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Aim To provide an electrophysiological basis for hippocampus involved emotional changes caused by tinnitus, the effects of salicylate on electro-physiological characteristics of the voltage-gated calci-um channels in hippocampal neurons were performed. Method The effects of salicylate on voltage-gated cal-cium channels in rat hippocampal neurons were stud-ied, using the whole-cell voltage clamp method. Re-sults Salicylate blocked the voltage-gated calcium channels ( ICa ) in a concentration-dependent manner (0.1~10 mmol · L-1 ) . The half-inhibition concen-tration ( IC50 ) values for the blocking action of salicy-late on ICa were 1.64 mmol·L-1 . With 1 mmol·L-1 salicylate applicalted into bath solution, the steady-state activation curve of calcium channel was shifted by about 9 mV in the hyperpolarizing direction, and its steady-state inactivation curve was not changed. Con-clusion Salicylate inhibits ICa in rat hippocampal neu-rons and significantly affects the activation kinetics of ICa ,which could be related to emotional changes caused by tinnitus.
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Objective To investigate the morphological change and SHP -2(src -homology domain contai-ning protein tygosine phosphatase type 2) gene expression in auditory cortical neuron after auditory deprivation in rat .Methods A total of 48 SD rats were randomly divided into 2-week group ,4-week group ,6-week group ,8-week group and 4 corresponding control groups with 6 rats in each group .Bilateral cochlear ablation was done to traumatized groups to ensure their postoperative ABR threshold was above 90 dB SPL .Then paraffin sectioning and HE and Nissl staining were used to detect morphological change of auditory cortical neuron ,simultaneously the RT-PCR was used to measure the expression of SHP -2 gene in auditory cortical neuron of each group ,and relative quantitative analysis was used .Results The HE and Nissl staining revealed that apoptotic shape of auditory cortical neuron became serious by time ,with the diversified cellular morphology .The relative quantity of SHP -2 gene showed statistical differences between any two groups by the method of one -way ANOVA ,showing a rising trend by time (P<0 .05) .Conclusion Along with time ,auditory cortex ,auditory deprivation showed increasing neuronic apoptosis and neuronic proliferation .Apoptosis was the final result from the mutual antagonism by the 2 factors .
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OBJECTIVE@#To investigate the mechanism of the tinnitus inducer, sodium salicylate, on voltage-gated sodium channels.@*METHOD@#The effects of salicylate on voltage-gated sodium channels in freshly dissociated inferior colliculus neurons of rats were studied, using the whole-cell voltage clamp method.@*RESULT@#Salicylate blocked sodium current (INa) in concentration-dependent manner (0.1-10 mmol/L). The IC50 value for the blocking action of salicylate was 1.43 mmol/L. Salicylate did not affect the conductance-voltage curve and the steady-state activation curve of INa. The steady-state INa inactivation curve of INa was shifted by about 9 mV in the hyperpolarizing direction. In addition, salicylate delayed the sodium channel recovery from INa inactivation by increasing the slow time constant.@*CONCLUSION@#Our results suggest that salicylate causes a concentration-dependent blockade of INa and shifts the INa inactivation curve to more hyperpolarized potentials, which could be related to the mechanism of salicylate-induced tinnitus.
Subject(s)
Animals , Male , Rats , Inferior Colliculi , Cell Biology , Neurons , Metabolism , Patch-Clamp Techniques , Rats, Wistar , Sodium Channels , Metabolism , Sodium Salicylate , PharmacologyABSTRACT
OBJECTIVE To understand what role of the L-type calcium channels play in the mechanism of salicylate-induced tinnitus. METHODS The effects of salicylate on L-type calcium channels in freshly dissociated inferior colliculus neurons of rats were studied using the whole-cell voltage clamp method. RESULTS Salicylate blocked L-type calcium channel current (ICa,L) in concentration-dependent manner. The half-blocking concentration of salicylate was 1.99 mmol/L. Salicylate did not affect the conductance-voltage curve and the steady-state activation curve of ICa,L, shifted the steady-state inactivation curve of ICa,L by about 8 mV in the hyperpolarizing direction, and delayed the recovery from inactivation of ICa,L. CONCLUSION Our results suggest that salicylate’s blocking of L-type calcium channels may contribute to salicylate-induced tinnitus by decreasing the release of ?-aminobutyric acid in the inferior colliculus.