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

Auditory Pathway

Auditory Pathway

Auditory pathways constitute the complex neural circuits responsible for transmitting and interpreting auditory information from the peripheral auditory system to the brain. Sound waves are initially captured by the outer ear, funneled through the ear canal, and reach the tympanic membrane (eardrum). These vibrations are transmitted via the middle ear's ossicles to the inner ear's cochlea.
When viewed cross-sectionally, the cochlea reveals the scala vestibuli and scala tympani flanking the...

Pleiotropy

Pleiotropy

Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...

You might also read

Related Articles

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

Sort by

Same author

Conserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling.

The Journal of clinical investigation·2026

Same author

Patterns of language and visuospatial lateralisation in three-year-old children.

Neuropsychologia·2026

Same author

Structural and functional brain asymmetry in relation to heterogeneous causes of situs inversus totalis.

Brain structure & function·2026

Same author

Genetic underpinnings of chills from art and music.

PLoS genetics·2026

Same author

Whole-exome sequencing in children with dyslexia implicates rare variants in CLDN3 and ion channel genes.

Human genetics·2025

Same author

Evaluating the effects of archaic protein-altering variants in living human adults.

Science advances·2025

Search research articles

Related Experiment Video

Updated: May 24, 2026

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation

Published on: July 6, 2022

Foxp2 mutations impair auditory-motor association learning.

Simone Kurt¹, Simon E Fisher, Günter Ehret

¹Institute of Neurobiology, University of Ulm, Ulm, Germany.

|March 14, 2012

Summary

This summary is machine-generated.

Mutations in the FOXP2 gene impair auditory-motor learning in mice, impacting speech development. Different mutations cause varying degrees of learning deficits, offering insights into speech and language disorders.

More Related Videos

Investigating Protein-protein Interactions in Live Cells Using Bioluminescence Resonance Energy Transfer

Investigating Protein-protein Interactions in Live Cells Using Bioluminescence Resonance Energy Transfer

Published on: May 26, 2014

Morphological and Functional Evaluation of Ribbon Synapses at Specific Frequency Regions of the Mouse Cochlea

Morphological and Functional Evaluation of Ribbon Synapses at Specific Frequency Regions of the Mouse Cochlea

Published on: May 10, 2019

Related Experiment Videos

Last Updated: May 24, 2026

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation

Published on: July 6, 2022

Investigating Protein-protein Interactions in Live Cells Using Bioluminescence Resonance Energy Transfer

Investigating Protein-protein Interactions in Live Cells Using Bioluminescence Resonance Energy Transfer

Published on: May 26, 2014

Morphological and Functional Evaluation of Ribbon Synapses at Specific Frequency Regions of the Mouse Cochlea

Morphological and Functional Evaluation of Ribbon Synapses at Specific Frequency Regions of the Mouse Cochlea

Published on: May 10, 2019

Area of Science:

Neuroscience
Genetics
Developmental Biology

Background:

The FOXP2 gene is crucial for speech and language development in humans.
Monogenic speech and language disorders are often linked to heterozygous mutations in the FOXP2 gene.
The role of Foxp2 mutations in auditory-motor association learning in mammals remains unclear.

Purpose of the Study:

To investigate the impact of etiological Foxp2 mutations on auditory-motor association learning in mice.
To assess deficits in learning new motor skills and auditory-motor associations.
To compare the effects of different Foxp2 mutations on learning capabilities.

Main Methods:

A novel conditioned avoidance paradigm in a shuttle-box was developed for mice.
Mice heterozygous for two distinct Foxp2 mutations were studied.
Learning acquisition and motor skill development were directly assessed.

Main Results:

Mice with Foxp2 mutations exhibited significant deficits in auditory-motor association learning.
Both mutations led to delays in acquiring new motor skills.
The severity of learning impairment varied with the specific Foxp2 mutation: missense mutations caused slower learning, while nonsense mutations resulted in minimal learning.

Conclusions:

Foxp2 mutations differentially affect auditory-motor association learning in mice.
Findings align with Foxp2 expression in brain circuits vital for motor skill and sensory-motor learning.
Mouse models with Foxp2 mutations provide valuable insights into the pathways underlying human speech and language disorders.