Evaluation of the synaptic plasticity via long term potentiation in the acoustic trauma tinnitus model of mice

Aim and HypothesisTinnitus is the perception of a sound in the absence of any external stimulus. Though its pathophysiological process still remains obscure, tinnitus has been under investigation for its association with synaptic plasticity in recent years.Synaptic plasticity is the differentiation of a synapse between two neurons due to the changes in external or internal environment. Synaptic plasticity can be evaluated by some electrophysiological measurements. Patch clamp is among the procedures, which are used for this purpose, and the long term potentiation is the electrical activity which is observed as the change.This study aimed to indicate the existence of the synaptic plasticity by figuring out the long term potentiation in the pathophysiology of tinnitus which was induced by the acoustic trauma model.MethodA total of 30 postnatal 16-day BABL/c mice consisting of 15 mice as the control group and 15 mice as the tinnitus induced group were used in the study. Tinnitus was induced in the mice through the acoustic trauma model. The induction of tinnitus in the mice and the hearing level was found by the startle reflex time and gap detection time measurements.The probability of the long term potentiation was searched by using the whole cell patch clamp technique in the fusiform cells which were isolated from the dorsal cochlear nucleus of the mice on their postnatal day 17.ResultsThe measurements, which were made on all experiment mice on their postnatal day 16 by using 90 dB SPL pure tone, gave the startle reflex time less than 5 seconds. No statistical difference was found between the control group and the pre-trauma acoustic trauma group with regard to gap detection time (p=0,604). The experiments performed by using 100 dB SPL pure tone after acoustic trauma. While the startle reflex time of the experiment mice was found to be less than 5 seconds with 100 dB SPL pure tone in the acoustic trauma group, a statistically significant increase was found in their gap detection times compared to the pre-trauma period and tinnitus was observed to have been induced, so ( 9,58+/-1,65 sec. in the pre-trauma period?? and 36,89+/-5,08 sec. in the post-trauma period p=0,001).In the tinnitus induced group, the long term potentiation was found to be meaningfully higher than the control group (86,7 % in the acoustic trauma group and 13,3 % in the control group p=0.000).ConclusionThe existence of synaptic plasticity in tinnitus drew attention as a result of the increased activity some cortical and subcortical areas of patients complaining about tinnitus and experiment mice. It is considered that dorsal cochlear nucleus, with its multilayer anatomical structure and physiological characteristics that allow associations with various cortical and subcortical regions, can be the key point of synaptic plasticity in tinnitus. The fact that the long term potentiation, which is one of the key indicators of synaptic plasticity, can be observed in some cells raise concerns about dorsal cochlear nucleus in this subject.The long term potentiation, which was found to be meaningfully higher in the dorsal cochlear nuclei of the mice with tinnitus than the control group (p=0.000), constitutes a strong evidence of the existence of synaptic plasticity in the pathophysiological mechanism of tinnitus.