Scientific American Mind-June/July 2007

JIM BRANDENBURG Minden Pictures
and human speech run even deeper. Both humans
and songbirds have developed neuronal
structures that specialize in the perception and
production of sounds. Compared with humans,
whose brains use parallel processing to comprehend
speech, songbirds have a rather more modularly
constructed brain in which various centers
assume specifi c roles. In the avian brain, auditory
stimuli reach the high vocal center, which
controls the muscular movements of the vocal
organ via the motor center; damage to this region
prevents singing.
Another important data path in bird brains
extends from the high vocal center via area X—a
song-learning center in the basal ganglia—to the
thalamus and from there back to the cortex. This
so-called corticobasal ganglia loop also exists
in the brains of mammals, including humans,
where it is vital for learning. In young birds, lesions
in area X lead to abnormal twittering,
whereas such lesions seem to have no effect in the
adults of most songbird species— until they try to
learn a new song. Apparently the corticobasal
network is important for learning songs but not
necessarily for singing them. In humans also,
FOXP2 proteins are produced in large quantities
in the basal ganglia, which is where the structural
and functional anomalies occur in patients
with FOXP2-related speech defects.
Genetic Songwriter
In the brains of zebra fi nches, area X contains
more FOXP2 during the song-learning phase
than during infancy or adulthood. Likewise in
the canary, which changes its melody once a year
after breeding season, FOXP2 is expressed particularly
strongly in area X during this learning
phase [see illustration on opposite page].
Accordingly, FOXP2 may well be involved in
song plasticity—the ability to learn new songs.
To explore this possibility, our team genetically
reduced the amount of FOXP2 in area X in zebra
fi nches to artifi cially induce a situation similar to
a FOXP2 mutation in humans. The crucial question
is, What happens to a melody if less FOXP2
is expressed in area X while it is being learned?
Our initial results show that the zebra fi nches
have diffi culty learning their songs when they
have less than the normal amount of the FOXP2
transcription factor. We concluded that this protein
is necessary for zebra fi nches to learn a song,
but it is less important for motor functions overall.
Thus, a FOXP2 mutation does not simply
cause the brain to develop abnormally. The defect
continues to play a role once the brain has
become fully developed—an important clue
about what happens in humans who have the
speech problems displayed by the KE family.
Careful analogy of the zebra fi nch’s impaired
song learning with the problems seen in the KE
family leads us to believe that affected family
members may have diffi culty imitating the sounds
made by their parents. They are unable to harmonize
their own speech with that of others. Should
this suspicion be borne out, it would mean that
the similarity between avian song learning and
human speech acquisition extends all the way to
the molecular level.
The logical implication is that the evolution
of language is not a unique feature of the human
lineage. Many species share the structure and
molecular makeup of the brain that was already
in place as our ancestors began to speak. Only as
existing genes and neuronal systems continued
to develop was the path cleared for the uniquely
human capacity for speech. M
(Further Reading)
Songbirds such
as this warbling
western meadowlark
could help provide
clues about
how genes regulate
human speech.
◆ FOXP2 in Focus: What Can Genes Tell Us about Speech and Language?
Gary F. Marcus and Simon E. Fisher in Trends in Cognitive Sciences, Vol. 7,
No. 6, pages 257–262; June 2003.
◆ FOXP2 Expression in Avian Vocal Learners and Non-Learners. Sebastian
Haesler, Kazuhiro Wada, A. Nshdejan, Edward E. Morrisey, Thierry Lints,
Eric D. Jarvis and Constance Scharff in Journal of Neuroscience, Vol. 24,
No. 13, pages 3164–3175; March 31, 2004.
◆ Singing Mice, Songbirds, and More: Models for FOXP2 Function and
Dysfunction in Human Speech and Language. Stephanie A. White, Simon
E. Fisher, Daniel H. Geschwind, Constance Scharff and Timothy E. Holy
in Journal of Neuroscience, Vol. 26, No. 41, pages 10376–10379;
October 11, 2006.
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