FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2933402327> ?p ?o ?g. }

• W2933402327 endingPage "4447" @default.
• W2933402327 startingPage "4434" @default.
• W2933402327 abstract "Noise-induced excitotoxicity is thought to depend on glutamate. However, the excitotoxic mechanisms are unknown, and the necessity of glutamate for synapse loss or regeneration is unclear. Despite absence of glutamatergic transmission from cochlear inner hair cells in mice lacking the vesicular glutamate transporter-3 (<i>Vglut3^KO</i>), at 9–11 weeks, approximately half the number of synapses found in <i>Vglut3^WT</i> were maintained as postsynaptic AMPA receptors juxtaposed with presynaptic ribbons and voltage-gated calcium channels (Ca_V1.3). Synapses were larger in <i>Vglut3^KO</i> than <i>Vglut3^WT</i>. In <i>Vglut3^WT</i> and <i>Vglut3</i>^+/− mice, 8–16 kHz octave-band noise exposure at 100 dB sound pressure level caused a threshold shift (∼40 dB) and a loss of synapses (>50%) at 24 h after exposure. Hearing threshold and synapse number partially recovered by 2 weeks after exposure as ribbons became larger, whereas recovery was significantly better in <i>Vglut3^WT</i>. Noise exposure at 94 dB sound pressure level caused auditory threshold shifts that fully recovered in 2 weeks, whereas suprathreshold hearing recovered faster in <i>Vglut3^WT</i> than <i>Vglut3</i>^+/−. These results, from mice of both sexes, suggest that spontaneous repair of synapses after noise depends on the level of Vglut3 protein or the level of glutamate release during the recovery period. Noise-induced loss of presynaptic ribbons or postsynaptic AMPA receptors was not observed in <i>Vglut3^KO</i>, demonstrating its dependence on vesicular glutamate release. In <i>Vglut3^WT</i> and <i>Vglut3</i>^+/−, noise exposure caused unpairing of presynaptic ribbons and presynaptic Ca_V1.3, but not in <i>Vglut3^KO</i> where Ca_V1.3 remained clustered with ribbons at presynaptic active zones. These results suggest that, without glutamate release, noise-induced presynaptic Ca²⁺ influx was insufficient to disassemble the active zone. However, synapse volume increased by 2 weeks after exposure in <i>Vglut3^KO</i>, suggesting glutamate-independent mechanisms. <b>SIGNIFICANCE STATEMENT</b> Hearing depends on glutamatergic transmission mediated by Vglut3, but the role of glutamate in synapse loss and repair is unclear. Here, using mice of both sexes, we show that one copy of the <i>Vglut3</i> gene is sufficient for noise-induced threshold shift and loss of ribbon synapses, but both copies are required for normal recovery of hearing function and ribbon synapse number. Impairment of the recovery process in mice having only one functional copy suggests that glutamate release may promote synapse regeneration. At least one copy of the <i>Vglut3</i> gene is necessary for noise-induced synapse loss. Although the excitotoxic mechanism remains unknown, these findings are consistent with the presumption that glutamate is the key mediator of noise-induced synaptopathy." @default.
• W2933402327 created "2019-04-11" @default.
• W2933402327 creator A5006872617 @default.
• W2933402327 creator A5016627436 @default.
• W2933402327 creator A5025749417 @default.
• W2933402327 creator A5027605173 @default.
• W2933402327 creator A5037849815 @default.
• W2933402327 creator A5046422599 @default.
• W2933402327 creator A5048731578 @default.
• W2933402327 creator A5053343606 @default.
• W2933402327 creator A5069013290 @default.
• W2933402327 creator A5075855267 @default.
• W2933402327 creator A5080915544 @default.
• W2933402327 creator A5083324348 @default.
• W2933402327 creator A5088074924 @default.
• W2933402327 date "2019-03-29" @default.
• W2933402327 modified "2023-10-16" @default.
• W2933402327 title "Vesicular Glutamatergic Transmission in Noise-Induced Loss and Repair of Cochlear Ribbon Synapses" @default.
• W2933402327 cites W1517515161 @default.
• W2933402327 cites W1534296897 @default.
• W2933402327 cites W1966272280 @default.
