Neural plasticity expressed in human auditory cortex

 
 

Animal studies have shown that several response properties of neurons in primary auditory cortex are modified by training at acoustic discrimination.  While human studies (including several of our own) have shown that neurons in secondary auditory cortex are highly plastic, evidence for plasticity in A1 has been elusive.  Experiments conducted recently by our PhD student Phillip Gander and published in Hearing Research (2010) have changed this picture.   Gander found that plasticity was robustly expressed in the temporal properties of the 40-Hz auditory steady state response (ASSR) that localizes tonotopically to primary auditory cortex in the human brain.  Companion experiments by Gander and reported in the same journal used the ASSR to show that neurons in this region are highly sensitive to top-down attention.  Reprints of Phillip’s two papers can be obtained by clicking the citations below.

Our student Scott Baynton recently completed a complementary study of auditory plasticity in groups of children and adults spanning the age range 5 to 28 years.  The results suggest that neural remodeling is driven largely by the spectrotemporal statistics of the acoustic input in adults as well as in children, such that neural representations become tuned to the sounds that are present in the environment.  Attention becomes increasingly important after maturity, but appears to exert its selective effects principally on higher order auditory processing required for complex skill, adaptive behaviour, and memory.  Scott will defend his dissertation reporting this research on December 9th of this year.

Gander PE, Bosnyak, DJ, and Roberts LE (2010). Acoustic experience but not attention modifies neural population phase expressed in human primary auditory cortex. Hearing Research 269:81-94

Gander PE, Bosnyak, DJ, and Roberts LE (2010). Evidence for modality-specific but not frequency-specific modulation of human primary auditory cortex by attention. Hearing Research 268:213-226