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Brain Sciences
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Brain-Derived Neurotrophic Factor in the Auditory System
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Brain-Derived Neurotrophic Factor in the Auditory System

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Systems Neuroscience".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 16178

Special Issue Editor

Dr. Huib Versnel

E-Mail Website
Guest Editor
Department of Otorhinolaryngology and Head & Neck Surgery, University Medical Center Utrecht, Utrecht University, Room G.02.531, P.O. Box 85500, 3508 GA Utrecht, The Netherlands
Interests: auditory system; cochlear implantation; hearing loss; neuroprotection; plasticity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain-derived neurotrophic factor (BDNF), one of the four neurotrophins present in mammalians, plays a crucial role in development and maintenance of the peripheral and central nervous system. In the auditory system BDNF supports maintenance of the auditory nerve and strengthens inhibition in the central auditory nuclei. The maintenance role triggered research aimed at protection of the auditory nerve which degenerates following either severe cochlear hair cell loss as encountered in deafness or synaptic trauma as induced by exposure to loud sounds. Among the various compounds tested in animal models, BDNF seems to have the better protective effect so far.

This special issue shares state-of-the-art research examining the roles of BDNF in the auditory system. This research includes 1) the role of BDNF in responsiveness of the auditory nerve and central nuclei; 2) the effect of exogenous BDNF on dendritic outgrowth, in particular regarding improvement of the neural connection with a cochlear implant; 3) the role of BDNF in changes in central auditory nuclei after cochlear damage, including mechanisms causing tinnitus; 4) the potential for treatment of hearing disorders.

Dr. Huib Versnel
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Cochlea
  • Hearing
  • Neurotrophic Treatment
  • Auditory Nerve

Published Papers (5 papers)

