Masashi Sakai

Department of Physiology, University of Yamanashi, Yamanashi 409-3898, Japan

Abstract:

Stimulus-locking discharges of the primary auditory cortex neurons (AI) are critically involved in encoding temporal variance of acoustic signals in the milliseconds to tens-of-milliseconds frame, which is necessary for voice-onset time (VOT) dependent categorical perception” (ex., /ba/-/pa/ distinction) (Sakai and Sato, 2011). Such fine-grained auditory processing has been considered as one of the bottlenecks for development of verbal acuity: its deficit is often accompanied with specific language impairment (SLI) (Tallal et al., 1993). SLI is diagnosed when a child's language does not develop normally and the difficulties cannot be accounted for malformation of nervous system, hearing deficits, mental retardation, emotional disturbance, etc. (Bishop, 1992). In USA, as much as 5-10 % of population below 6-7 years old is affected by SLI (Tomblin et al., 1997). Currently no unequivocal evidence is available as to neural basis of SLI.

First, I introduce our physiology-based neuro-computational model which well captures synaptic mechanism of AI stimulus-locking discharges (Sakai et al., 2009, Sakai, 2012). The model incorporates four post-synaptic potentials (PSPs) in the AI neuron and short-term plasticity of thalamocortical synaptic connections. Then, I present results of animal studies showing such pharmacological treatment as to modify GABAA-receptor-mediated IPSP, NMDAreceptor- mediated EPSP and/or short-term plasticity specifically altered (1) stimulus-locking capacity of AI neurons and (2) behaviorally-assessed perceptual capacity for /ba/-/pa/ discrimination in cats. These findings raise a possibility that some CNS drugs, or environmental chemicals, heighten the risk of SLI.