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

Lethal Alleles

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...

You might also read

Related Articles

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

Sort by

Same author

The Putative Role of 1,25(OH)<sub>2</sub>D<sub>3</sub> in the Association of Milk Consumption and Parkinson's Disease.

Neuro-Signals·2021

Same author

The Putative Role of 1,25(OH)<sub>2</sub>D<sub>3</sub> in the Association of Milk Consumption and Parkinson's Disease.

Neuro-Signals·2020

Same author

1,25(OH)<sub>2</sub>D<sub>3</sub> in Brain Function and Neuropsychiatric Disease.

Neuro-Signals·2019

Same author

Partial Reversal of Tissue Calcification and Extension of Life Span following Ammonium Nitrate Treatment of Klotho-Deficient Mice.

Kidney & blood pressure research·2016

Same author

Bicarbonate-sensitive calcification and lifespan of klotho-deficient mice.

American journal of physiology. Renal physiology·2015

Same author

Acetazolamide sensitive tissue calcification and aging of klotho-hypomorphic mice.

Journal of molecular medicine (Berlin, Germany)·2015

Search research articles

Related Experiment Video

Updated: Mar 22, 2026

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

1,25(OH)2D3 dependent overt hyperactivity phenotype in klotho-hypomorphic mice.

Christina B Leibrock¹, Jakob Voelkl¹, Makoto Kuro-O²

¹Department of Physiology, Cardiology &Vascular Medicine, University of Tübingen, Gmelinstr. 5, 72076 Tübingen, Germany.

Scientific Reports

|April 26, 2016

Summary

Klotho deficiency causes high vitamin D levels, leading to calcification and aging. NH4Cl treatment in deficient mice altered behavior, suggesting vitamin D

More Related Videos

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

Elevated Plus Maze for Mice

Elevated Plus Maze for Mice

Published on: December 22, 2008

Related Experiment Videos

Last Updated: Mar 22, 2026

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

Elevated Plus Maze for Mice

Elevated Plus Maze for Mice

Published on: December 22, 2008

Area of Science:

Endocrinology
Neuroscience
Gerontology

Background:

Klotho is a key regulator of vitamin D (1,25(OH)2D3) formation, primarily in the kidneys and choroid plexus.
Klotho-deficient (kl/kl) mice exhibit hypervitaminosis D, hypercalcemia, hyperphosphatemia, soft tissue calcification, and accelerated aging.
NH4Cl treatment mitigates calcification and aging in kl/kl mice without altering 1,25(OH)2D3 levels.

Purpose of the Study:

To investigate the behavioral impact of excessive 1,25(OH)2D3 formation in NH4Cl-treated kl/kl mice.
To determine if vitamin D deficiency (LVD) can reverse behavioral changes induced by NH4Cl treatment in kl/kl mice.

Main Methods:

Kl/kl mice and wild-type littermates were administered NH4Cl and fed either a control or a low-vitamin-D (LVD) diet.
Behavioral assessments included open field, dark-light box, and O-maze tests for exploratory behavior, and a forced swimming test for depressive-like behavior.
Plasma levels of 1,25(OH)2D3, calcium, and phosphate were measured.

Main Results:

NH4Cl-treated kl/kl mice exhibited significantly higher plasma 1,25(OH)2D3, calcium, and phosphate levels compared to wild-type mice, an effect normalized by LVD.
NH4Cl-treated kl/kl mice displayed increased exploratory behavior in multiple tests, which was abrogated by LVD.
NH4Cl-treated kl/kl mice showed reduced floating time in the forced swimming test, indicating decreased depressive-like behavior.

Conclusions:

Excessive 1,25(OH)2D3 formation in klotho-hypomorphic mice significantly impacts murine behavior, including exploration and depressive-like behaviors.
The behavioral alterations observed in NH4Cl-treated kl/kl mice are dependent on elevated 1,25(OH)2D3 levels.
NH4Cl treatment in wild-type mice did not induce significant changes in behavior or biochemical parameters, highlighting the specific role of klotho deficiency.