Stroke recovery and sensory plasticity: Common mechanisms?

Abstract

Presentations in this symposium are considered in the context of mechanisms of sensory plasticity, particularly in the auditory system. The auditory nervous system has two discrete end organs that are separately vulnerable to clinical and experimental injury, and brainstem processing mechanisms that are highly specialized for temporal, spectral, and spatial coding. These include giant axo-somatic synapses and neurons with spatially segregated bipolar dendrites, each innervated exclusively from one ear. This architecture allows exquisite control of afferent-target interactions, including known excitatory and inhibitory couplings, and consequently enhanced interpretation of data from other brain systems. For example, deafening can silence the auditory nerve, but has surprisingly little impact on normal brain function, as evidenced by the success of cochlear implants. The observed amplification from one brain region to another of degeneration following stroke or discrete brain lesions may thus be due to secondary rather than primary afferent consequences of the lesion.