According to a new study published in the journal Frontiers in Behavioral Neuroscience, ultrasonic vocal communication in adult mice is affected by the same gene needed for speech in humans.

The study’s authors report the results of their investigation into the effect of a genetic mutation in the Forkhead box protein 2 (FOXP2) on the vocalization patterns of adult male mice.

The FOXP2 gene regulates speech production in humans. Genetic aberrations of this gene impair speech production and comprehension.

Although mice are unable to communicate using speech in the same way as humans, they do vocalize as a means of communicating with each other.

The current study sought to determine whether FOXP2 deficiencies have similar consequences for communication by mice as they do for humans.

“This study supports the ‘continuum hypothesis,’ which is that FOXP2 affects the vocal production of all mammals and not just humans,” said senior author Dr. Erich Jarvis, of Duke University Medical Center, Howard Hughes Medical Institute and the Rockefeller University.

The researchers investigated 26 male mice bred to have a FOXP2 mutation the same as that found in humans with speech deficits, and 24 male mice with a normal level of FOXP2 protein (wildtype mice).

Both types of mice were placed in several unique contexts — housed with an active wildtype female mouse, in proximity of only the urine of wildtype females, or housed with a sleeping female or sleeping male mouse. These particular contexts derived from a 2015 study by the same team.

This past study found that in these various social contexts, healthy males produced differences in the sequence and duration of the ultrasonic vocalizations (USVs), which are high-pitched sounds inaudible to humans, that mice make.

In the new study, Dr. Jarvis and co-authors wished to determine if there was an effect of a FOXP2 deficiency on the communication patterns of mice.

The results showed that the FOXP2 heterozygotes have difficulty producing the complex vocal communication patterns that wildtype mice can create with ease — as measured both by syllable length and the number of unique syllables produced over time.

These divergences are particularly strong when comparing the communication of FOXP2 heterozygotes and wildtype males while in the presence of active female mice.

In this context, the wildtype males were three times as likely as heterozygotes to produce the most complex syllable types and sequences available for review.

“Mice do not have the complex vocal learning behavior of humans and song-learning birds,” the authors said.

“Nonetheless, we find that the same FoxP2 mutation in mice and in humans leads to overlapping effects on sequencing of vocalizations.”

“In particular, against a background of preserved syllable acoustic structure, we see reductions in the length and complexity of syllable sequences.”

The scientists also performed intricate statistical analyses to validate the finding, and their conclusion held true.

Following the conclusion of all recordings, the team used a process known as transsynaptic tracing from vocal larynx muscles to compare the vocal brain regions of wildtype and heterozygote FOXP2 mice.

The research revealed that the heterozygote’s vocal motor neurons were more widely distributed across the cortex than was the case for wildtype mice.

This evidence suggests that the FOXP2 mutation affects both the placement and functioning of the neurons connected to effective communication, from mice all the way to humans.

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Jonathan Chabout et al. A Foxp2 Mutation Implicated in Human Speech Deficits Alters Sequencing of Ultrasonic Vocalizations in Adult Male Mice. Front. Behav. Neurosci, published online October 20, 2016; doi: 10.3389/fnbeh.2016.00197