International Journal of Molecular Sciences

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Ribbon Synapses: Molecular Mechanisms of Synaptic Signaling and Involvement in Diseases 2.0

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Dear Colleagues,

This Special Issue is a continuation of “Ribbon Synapses: Molecular Mechanisms of Synaptic Signaling and Involvement in Diseases”.

We welcome studies on ribbon synapses in the retina, inner ear, and pineal gland. These will include papers on the molecular anatomy and physiology of ribbon synapses. Studies on translational aspects/synaptic dysfunctions/diseases in which ribbon synapses play an important role are also welcome.

Prof. Dr. Ruth Heidelberger
Prof. Dr. Frank Schmitz
Prof. Dr. David Zenisek
Guest Editors

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Keywords

ribbon synapses
molecular anatomy and physiology of ribbon synapses
retina, inner ear ribbon synapses
pineal gland
synaptic ribbon
exocytosis
endocytosis
neuronal networks
circadian rhythms and circadian signaling

Published Papers (2 papers)

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16 pages, 3459 KiB

Open AccessArticle

Cochlear Ribbon Synapses in Aged Gerbils

by Sonny Bovee, Georg M. Klump, Sonja J. Pyott, Charlotte Sielaff and Christine Köppl

Int. J. Mol. Sci. 2024, 25(5), 2738; https://doi.org/10.3390/ijms25052738 - 27 Feb 2024

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Abstract

In mammalian hearing, type-I afferent auditory nerve fibers comprise the basis of the afferent auditory pathway. They are connected to inner hair cells of the cochlea via specialized ribbon synapses. Auditory nerve fibers of different physiological types differ subtly in their synaptic location and morphology. Low-spontaneous-rate auditory nerve fibers typically connect on the modiolar side of the inner hair cell, while high-spontaneous-rate fibers are typically found on the pillar side. In aging and noise-damaged ears, this fine-tuned balance between auditory nerve fiber populations can be disrupted and the functional consequences are currently unclear. Here, using immunofluorescent labeling of presynaptic ribbons and postsynaptic glutamate receptor patches, we investigated changes in synaptic morphology at three different tonotopic locations along the cochlea of aging gerbils compared to those of young adults. Quiet-aged gerbils showed about 20% loss of afferent ribbon synapses. While the loss was random at apical, low-frequency cochlear locations, at the basal, high-frequency location it almost exclusively affected the modiolar-located synapses. The subtle differences in volumes of pre- and postsynaptic elements located on the inner hair cell’s modiolar versus pillar side were unaffected by age. This is consistent with known physiology and suggests a predominant, age-related loss in the low-spontaneous-rate auditory nerve population in the cochlear base, but not the apex. Full article

(This article belongs to the Special Issue Ribbon Synapses: Molecular Mechanisms of Synaptic Signaling and Involvement in Diseases 2.0)

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18 pages, 4014 KiB

Open AccessArticle

A Novel Cre Recombinase Mouse Strain for Cell-Specific Deletion of Floxed Genes in Ribbon Synapse-Forming Retinal Neurons

by Shweta Suiwal, Philipp Wartenberg, Ulrich Boehm, Frank Schmitz and Karin Schwarz

Int. J. Mol. Sci. 2024, 25(3), 1916; https://doi.org/10.3390/ijms25031916 - 05 Feb 2024

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Abstract

We generated a novel Cre mouse strain for cell-specific deletion of floxed genes in ribbon synapse-forming retinal neurons. Previous studies have shown that the RIBEYE promotor targets the expression of recombinant proteins such as fluorescently tagged RIBEYE to photoreceptors and retinal bipolar cells and generates fluorescent synaptic ribbons in situ in these neurons. Here, we used the same promotor to generate a novel transgenic mouse strain in which the RIBEYE promotor controls the expression of a Cre-ER(T2) recombinase (RIBEYE-Cre). To visualize Cre expression, the RIBEYE-Cre animals were crossed with ROSA26 tau-GFP (R26-τGFP) reporter mice. In the resulting RIBEYE-Cre/R26 τGFP animals, Cre-mediated removal of a transcriptional STOP cassette results in the expression of green fluorescent tau protein (tau-GFP) that binds to cellular microtubules. We detected robust tau-GFP expression in retinal bipolar cells. Surprisingly, we did not find fluorescent tau-GFP expression in mouse photoreceptors. The lack of tau-GFP reporter protein in these cells could be based on the previously reported absence of tau protein in mouse photoreceptors which could lead to the degradation of the recombinant tau protein. Consistent with this, we detected Cre and tau-GFP mRNA in mouse photoreceptor slices by RT-PCR. The transgenic RIBEYE-Cre mouse strain provides a new tool to study the deletion of floxed genes in ribbon synapse-forming neurons of the retina and will also allow for analyzing gene deletions that are lethal if globally deleted in neurons. Full article

(This article belongs to the Special Issue Ribbon Synapses: Molecular Mechanisms of Synaptic Signaling and Involvement in Diseases 2.0)

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