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Research

19 pages, 5054 KiB  
Article
No Protective Effects of Hair Cells or Supporting Cells in Ototoxically Deafened Guinea Pigs upon Administration of BDNF
by Annamaria Tisi, Jochebed Rovers, Henk A. Vink, Dyan Ramekers, Rita Maccarone and Huib Versnel
Brain Sci. 2022, 12(1), 2; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci12010002 - 21 Dec 2021
Cited by 6 | Viewed by 2565
Abstract
We investigated whether treatment with brain-derived neurotrophic factor (BDNF), which is known to protect spiral ganglion cells (SGCs), could also protect hair cells (HCs) and supporting cells (SCs) in the organ of Corti of a guinea pig model of sensorineural hearing loss. Hearing [...] Read more.
We investigated whether treatment with brain-derived neurotrophic factor (BDNF), which is known to protect spiral ganglion cells (SGCs), could also protect hair cells (HCs) and supporting cells (SCs) in the organ of Corti of a guinea pig model of sensorineural hearing loss. Hearing loss was induced by administration of kanamycin/furosemide and two BDNF treatments were performed: (1) by gelatin sponge (BDNF-GS) with acute cochlear implantation (CI), and (2) through a mini-osmotic pump (BDNF-OP) with chronic CI. Outer HCs (OHCs), inner HCs (IHCs), Border, Phalangeal, Pillar, Deiters’, and Hensen’s cells were counted. The BDNF-GS cochleas had significantly fewer OHCs compared to the untreated ones, while the IHC and SC numbers did not differ between treated and untreated cochleas. The BDNF-OP group showed similar cell numbers to the untreated group. SGC packing density was not correlated with the total number of SCs for either BDNF group. Our data suggest that: (1) BDNF does not prevent cell death in the organ of Corti, and that the protection of SGCs could result from a direct targeting by BDNF; (2) BDNF might induce a different function/activity of the remaining cells in the organ of Corti (independently from cell number). Full article
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor in the Auditory System)
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20 pages, 5570 KiB  
Article
BDNF Outperforms TrkB Agonist 7,8,3′-THF in Preserving the Auditory Nerve in Deafened Guinea Pigs
by Henk A. Vink, Willem C. van Dorp, Hans G. X. M. Thomeer, Huib Versnel and Dyan Ramekers
Brain Sci. 2020, 10(11), 787; https://doi.org/10.3390/brainsci10110787 - 28 Oct 2020
Cited by 15 | Viewed by 2929
Abstract
In deaf subjects using a cochlear implant (CI) for hearing restoration, the auditory nerve is subject to degeneration, which may negatively impact CI effectiveness. This nerve degeneration can be reduced by neurotrophic treatment. Here, we compare the preservative effects of the naturally occurring [...] Read more.
In deaf subjects using a cochlear implant (CI) for hearing restoration, the auditory nerve is subject to degeneration, which may negatively impact CI effectiveness. This nerve degeneration can be reduced by neurotrophic treatment. Here, we compare the preservative effects of the naturally occurring tyrosine receptor kinase B (TrkB) agonist brain-derived neurotrophic factor (BDNF) and the small-molecule TrkB agonist 7,8,3′-trihydroxyflavone (THF) on the auditory nerve in deafened guinea pigs. THF may be more effective than BDNF throughout the cochlea because of better pharmacokinetic properties. The neurotrophic compounds were delivered by placement of a gelatin sponge on the perforated round window membrane. To complement the histology of spiral ganglion cells (SGCs), electrically evoked compound action potential (eCAP) recordings were performed four weeks after treatment initiation. We analyzed the eCAP inter-phase gap (IPG) effect and measures derived from pulse-train evoked eCAPs, both indicative of SGC healthiness. BDNF but not THF yielded a significantly higher survival of SGCs in the basal cochlear turn than untreated controls. Regarding IPG effect and pulse-train responses, the BDNF-treated animals exhibited more normal responses than both untreated and THF-treated animals. We have thus confirmed the protective effect of BDNF, but we have not confirmed previously reported protective effects of THF with our clinically applicable delivery method. Full article
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor in the Auditory System)
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26 pages, 12082 KiB  
Article
Age-Dependent Auditory Processing Deficits after Cochlear Synaptopathy Depend on Auditory Nerve Latency and the Ability of the Brain to Recruit LTP/BDNF
by Philine Marchetta, Daria Savitska, Angelika Kübler, Giulia Asola, Marie Manthey, Dorit Möhrle, Thomas Schimmang, Lukas Rüttiger, Marlies Knipper and Wibke Singer
Brain Sci. 2020, 10(10), 710; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci10100710 - 06 Oct 2020
Cited by 9 | Viewed by 3975
Abstract
Age-related decoupling of auditory nerve fibers from hair cells (cochlear synaptopathy) has been linked to temporal processing deficits and impaired speech recognition performance. The link between both is elusive. We have previously demonstrated that cochlear synaptopathy, if centrally compensated through enhanced input/output function [...] Read more.
