Cellular and molecular bases of neuroplasticity: brainstem effects after cochlear damage

Abstract

After a cochlear lesion or auditory nerve damage, afferent connections from auditory ganglia can be highly altered. This results in a clear reduction of auditory input and an alteration of connectivity of terminals on cochlear nuclei neurons. Such a process could stimulate the reorganization of the neural circuits and neuroplasticity. Cochlea removal has been demonstrated to be a good model in which to analyse brainstem neuroplasticity, particularly with regard to the cochlear nuclei. After cochlea removal three main periods of degeneration and regeneration were observed. Early effects, during the first week post lesion, involved acute degeneration with nerve ending oedema and degeneration. During the second and, probably, the third post lesion weeks, degeneration was still present, even though a limited and diffuse expression of GAP-43 started. Around 1 month post lesion, degeneration at the cochlear nuclei progressively disappeared and a relevant GAP-43 expression was found. We conclude that neuroplasticity leads neurons to modify their activity and/or their synaptic tree as a consequence of animal adaptation to learning and memory. For the human being neuroplasticity is involved in language learning and comprehension, particularly the acquisition of a second language. Neuroplasticity is important for therapeutic strategies, such as hearing aids and cochlear implants.