| Literature DB >> 31658367 |
Qiang Li1,2, Tianhao Lu1,2, Chen Zhang1,2, Marlan R Hansen3, Shufeng Li1,2.
Abstract
Since a rapidly increasing number of neurostimulation devices are used clinically to modulate specific neural functions, the impact of electrical stimulation on targeted neural structure and function has become a key issue. In particular, the specific effect of electrical stimulation via a cochlear implant (CI) on inner hair cell (IHC) synapses remains unclear. Importantly, CI candidacy has recently expanded to include patients with partial hearing loss. Unfortunately, some CI recipients experience progressive hearing loss after activation of electrical stimulation. The mechanism(s) accounting for loss of residual hearing following electrical stimulation is unknown. Here normal-hearing guinea pigs were implanted with customized CIs. Intracochlear electrical stimulation with an intensity equal to or above electrically evoked compound action potential (ECAP) threshold decreased the excitability of auditory nerve. Furthermore, the number of synapses between IHCs and the afferent spiral ganglion neurons (SGNs) also decreased after electrical stimulation with higher intensities. However, no significant change was observed in the packing density and perikaryal area of SGNs as well as the quantity of hair cells. These results carry important implications for use of CIs in patients with residual hearing and for an increasing number of patients treated with other neurostimulation devices. Notably, the results were based on acute electrical stimulation. Considering the complex interaction between CIs and targeted tissues, it is urgent to conduct further research to clarify whether the similar changes could be induced by chronic electrical stimulation.Entities:
Keywords: RRID: AB_2113875; RRID: AB_2535764; RRID: AB_2535776; RRID: AB_399431; cochlear implant; electrical stimulation; electrically evoked compound action potential, ECAP; inner hair cells; spiral ganglion neuron; synapse
Year: 2019 PMID: 31658367 DOI: 10.1002/cne.24802
Source DB: PubMed Journal: J Comp Neurol ISSN: 0021-9967 Impact factor: 3.215