Autophagy mediates the degradation of synaptic vesicles: A potential mechanism of synaptic plasticity injury induced by microwave exposure in rats

Hao, Yanhui; Li, Wenchao; Wang, Hui; Zhang, Jing; Yu, Chao; Tan, Shengzhi; Wang, Haoyu; Xu, Xinping; Dong, Ji; Yao, Baojin; Zhou, Hongmei; Zhao, Li; Peng, Ruiyun

doi:10.1016/j.physbeh.2018.02.005

Cited by 20 publications

(24 citation statements)

References 43 publications

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“…Interestingly, previous studies showed that the expression of LC3-II was increased in sevoflurane induced cognitive impairment, while p62 was decreased (Li X. et al, 2017), which is consistent with our results. Based on the evidence that excessive autophagy in hippocampus is closely associated with cognitive impairment (Xu et al, 2016; Li X. et al, 2017; Hao et al, 2018), our present results suggested that excessive hippocampal autophagy is an important pathological mechanism involved in the SD-induced cognitive impairment.…”

Section: Discussionsupporting

confidence: 54%

“…Sleep deprivation (SD) is considered as a common social phenomenon and is a frequent cause of cognitive impairment (Miller, 2015; Feng et al, 2016; Hao et al, 2018). It is well established that H 2 S regulates learning and memory (Nagpure and Bian, 2015; Zhuang et al, 2016; Tang et al, 2018) and that excessive autophagy in hippocampus causes cognitive impairment (Xu et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Autophagy is essential for maintaining metabolic balance by digestion of misfolded proteins and dysfunctional organelles (Mizushima and Komatsu, 2011; Shehata and Inokuchi, 2014). However, it has been reported that excessive activation of autophagy damages synaptic plasticity in hippocampus (Hao et al, 2018) and that excessive activation of autophagy in hippocampus is responsible for cognitive impairment induced by hypoxic-ischemic brain injury (Xu et al, 2016) and sevoflurane (Li X. et al, 2017). Interestingly, inhibition of autophagy has a protective effect on cognitive impairment (Wang et al, 2015, 2017; Kong et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

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Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment

et al. 2019

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Background and Aim: Sleep deprivation (SD) causes deficit of cognition, but the mechanisms remain to be fully established. Hydrogen sulfide (H2S) plays an important role in the formation of cognition, while excessive and prolonged autophagy in hippocampus triggers cognitive disorder. In this work, we proposed that disturbances in hippocampal endogenous H2S generation and autophagy might be involved in SD-induced cognitive impairment.Methods: After treatment of adult male wistar rats with 72-h SD, the Y-maze test, object location test (OLT), novel object recognition test (NORT) and the Morris water maze (MWM) test were performed to determine the cognitive function. The autophagosome formation was observed with electron microscope. Generation of endogenous H2S in the hippocampus of rats was detected using unisense H2S microsensor method. The expressions of cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), beclin-1, light chain LC3 II/LC3 I, and p62 in the hippocampus were assessed by western blotting.Results: The Y-maze, OLT, NORT, and MWM test demonstrated that SD-exposed rats exhibited cognitive dysfunction. SD triggered the elevation of hippocampal autophagy as evidenced by enhancement of autophagosome, up-regulations of beclin-1 and LC3 II/LC3 I, and down-regulation of p62. Meanwhile, the generation of endogenous H2S and the expressions of CBS and 3-MST (H2S producing enzyme) in the hippocampus of SD-treated rats were reduced.Conclusion: These results suggested that inhibition of endogenous H2S generation and excessiveness of autophagy in hippocampus are involved in SD-induced cognitive impairment.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment

et al. 2019

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“…Autophagy is known to contribute to changes in synaptic plasticity. While increased autophagy activation through mTOR inhibitors such as rapamycin [23,26,69] as well as quantum dots [27] and increased autophagy through microwave radiation [70] reduced LTP, also the reduction of autophagy might impair synaptic plasticity as it seems to be necessary for LTP [71,72]. Together, this suggests that a sensitive balance between protein degradation systems but also within individual protein degradation systems is required to maintain synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

