Streptozotocin inhibits synaptic transmission and edaravone attenuates streptozotocin-induced electrophysiological changes in CA1 pyramidal neurons of rat hippocampal slices

Ju, Ting; Wang, Xiaoran; Zhou, Shanshan; Zhao, Tingting; Yang, Meimei; Lin, Jinghan; Sun, Lina; Liu, Tingjiao; Xu, Yi; Zhang, Liming

doi:10.1016/j.neuro.2016.09.005

Cited by 6 publications

(11 citation statements)

References 52 publications

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“…Moreover, EDA alone did not affect synaptic transmission compared with the control state [24]. Accordingly, EDAinduced changes could not compensate for the STZ-induced changes.…”

Section: Resultsmentioning

confidence: 75%

“…As a result of our previous work indicating that the wash-out of STZ state showed no effects compared to STZ state, currents were tested in the pre-treatment of STZ for at least 30 minutes before application of EDA, which could then avoid a direct interaction between STZ and EDA and also represent a co-application of STZ and EDA [24]. Moreover, EDA alone did not affect synaptic transmission compared with the control state [24].…”

Section: Resultsmentioning

confidence: 99%

“…Specifically, as revealed from measures of spontaneous excitatory postsynaptic current (sEPSC), miniature excitatory postsynaptic current (mEPSC), spontaneous inhibitory postsynaptic current (sIPSC) and miniature inhibitory postsynaptic current (mIPSC), we found that EDA could attenuate acute and chronic neurotoxicity of STZ within CA1 pyramidal neurons of rat hippocampal slices [24]. In this study, we directed our investigation toward examining the effects of EDA on the CA3-CA1 synaptic pathway in this STZ model as achieved by measuring evoked excitatory postsynaptic currents (eEPSCs), AMPAR-mediated eEPSCs (eEPSCs AMPA ), evoked inhibitory postsynaptic currents (eIPSCs), evoked excitatory postsynaptic current paired pulse ratio (eEPSC PPR) and evoked inhibitory postsynaptic current paired pulse ratio (eIPSC PPR).…”

Section: Introductionmentioning

confidence: 95%

“…Within our laboratory, we have demonstrated neuroprotective effects of EDA upon STZ-induced models of AD [11] and STZ-induced electrophysiological changes in CA1 pyramidal neurons of rat hippocampal slices [24]. Specifically, as revealed from measures of spontaneous excitatory postsynaptic current (sEPSC), miniature excitatory postsynaptic current (mEPSC), spontaneous inhibitory postsynaptic current (sIPSC) and miniature inhibitory postsynaptic current (mIPSC), we found that EDA could attenuate acute and chronic neurotoxicity of STZ within CA1 pyramidal neurons of rat hippocampal slices [24].…”

Section: Introductionmentioning

confidence: 98%

“…As oxidative imbalance represents a manifestation of AD, even preceding Aβ deposition and neurofibrillary tangles [20][21][22][23], ICV-STZ treated rats could serve as a model of AD. We have demonstrated previously that STZ was effective in inducing neurotoxicity upon synaptic transmission [24], but much work remains to be done with regard to these STZ-induced effects in CA1 pyramidal neurons of rat hippocampal slices.…”

Section: Introductionmentioning

confidence: 99%

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Streptozotocin Inhibits Electrophysiological Determinants of Excitatory and Inhibitory Synaptic Transmission in CA1 Pyramidal Neurons of Rat Hippocampal Slices: Reduction of These Effects by Edaravone

Wang

et al. 2016

Cell Physiol Biochem

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Background: Streptozotocin (STZ) has served as an agent to generate an Alzheimer's disease (AD) model in rats, while edaravone (EDA), a novel free radical scavenger, has recently emerged as an effective treatment for use in vivo and vitro AD models. However, to date, these beneficial effects of EDA have only been clearly demonstrated within STZ-induced animal models of AD and in cell models of AD. A better understanding of the mechanisms of EDA may provide the opportunity for their clinical application in the treatment of AD. Therefore, the purpose of this study was to investigate the underlying mechanisms of STZ and EDA as assessed upon electrophysiological alterations in CA1 pyramidal neurons of rat hippocampal slices. Methods: Through measures of evoked excitatory postsynaptic currents (eEPSCs), AMPAR-mediated eEPSCs (eEPSCs_AMPA), evoked inhibitory postsynaptic currents (eIPSCs), evoked excitatory postsynaptic current paired pulse ratio (eEPSC PPR) and evoked inhibitory postsynaptic current paired pulse ratio (eIPSC PPR), it was possible to investigate mechanisms as related to the neurotoxicity of STZ and reductions in these effects by EDA. Results: Our results showed that STZ (1000 µM) significantly inhibited peak amplitudes of eEPSCs, eEPSCs_AMPA and eIPSCs, while EDA (1000 µM) attenuated these STZ-induced changes at holding potentials ranging from -60mV to +40 mV for EPSCs and -60mV to +20 mV for IPSCs. Our work also indicated that mean eEPSC PPR were substantially altered by STZ, effects which were partially restored by EDA. In contrast, no significant effects upon eIPSC PPR were obtained in response to STZ and EDA. Conclusion: Our data suggest that STZ inhibits glutamatergic transmission involving pre-synaptic mechanisms and AMPAR, and that STZ inhibits GABAergic transmission by post-synaptic mechanisms within CA1 pyramidal neurons. These effects are attenuated by EDA.

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“…Moreover, EDA alone did not affect synaptic transmission compared with the control state [24]. Accordingly, EDAinduced changes could not compensate for the STZ-induced changes.…”

Section: Resultsmentioning

confidence: 75%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%