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UT Dallas researcher studing how 6-month-olds distinguish between speech sounds. Through cochlear
implant simulations, she found that infants process speech differently than older children and adults.
Rhythmic electric pulses teach brain to hear
Precise rhythms of impulses transmitted from cells of the inner ear, coach the brain how to hear.
Researchers at the University of Pittsburgh School of Medicine report the first evidence of this developmental process in the online version of Neuron.
The ear generates spontaneous electrical activity triggering a response in the brain before hearing actually begins.
These patterned bursts start at inner hair cells in the cochlea, part of the inner ear, and travel along the auditory nerve to the brain, according to senior investigator Karl Kandler.
"It's long been speculated that these impulses are intended to 'wire' the brain auditory centers. Until now, however, no one has been able to provide experimental evidence to support this concept," says Karl Kandler, Ph.D., professor of otolaryngology and neurobiology at the University of Pittsburgh School of Medicine.
To map neural connectivity, Dr. Kandler's team prepared mouse brain sections of auditory pathways using an inert chemical made active by UV light.
When pulsed laser light is absorbed by a neuron in these auditory pathways, it excites the nerve generating an electrical impulse.
Tracking the spread of an impulse to adjacent cells, creates a map of that neural network over an interval of time.
All mice are born unable to hear - a sense that develops around two weeks after birth. But even before hearing starts, their ears produce rhythmic pulses of electrical activity causing broad reactions in their brain's auditory processing centers.
The brain organizes itself aound these pulses, pruning unneeded neural connections and strengthening others.
To investigate whether the pulses are important to this reorganization, the team genetically engineered mice not to have a key receptor on their inner ear hair cells.
Dr. Kandler: "In normal mice, the wiring diagram of the brain gets sharper and more efficient over time and the pups begin to hear. But this doesn't happen when the inner ear pulses in a different rhythm. The brain isn't getting the instructions it needs to wire itself correctly. We see that these mice can detect sound, but have problems perceiving pitch."
In humans, such subtle hearing deficits are associated with Central Auditory-Processing Disorders (CAPD), difficulty processing the meaning of sound.
About 2 to 3 percent of children are affected with CAPD and often have speech and language disorders or delays, and sometimes learning disabilities such as dyslexia. In contrast to impairments due to ear structural deficits, the causes underlying CAPD have remained obscure.
"Our findings suggest that an abnormal rhythm in electrical impulses early in life may be an important contributing factor in the development of Central Auditory-Processing Disorders - CAPD. More research is needed to find out whether this also holds true for humans, but our results point us in a new direction that is worth following,"
Karl Kandler, Ph.D., professor of otolaryngology and neurobiology, University of Pittsburgh School of Medicine
•Deletion of nicotinic α9 subunit alters spontaneous activity in auditory system
•α9 KO mice have impaired refinement of an inhibitory tonotopic map
•Imprecise tonotopy in α9 KO mice is present on functional and structural levels
Patterned spontaneous activity is a hallmark of developing sensory systems. In the auditory system, rhythmic bursts of spontaneous activity are generated in cochlear hair cells and propagated along central auditory pathways. The role of these activity patterns in the development of central auditory circuits has remained speculative. Here we demonstrate that blocking efferent cholinergic neurotransmission to developing hair cells in mice that lack the α9 subunit of nicotinic acetylcholine receptors (α9 KO mice) altered the temporal fine structure of spontaneous activity without changing activity levels. KO mice showed a severe impairment in the functional and structural sharpening of an inhibitory tonotopic map, as evidenced by deficits in synaptic strengthening and silencing of connections and an absence in axonal pruning. These results provide evidence that the precise temporal pattern of spontaneous activity before hearing onset is crucial for the establishment of precise tonotopy, the major organizing principle of central auditory pathways.
The study team included Amanda Clause, Ph.D., Gunsoo Kim, Ph.D., and Catherine Weisz, Ph.D., all of the University of Pittsburgh School of Medicine; Mandy Sonntag, Ph.D., and Rudolf R?bsamen, Ph.D., both of the University of Leipzig; and Douglas E. Vetter, Ph.D., of the University of Mississippi Medical Center.
The project was funded by the National Institute on Deafness and Other Communication Disorders grants 04199 and DC011499 and National Institutes of Health grant NS007433; the National Science Foundation; the Pennsylvania Lions Hearing Research Foundation; and Deutsche Forschungsgemeinschaft.
About the University of Pittsburgh School of Medicine
As one of the nation's leading academic centers for biomedical research, the University of Pittsburgh School of Medicine integrates advanced technology with basic science across a broad range of disciplines in a continuous quest to harness the power of new knowledge and improve the human condition. Driven mainly by the School of Medicine and its affiliates, Pitt has ranked among the top 10 recipients of funding from the National Institutes of Health since 1998. In rankings recently released by the National Science Foundation, Pitt ranked fifth among all American universities in total federal science and engineering research and development support.
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