Seminar
Abstract:
In humans, speech experience alters vowel perception before shaping the perception of acoustically distinct consonants (Kuhl et al., 1992; Welker and Tees, 2005). Similarly, the time window of enhanced plasticity for pure tone exposure precedes sensitive periods for more complex sounds in rodents (Insanally et al.,2009). This suggests that distinct sound features might be processed by different neuronal circuits. By characterizing the development and plasticity of auditory responses to sensory inputs of increasing complexity, we aim at determining what neuronal circuits are engaged by specific sound features.
We identified the neuronal circuit crucial for processing pure frequency tones through voltage-sensitive dye imaging in an acute mouse brain slice preparation. Passive tone-rearing modified response strength and topography within mouse primary auditory cortex during a brief, three-day window. To determine a cortical site of origin for these experience-dependent modifications, we examined a gene-targeted manipulation restricted to the forebrain with Icam5 knockout mice. These mice exhibited an accelerated auditory critical period for thalamocortical modification when compared to wild-type animals. Using in vivo recordings in the auditory cortex of anesthetized mouse, we then identified a late critical period for another sound feature,the direction of frequency modulated sweep. This seven-day window happened three weeks later than the critical period for pure frequency tone, indicating not only that the auditory cortex is still developing until adulthood, but also that there are different windows of plasticity for different sound features. Furthermore, we demonstrated that although the imbalance of excitatory and inhibitory ratio might be triggering both critical periods, it does it in independent and distinct ways.
Our results reveal the existence of asynchronous critical periods for plasticity in the mouse auditory system and the crucial role of the excitatory inhibitory ratio imbalance in triggering this plasticity. They contribute to understanding the mechanisms behind developmental plasticity and could be explored to reinstate adult plasticity in cases of auditory malfunction.