Prof Victoria M Bajo Lorenzana, MD PhD
Targeting neural plasticity by optogenetic silencing in the auditory cortex
Training can improve perceptual skills and be harnessed for treating sensory disorders included reversing age-related deficits in sensory processing. Plasticity of cortical function is generally considered to underpin perceptual learning but the neural circuits responsible for this processing remain poorly understood.
Our aim is deciphering the role of the auditory cortex, mainly primary auditory cortex (A1) in adult learning. We are working with two models of auditory cortical plasticity using the ferret as animal model and optogenetic silencing to manipulate cortical activity.
Unilateral and reversible conductive hearing loss by plugging one ear canal produces changes in the binaural cue values and needs further training in sound localisation behaviour to regain quasi-normal performance. This learning-induced auditory plasticity requires the functional integrity of the auditory cortex. Using optogenetic silencing of ArchT-expressing neurons in adult ferrets, we show that within-trial activity in the auditory cortex is required for training-dependent recovery in sound-localization accuracy following monaural deprivation. In control animals, the adaptation process appears to leave a memory trace, facilitating adaptation during a second period of monaural deprivation. However, in ferrets in which learning was initially disrupted by perturbing optogenetically cortical activity, subsequent optogenetic suppression during training no longer altered localization accuracy when one ear was occluded.
In the second model, and to investigate sensorineural hearing-loss-neuroplasticity, ferrets underwent a partial, unilateral lesion of the spiral ganglion, replicating aspects of otopathology described in age-related hearing loss and/or tinnitus. Ferrets were tested on a gap-in-noise detection task to assess auditory temporal processing before and after the peripheral lesion and hearing loss was assessed by recordings auditory brainstem evoked recorded (ABRs). In cases with behavioural impairments in gap detection performance was rescued by silencing the auditory cortex contralateral to the peripheral lesion.
Those results show the essential role of the auditory cortex in mediating peripheral-related neuroplasticity.
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