Paraflocculus plays a role in salicylate-induced tinnitus

Du, Yali; Liu, Junxiu; Jiang, Qin; Duan, Qingyun; Mao, Lanqun; Ma, Furong

doi:10.1016/j.heares.2017.06.013

Cited by 16 publications

(16 citation statements)

References 51 publications

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“…The specificity study shown in Figure 3 demonstrates that online electrochemical method has a good selectivity and linear response for ascorbate and has been confirmed that it's very suitable for studying the changes of ascorbate independent of O2 and pH fluctuation and other co-existing interference in the spinal cord. As shown in our earlier research [21,25,26], our OECS coupled with in vivo micro-dialysis has high specificity, good accuracy, and stability for monitoring ascorbate continuously in the study of different pathophysiological mechanisms. As depicted in Figure 4, in the first 30 min after beginning the recording, the current response recorded for the spinal cord microdialysate continuously sampled from the spinal cord remained constant indicating that after 90 minutes of equilibrating, the local microenvironment of the spinal cord reaches to steady state.…”

Section: Discussionmentioning

confidence: 63%

Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels

Zhang¹,

Hou²,

Ji³

et al. 2020

Int. J. Med. Sci.

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Background: Surgical decompression after acute spinal cord injury has become the consensus of orthopaedic surgeons. However, the choice of surgical decompression time window after acute spinal cord injury has been one of the most controversial topics in orthopaedics. Objective: We apply an online electrochemical system (OECS) for continuously monitoring the ascorbate of the rats' spinal cord to determine the extent to which ascorbate levels were influenced by contusion or sustained compression. Methods: Adult Sprague-Dawley rats (n=10) were instrumented for ascorbate concentration recording and received T11 drop spinal cord injury (SCI). The Group A (n=5) were treated with immediately decompression after SCI. The Group B (n=5) were contused and oppressed until 1 h after the injury to decompress.Results: The ascorbate level of spinal cord increased immediately by contusion injury and reached to 1.62 μmol/L ± 0.61 μmol/L (217.30% ± 95.09% of the basal level) at the time point of 60 min after the injury. Compared with the Group A, the ascorbate level in Group B increased more significantly at 1 h after the injury, reaching to 3.76 μmol/L ± 1.75 μmol/L (430.25% ± 101.30% of the basal level). Meanwhile, we also found that the decompression after 1 hour of continuous compression will cause delayed peaks of ascorbate reaching to 5.71 μmol/L ± 2.69 μmol/L (627.73% ± 188.11% of the basal level). Conclusion:Our study provides first-hand direct experimental evidence indicating ascorbate is directly involved in secondary spinal cord injury and exhibits the dynamic time course of microenvironment changes after continuous compression injury of the spinal cord.

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Section: Discussionmentioning

confidence: 63%

Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels

Zhang¹,

Hou²,

Ji³

et al. 2020

Int. J. Med. Sci.

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“…In our study, we treated rats with a high dose of SS (350 mg/kg) to investigate changes in the AC during tinnitus. This dose was the same as that used by Jastrboff and has been used in many behavioral experiments, with a reliable behavioral manifestation of tinnitus …”

Section: Discussionmentioning

confidence: 99%

“…This dose was the same as that used by Jastrboff and has been used in many behavioral experiments, with a reliable behavioral manifestation of tinnitus. 21,[23][24][25] AA reaches the highest concentration in the brain. 12 As an important endogenous antioxidant, SS is considered to be neuroprotective.…”

Section: Effects Of Lidocaine On Ss-induced Single-unit Ac Neuron Dismentioning

confidence: 98%

Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex

Duan

Zhang

2019

Pediatric Investigation

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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.

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“…The output of the electrode was connected to a 16-channel preamplifier (Plexon Inc, Dallas, TX, USA) using a flexible low-noise cable. [ 23 ] Signals were sent to a multichannel acquisition processor and recorded. Signals were analyzed using Offline Sorter (Plexon Inc, Dallas, TX, USA) and NeuroExplorer (Nex Technologies, Madison, AL, USA) for spike sorting.…”

Section: Ethodsmentioning

confidence: 99%

Effect of Neuronal Excitability in Hippocampal CA1 Area on Auditory Pathway in a Rat Model of Tinnitus

Ding

Song

Liu

et al. 2018

Chinese Medical Journal

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Background:Tinnitus is a common disorder that causes significant morbidity; however, the neurophysiological mechanism is not yet fully understood. A relationship between tinnitus and limbic system has been reported. As a significant component of the limbic system, the hippocampus plays an important role in various pathological processes, such as emotional disturbance, decreased learning ability, and deterioration of memory. This study was aimed to explore the role of the hippocampus in the generation of tinnitus by electrophysiological technology.Methods:A tinnitus model was established in rats through intraperitoneal injection of salicylate (SA). Subsequently, the spontaneous firing rate (SFR) of neurons in the hippocampal CA1 area was recorded with in vivo multichannel recording technology to assess changes in excitability induced by SA. To investigate the effect of excitability changes of hippocampus on the auditory pathway, the hippocampus was electrically stimulated and neural excitability in the auditory cortex (AC) was monitored.Results:Totally 65 neurons in the hippocampal CA1 area were recorded, 45 from the SA group (n = 5), and 20 from the saline group (n = 5). Two hours after treatment, mean SFR of neurons in the hippocampal CA1 area had significantly increased from 3.06 ± 0.36 Hz to 9.18 ± 1.30 Hz in the SA group (t = −4.521, P < 0.05), while no significant difference was observed in the saline group (2.66 ± 0.36 Hz vs. 2.16 ± 0.36 Hz, t = 0.902, P > 0.05). In the AC, 79.3% (157/198) of recorded neurons showed responses to electrical stimulation of the hippocampal CA1 area. Presumed pyramidal neurons were excited, while intermediate neurons were inhibited after electrical stimulation of the hippocampus.Conclusions:The study shows that the hippocampus is excited in SA-induced tinnitus, and stimulation of hippocampus could modulate neuronal excitability of the AC. The hippocampus is involved in tinnitus and may also have a regulatory effect on the neural center.

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Paraflocculus plays a role in salicylate-induced tinnitus

Cited by 16 publications

References 51 publications

Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels

Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels

Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex

Effect of Neuronal Excitability in Hippocampal CA1 Area on Auditory Pathway in a Rat Model of Tinnitus

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