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Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex
IMPORTANCE: Clinical observations have implied a central origin for tinnitus and potential therapeutic effects of ascorbic acid (AA); however, the detailed mechanisms remain undetermined. OBJECTIVE: To investigate changes in the AA levels and neural activity in the auditory cortex (AC) during salicy...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7331419/ https://www.ncbi.nlm.nih.gov/pubmed/32851309 http://dx.doi.org/10.1002/ped4.12143 |
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author | Duan, Qingchuan Ma, Furong Zhang, Jie |
author_facet | Duan, Qingchuan Ma, Furong Zhang, Jie |
author_sort | Duan, Qingchuan |
collection | PubMed |
description | IMPORTANCE: Clinical observations have implied a central origin for tinnitus and potential therapeutic effects of ascorbic acid (AA); however, the detailed mechanisms remain undetermined. OBJECTIVE: To investigate changes in the AA levels and neural activity in the auditory cortex (AC) during salicylate‐induced tinnitus. METHODS: Rats were randomly divided into 3 groups: (1) saline group, which received an intraperitoneal saline injection; (2) SS group, which received an intraperitoneal sodium salicylate (SS) injection (350 mg/kg); and (3) SS+Lido group, which received an intraperitoneal SS injection (350 mg/kg) and lidocaine delivered to the AC by microdialysis. For each group, we firstly used an in vivo microdialysis technique to investigate the concentrations of AA in the AC; and secondly, we recorded the neural activity in the AC using a single‐unit recording technique. RESULTS: The AA concentration in the SS group significantly increased after SS injection, whereas that of the saline group did not change. The AA concentration in the SS+Lido group also showed an increasing trend but was significantly lower than that in the SS group. In the electrophysiological study, the spontaneous firing rate of the SS group was significantly higher than that of the saline group. In addition, the proportion of short interval discharges was also higher in the SS group than in the saline group. Both differences were reversed by lidocaine treatment. INTERPRETATION: Our data suggest that the elevation of AA levels in the AC may be related to increased neuronal activity, which may represent the mechanism underlying salicylate‐induced tinnitus. |
format | Online Article Text |
id | pubmed-7331419 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73314192020-08-25 Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex Duan, Qingchuan Ma, Furong Zhang, Jie Pediatr Investig Original Articles IMPORTANCE: Clinical observations have implied a central origin for tinnitus and potential therapeutic effects of ascorbic acid (AA); however, the detailed mechanisms remain undetermined. OBJECTIVE: To investigate changes in the AA levels and neural activity in the auditory cortex (AC) during salicylate‐induced tinnitus. METHODS: Rats were randomly divided into 3 groups: (1) saline group, which received an intraperitoneal saline injection; (2) SS group, which received an intraperitoneal sodium salicylate (SS) injection (350 mg/kg); and (3) SS+Lido group, which received an intraperitoneal SS injection (350 mg/kg) and lidocaine delivered to the AC by microdialysis. For each group, we firstly used an in vivo microdialysis technique to investigate the concentrations of AA in the AC; and secondly, we recorded the neural activity in the AC using a single‐unit recording technique. RESULTS: The AA concentration in the SS group significantly increased after SS injection, whereas that of the saline group did not change. The AA concentration in the SS+Lido group also showed an increasing trend but was significantly lower than that in the SS group. In the electrophysiological study, the spontaneous firing rate of the SS group was significantly higher than that of the saline group. In addition, the proportion of short interval discharges was also higher in the SS group than in the saline group. Both differences were reversed by lidocaine treatment. INTERPRETATION: Our data suggest that the elevation of AA levels in the AC may be related to increased neuronal activity, which may represent the mechanism underlying salicylate‐induced tinnitus. John Wiley and Sons Inc. 2019-09-26 /pmc/articles/PMC7331419/ /pubmed/32851309 http://dx.doi.org/10.1002/ped4.12143 Text en © 2019 Chinese Medical Association. Pediatric Investigation published by John Wiley & Sons Australia, Ltd on behalf of Futang Research Center of Pediatric Development. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Duan, Qingchuan Ma, Furong Zhang, Jie Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
title | Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
title_full | Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
title_fullStr | Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
title_full_unstemmed | Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
title_short | Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
title_sort | salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7331419/ https://www.ncbi.nlm.nih.gov/pubmed/32851309 http://dx.doi.org/10.1002/ped4.12143 |
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