Proteasome and Autophagy-Mediated Impairment of Late Long-Term Potentiation (l-LTP) after Traumatic Brain Injury in the Somatosensory Cortex of Mice

Feldmann

Prieult

Felzen

et al. 2019

IJMS

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Traumatic brain injury (TBI) can lead to impaired cognition and memory consolidation.The acute phase (24–48 h) after TBI is often characterized by neural dysfunction in the vicinity ofthe lesion, but also in remote areas like the contralateral hemisphere. Protein homeostasis is crucialfor synaptic long-term plasticity including the protein degradation systems, proteasome andautophagy. Still, little is known about the acute effects of TBI on synaptic long-term plasticity andprotein degradation. Thus, we investigated TBI in a controlled cortical impact (CCI) model in themotor and somatosensory cortex of mice ex vivo-in vitro. Late long-term potentiation (l-LTP) wasinduced by theta-burst stimulation in acute brain slices after survival times of 1–2 days. Proteinlevels for the plasticity related protein calcium/calmodulin-dependent protein kinase II (CaMKII)was quantified by Western blots, and the protein degradation activity by enzymatical assays. Weobserved missing maintenance of l-LTP in the ipsilateral hemisphere, however not in thecontralateral hemisphere after TBI. Protein levels of CaMKII were not changed but, interestingly,the protein degradation revealed bidirectional changes with a reduced proteasome activity and anincreased autophagic flux in the ipsilateral hemisphere. Finally, LTP recordings in the presence ofpharmacologically modified protein degradation systems also led to an impaired synaptic plasticity:bath-applied MG132, a proteasome inhibitor, or rapamycin, an activator of autophagy, bothadministered during theta burst stimulation, blocked the induction of LTP. These data indicate thatalterations in protein degradation pathways likely contribute to cognitive deficits in the acute phaseafter TBI, which could be interesting for future approaches towards neuroprotective treatmentsearly after traumatic brain injury.

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“…Importantly, previous research has established that MW exposure impaired N-methyl-D-aspartate Recepto (NMDAR) signaling molecules, neurotransmitter release, and calcium influx in the hippocampus, which may be related to synaptic plasticity deficit (Xiong et al, 2015). It has also been suggested that the MW exposure increases autophagy in the hippocampus and may lead to synaptic plasticity impairment via degradation of synaptic vesicles (Hao et al, 2018; Zhi et al, 2018). Thus, the impairment of LTP induction and decrease of synaptic vesicles might causes cognitive deficits after MW exposure (Wang et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

2.45 GHz microwave radiation impairs learning, memory, and hippocampal synaptic plasticity in the rat

et al. 2018

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Microwave (MW) radiation has a close relationship with neurobehavioral disorders. Due to the widespread usage of MW radiation, especially in our homes, it is essential to investigate the direct effect of MW radiation on the central nervous system. Therefore, this study was carried out to determine the effect of MW radiation on memory and hippocampal synaptic plasticity. The rats were exposed to 2.45 GHz MW radiation (continuous wave with overall average power density of 0.016 mW/cm2 and overall average whole-body specific absorption rate value of 0.017 W/kg) for 2 h/day over a period of 40 days. Spatial learning and memory were tested by radial maze and passive avoidance tests. We evaluated the synaptic plasticity and hippocampal neuronal cells number by field potential recording and Giemsa staining, respectively. Our results showed that MW radiation exposure decreased the learning and memory performance that was associated with decrement of long-term potentiation induction and excitability of CA1 neurons. However, MW radiation did not have any effects on short-term plasticity and paired-pulse ratio as a good indirect index for measurement of glutamate release probability. The evaluation of hippocampal morphology indicated that the neuronal density in the hippocampal CA1 area was significantly decreased by MW.

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Autophagy mediates the degradation of synaptic vesicles: A potential mechanism of synaptic plasticity injury induced by microwave exposure in rats

Cited by 20 publications

References 43 publications

Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment

Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment

Proteasome and Autophagy-Mediated Impairment of Late Long-Term Potentiation (l-LTP) after Traumatic Brain Injury in the Somatosensory Cortex of Mice

2.45 GHz microwave radiation impairs learning, memory, and hippocampal synaptic plasticity in the rat

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