Age-related decoupling of auditory nerve fibers from hair cells (cochlear synaptopathy) has been linked to temporal processing deficits and impaired speech recognition performance. The link between both is elusive. We have previously demonstrated that cochlear synaptopathy, if centrally compensated through enhanced input/output function (neural gain), can prevent age-dependent temporal discrimination loss. It was also found that central neural gain after acoustic trauma was linked to hippocampal long-term potentiation (LTP) and upregulation of brain-derived neurotrophic factor (BDNF). Using middle-aged and old BDNF-live-exon-visualization (BLEV) reporter mice we analyzed the specific recruitment of LTP and the activity-dependent usage of Bdnf exon-IV and -VI promoters relative to cochlear synaptopathy and central (temporal) processing. For both groups, specimens with higher or lower ability to centrally compensate diminished auditory nerve activity were found. Strikingly, low compensating mouse groups differed from high compensators by prolonged auditory nerve latency. Moreover, low compensators exhibited attenuated responses to amplitude-modulated tones, and a reduction of hippocampal LTP and Bdnf transcript levels in comparison to high compensators. These results suggest that latency of auditory nerve processing, recruitment of hippocampal LTP, and Bdnf transcription, are key factors for age-dependent auditory processing deficits, rather than cochlear synaptopathy or aging per se. Full article
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor in the Auditory System)
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19 pages, 3041 KiB  
Article
Age-Dependency of Neurite Outgrowth in Postnatal Mouse Cochlear Spiral Ganglion Explants
by Claudia Frick, Stefan Fink, Dominik Schmidbauer, Francis Rousset, Holger Eickhoff, Anke Tropitzsch, Benedikt Kramer, Pascal Senn, Rudolf Glueckert, Helge Rask-Andersen, Karl-Heinz Wiesmüller, Hubert Löwenheim and Marcus Müller
Brain Sci. 2020, 10(9), 580; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci10090580 - 21 Aug 2020
Cited by 7 | Viewed by 3363
Abstract
Background: The spatial gap between cochlear implants (CIs) and the auditory nerve limits frequency selectivity as large populations of spiral ganglion neurons (SGNs) are electrically stimulated synchronously. To improve CI performance, a possible strategy is to promote neurite outgrowth toward the CI, thereby [...] Read more.
Background: The spatial gap between cochlear implants (CIs) and the auditory nerve limits frequency selectivity as large populations of spiral ganglion neurons (SGNs) are electrically stimulated synchronously. To improve CI performance, a possible strategy is to promote neurite outgrowth toward the CI, thereby allowing a discrete stimulation of small SGN subpopulations. Brain-derived neurotrophic factor (BDNF) is effective to stimulate neurite outgrowth from SGNs. Method: TrkB (tropomyosin receptor kinase B) agonists, BDNF, and five known small-molecule BDNF mimetics were tested for their efficacy in stimulating neurite outgrowth in postnatal SGN explants. To modulate Trk receptor-mediated effects, TrkB and TrkC ligands were scavenged by an excess of recombinant receptor proteins. The pan-Trk inhibitor K252a was used to block Trk receptor actions. Results: THF (7,8,3′-trihydroxyflavone) partly reproduced the BDNF effect in postnatal day 7 (P7) mouse cochlear spiral ganglion explants (SGEs), but failed to show effectiveness in P4 SGEs. During the same postnatal period, spontaneous and BDNF-stimulated neurite outgrowth increased. The increased neurite outgrowth in P7 SGEs was not caused by the TrkB/TrkC ligands, BDNF and neurotrophin-3 (NT-3). Conclusions: The age-dependency of induction of neurite outgrowth in SGEs was very likely dependent on presently unidentified factors and/or molecular mechanisms which may also be decisive for the age-dependent efficacy of the small-molecule TrkB receptor agonist THF. Full article
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor in the Auditory System)
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13 pages, 2240 KiB  
Article
Consecutive Treatment with Brain-Derived Neurotrophic Factor and Electrical Stimulation Has a Protective Effect on Primary Auditory Neurons
by Verena Scheper, Ira Seidel-Effenberg, Thomas Lenarz, Timo Stöver and Gerrit Paasche
Brain Sci. 2020, 10(8), 559; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci10080559 - 15 Aug 2020
Cited by 13 | Viewed by 2743
Abstract
Degeneration of neurons, such as the inner ear spiral ganglion neurons (SGN), may be decelerated or even stopped by neurotrophic factor treatment, such as brain-derived neurotrophic factor (BDNF), as well as electrical stimulation (ES). In a clinical setting, drug treatment of the SGN [...] Read more.
Degeneration of neurons, such as the inner ear spiral ganglion neurons (SGN), may be decelerated or even stopped by neurotrophic factor treatment, such as brain-derived neurotrophic factor (BDNF), as well as electrical stimulation (ES). In a clinical setting, drug treatment of the SGN could start directly during implantation of a cochlear implant, whereas electrical stimulation begins days to weeks later. The present study was conducted to determine the effects of consecutive BDNF and ES treatments on SGN density and electrical responsiveness. An electrode drug delivery device was implanted in guinea pigs 3 weeks after deafening and five experimental groups were established: two groups received intracochlear infusion of artificial perilymph (AP) or BDNF; two groups were treated with AP respectively BDNF in addition to ES (AP + ES, BDNF + ES); and one group received BDNF from the day of implantation until day 34 followed by ES (BDNF ⇨ ES). Electrically evoked auditory brainstem responses were recorded. After one month of treatment, the tissue was harvested and the SGN density was assessed. The results show that consecutive treatment with BDNF and ES was as successful as the simultaneous combined treatment in terms of enhanced SGN density compared to the untreated contralateral side but not in regard to the numbers of protected cells. Full article
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor in the Auditory System)
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