation in regulating seizure susceptibility.
    • To elucidate the mechanisms by which palmitoylation affects AMPAR function and brain network stability.

    Main Methods:

    • Generation of GluA1 palmitoylation-deficient knock-in mice (Cys811 to Ser substitution).
    • Assessment of seizure susceptibility, neuronal activity, synaptic transmission, and behavior in mutant mice.

    More Related Videos

    Identification of Fatty Acids in Bacillus cereus
    08:41

    Identification of Fatty Acids in Bacillus cereus

    Published on: December 5, 2016

    10.1K
    Analysis of Fatty Acid Content and Composition in Microalgae
    07:44

    Analysis of Fatty Acid Content and Composition in Microalgae

    Published on: October 1, 2013

    61.5K

    Related Experiment Videos

    Last Updated: Jan 26, 2026

    Preparation, Purification, and Use of Fatty Acid-containing Liposomes
    10:43

    Preparation, Purification, and Use of Fatty Acid-containing Liposomes

    Published on: February 9, 2018

    83.1K
    Identification of Fatty Acids in Bacillus cereus
    08:41

    Identification of Fatty Acids in Bacillus cereus

    Published on: December 5, 2016

    10.1K
    Analysis of Fatty Acid Content and Composition in Microalgae
    07:44

    Analysis of Fatty Acid Content and Composition in Microalgae

    Published on: October 1, 2013

    61.5K
  • Analysis of GluA1 phosphorylation and protein expression in specific brain regions.

    • Main Results:

    • Mutant mice exhibited increased seizure susceptibility and neuronal activity without basal deficits.
    • Disruption of palmitoylation site upregulated GluA1 phosphorylation at Ser831 and increased cortical GluA1 expression.
    • GluA1 palmitoylation was found to suppress excessive spine enlargement post-long-term potentiation.

    Conclusions:

    • Abnormal GluA1 palmitoylation leads to cerebral hyperexcitability and epileptic seizures.
    • This study identifies a specific palmitoylated protein crucial for seizure suppression.
    • Findings suggest novel therapeutic targets for antiepileptic drug development.