• W2933402327 cites W1982682966 @default.
• W2933402327 cites W1984056122 @default.
• W2933402327 cites W1987022414 @default.
• W2933402327 cites W1991705397 @default.
• W2933402327 cites W1997896450 @default.
• W2933402327 cites W2013496968 @default.
• W2933402327 cites W2014428504 @default.
• W2933402327 cites W2023575573 @default.
• W2933402327 cites W2030430332 @default.
• W2933402327 cites W2033347933 @default.
• W2933402327 cites W2034060287 @default.
• W2933402327 cites W2037545143 @default.
• W2933402327 cites W2040476517 @default.
• W2933402327 cites W2041125175 @default.
• W2933402327 cites W2041901262 @default.
• W2933402327 cites W2048579894 @default.
• W2933402327 cites W2056239356 @default.
• W2933402327 cites W2058562909 @default.
• W2933402327 cites W2065874844 @default.
• W2933402327 cites W2080283839 @default.
• W2933402327 cites W2086185798 @default.
• W2933402327 cites W2087400174 @default.
• W2933402327 cites W2089138302 @default.
• W2933402327 cites W2090298016 @default.
• W2933402327 cites W2091127227 @default.
• W2933402327 cites W2091448118 @default.
• W2933402327 cites W2092609060 @default.
• W2933402327 cites W2097498366 @default.
• W2933402327 cites W2097997238 @default.
• W2933402327 cites W2110013008 @default.
• W2933402327 cites W2112722770 @default.
• W2933402327 cites W2115680008 @default.
• W2933402327 cites W2133421491 @default.
• W2933402327 cites W2140689828 @default.
• W2933402327 cites W2164589681 @default.
• W2933402327 cites W2305721862 @default.
• W2933402327 cites W2460054080 @default.
• W2933402327 cites W2482089764 @default.
• W2933402327 cites W2535589380 @default.
• W2933402327 cites W2591110364 @default.
• W2933402327 cites W2617438320 @default.
• W2933402327 cites W2789854767 @default.
• W2933402327 cites W2885349901 @default.
• W2933402327 cites W2886288118 @default.
• W2933402327 cites W2887693294 @default.
• W2933402327 cites W2891127204 @default.
• W2933402327 cites W2914239719 @default.
• W2933402327 cites W85196187 @default.
• W2933402327 doi "https://doi.org/10.1523/jneurosci.2228-18.2019" @default.
• W2933402327 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6554621" @default.
• W2933402327 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30926748" @default.
• W2933402327 hasPublicationYear "2019" @default.
• W2933402327 type Work @default.
• W2933402327 sameAs 2933402327 @default.
• W2933402327 citedByCount "67" @default.
• W2933402327 countsByYear W29334023272019 @default.
• W2933402327 countsByYear W29334023272020 @default.
• W2933402327 countsByYear W29334023272021 @default.
• W2933402327 countsByYear W29334023272022 @default.
• W2933402327 countsByYear W29334023272023 @default.
• W2933402327 crossrefType "journal-article" @default.
• W2933402327 hasAuthorship W2933402327A5006872617 @default.
• W2933402327 hasAuthorship W2933402327A5016627436 @default.
• W2933402327 hasAuthorship W2933402327A5025749417 @default.
• W2933402327 hasAuthorship W2933402327A5027605173 @default.
• W2933402327 hasAuthorship W2933402327A5037849815 @default.
• W2933402327 hasAuthorship W2933402327A5046422599 @default.
• W2933402327 hasAuthorship W2933402327A5048731578 @default.
• W2933402327 hasAuthorship W2933402327A5053343606 @default.
• W2933402327 hasAuthorship W2933402327A5069013290 @default.
• W2933402327 hasAuthorship W2933402327A5075855267 @default.
• W2933402327 hasAuthorship W2933402327A5080915544 @default.
• W2933402327 hasAuthorship W2933402327A5083324348 @default.
• W2933402327 hasAuthorship W2933402327A5088074924 @default.
• W2933402327 hasBestOaLocation W29334023271 @default.
• W2933402327 hasConcept C112592302 @default.
• W2933402327 hasConcept C12554922 @default.

• next