Synaptic Release Potentiation at Aging Auditory Ribbon Synapses
Autor: | Severin Belleudy, Thibault Peineau, Didier Dulon, yohan bouleau, Susanna Pietropaolo |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
auditory hair cells
synaptopathy Neurosciences. Biological psychiatry. Neuropsychiatry Neurotransmission Biology Ribbon synapse Synapse 03 medical and health sciences 0302 clinical medicine Postsynaptic potential medicine 030304 developmental biology 0303 health sciences synaptic ribbons Long-term potentiation medicine.disease medicine.anatomical_structure Synaptic plasticity Synaptopathy Hair cell sense organs Ca2+ channels exocytosis Neuroscience 030217 neurology & neurosurgery hyperacusis RC321-571 |
Zdroj: | Frontiers in Aging Neuroscience, Vol 13 (2021) |
ISSN: | 1663-4365 |
Popis: | Age-related hidden hearing loss is often described as a cochlear synaptopathy that results from a progressive degeneration of the inner hair cell (IHC) ribbon synapses. The functional changes occurring at these synapses during aging are not fully understood. Here, we characterized this aging process in IHCs of C57BL/6J mice, a strain which is known to carry a cadherin23 mutation and experiences early hearing loss with age. These mice, while displaying a large increase in auditory brainstem thresholds due to 50 % loss of IHC synaptic ribbons at middle age (postnatal day 365), paradoxically showed enhanced acoustic startle reflex suggesting a hyperacusis-like response. The auditory defect was associated with a large shrinkage of the IHCs’ cell body and a drastic enlargement of their remaining presynaptic ribbons which were facing enlarged postsynaptic AMPAR clusters. Presynaptic Ca2+ microdomains and the capacity of IHCs to sustain high rates of exocytosis were largely increased, while on the contrary the expression of the fast repolarizing BK channels, known to negatively control transmitter release, was decreased. This age-related synaptic plasticity in IHCs suggested a functional potentiation of synaptic transmission at the surviving synapses, a process that could partially compensate the decrease in synapse number and underlie hyperacusis. |
Databáze: | OpenAIRE |
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