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Targeted Training of Ultrasonic Vocalizations in Aged and Parkinsonian Rats

Targeted Training of Ultrasonic Vocalizations in Aged and Parkinsonian Rats

Published on: August 8, 2011

Ultrasonic vocalization changes and FOXP2 expression after experimental stroke.

Sarah J Doran¹, Cassandra Trammel¹, Sharon E Benashaski¹

¹Departments of Neuroscience, University of Connecticut Health Center, Farmington, CT 06030.

Behavioural Brain Research

|February 4, 2015

Summary

This summary is machine-generated.

Stroke survivors often experience speech impairments. This study shows that male mice exhibit quantifiable deficits in ultrasonic vocalizations (USVs) after cerebral ischemia, offering a potential model for studying stroke-related vocal deficits.

Keywords:

FOXP2/Foxp2 gene (in humans and other mammals Middle cerebral artery occlusion Ultrasonic vocalization respectively)

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Area of Science:

Neuroscience
Stroke Research
Animal Models

Background:

Speech impairments are common after stroke, affecting up to 25% of survivors.
Existing animal models for studying post-stroke vocalization deficits are limited.
Male mice produce ultrasonic vocalizations (USVs) when exposed to female mice, providing a basis for vocalization analysis.

Purpose of the Study:

To assess vocalization patterns and quantity in male mice following cerebral ischemia.
To investigate the role of the FOXP2 gene in post-stroke vocalization deficits.
To explore potential lateralization of vocalization impairments based on stroke hemisphere.

Main Methods:

Transient middle cerebral artery occlusion (MCAO) model in male mice to induce cerebral ischemia.
Assessment of vocalization quantity and patterns at multiple time points post-stroke.
Analysis of FOXP2 gene expression in brain tissue after ischemic injury.
Comparison of vocalization deficits between left and right hemispheric strokes.

Main Results:

Significant and persistent reductions in vocalization quantity were observed in stroke mice compared to sham controls for up to one month.
Left hemispheric strokes caused a more profound early reduction in vocalizations than right hemispheric strokes.
FOXP2 expression showed dynamic changes, with early elevation followed by a decrease, and increased neuronal expression at 4 weeks post-stroke.

Conclusions:

Quantifiable deficits in ultrasonic vocalizations (USVs) occur after experimental stroke in mice.
USV analysis may serve as a valuable tool for evaluating chronic behavioral recovery in murine stroke models.
The study highlights the potential of USVs for understanding and modeling speech impairments post-stroke.