Traditionally, brain function is considered to be exclusive to neuronal activity. Recent studies have shown that in addition to the classical bidirectional information flow between presynaptic and postsynaptic neurons, astrocytes also participate in the process of information exchange between synaptic neurons, response to synaptic activity, and regulation of synaptic transmission. We review herein astrocytes integrate and process synaptic information and finally regulate synaptic transmission and plasticity through releasing gliotransmitters.
Key words:
Tripartite synapse; Astrocyte; Synaptic transmission; Synaptic plasticity
This study explored the change in mortality rates of respiratory disease during the corona virus disease 2019 (COVID-19) pandemic. Death data of registered residents of Suzhou from 2014 to 2020 were collected and the weekly mortality rates due to respiratory disease and all deaths were analyzed. The differences in mortality rates during the pandemic and the same period in previous years were compared. Before the pandemic, the crude mortality rate (CMR) and standardized mortality rate (SMR) of Suzhou residents including respiratory disease, were not much different from those in previous years. During the emergency period, the CMR of Suzhou residents was 180.2/100,000 and the SMR was 85.5/100,000, decreasing by 9.1% and 14.6%, respectively; the CMR of respiratory disease was 16.4/100,000 and the SMR was 6.8/100,000, down 41.4% and 44.9%, respectively. Regardless of the mortality rates of all deaths or respiratory disease, the rates were higher in males than in females, although males had aslightly greater decrease in all deaths during the emergency period compared with females, and the opposite was true for respiratory disease. During the pandemic, the death rate of residents decreased, especially that due to respiratory disease.
Background: Isoflurane (IFL), one of the most widely used volatile anesthetics, has an anti-nociceptive effect at the spinal cord level. However, the reported spinal mechanisms of IFL analgesic action remain controversial. The aim of this study was to examine the effect of IFL on the excitability of spinal substantia gelatinosa (SG, lamina II) neurons and the synaptic transmission from primary nociceptive fibers to SG neurons.Methods: Parasagittal spinal slices with a dorsal root attached were cut from the Sprague-Dawley rats (4-6 weeks old). Whole-cell patch-clamp recordings were made from SG neurons at room temperature. Dorsal root stimulation was used to evoke excitatory postsynaptic currents (eEPSCs). Depolarizing current injection was used to display the firing pattern of action potentials. IFL was given as volume percent (3%) by passing the gas mixture (flow rate, 0.5 L/minute) into equilibrated artificial cerebral spinal fluid (ACSF) for at least 15 minutes at room temperature.Results: IFL significantly suppressed the peak amplitude of monosynaptic eEPSCs mediated by primary Aδ and C fibers. Regardless of neuron types, IFL significantly decreased the frequency of action potentials in all SG neurons tested.Conclusions: IFL may play analgesic role through inhibiting or weakening the excitability and synaptic transmission of spinal nociceptive pathway. Citation: Jie Liu, Gen-Lin Ji, Jian-Min Li, Tun Liu, Qun Wang, Ya-Nan Pu, et al. Isoflurane suppresses the excitability and synaptic transmission of spinal nociceptive pathway in rats. J Anesth Perioper Med 2015; 2: 61-5. doi: 10.24015/JAPM.2015.0010This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
The use of high-power microwave (HPM) in our daily live is becoming more and more widespread, but the safety has also caused our concern. And ferroptosis is a newly discovered modality that can regulate cell death in recent years. The aim of our study was to demonstrate whether ferroptosis is an important cause of myocardial injury caused by HPM. And whether myocardial injury caused by HPM can be alleviated by inhibiting ferroptosis.We verified the extent of myocardial damage by different doses of HPM through in vivo and in vitro assays, respectively. In addition, GPX4 was knocked down and overexpressed in cardiac myocytes to verify the altered sensitivity of cardiac myocytes to HPM. Finally, the therapeutic effect of Fer-1 and tanshinoneIIA on myocardial injury caused by HPM was verified in in vivo and in vitro assays.We found that cardiac tissue and cardiomyocyte injury in mice gradually increased with increasing HPM dose, while ferroptosis markers were consistent with the injury trend. Gpx4 had an important role in ferroptosis in cardiomyocytes caused by HPM. Finally, tanshinoneIIA and Fer-1 could attenuate the damage of cardiac tissues and cardiomyocytes caused by HPM.In conclusion, our study found that ferroptosis, a novel mode of cell death, is present in myocardial injury caused by HPM. Moreover, tanshinone, a drug already in clinical use, can significantly reduce myocardial injury caused by HPM, which is promising to provide new therapeutic ideas for myocardial injury caused by HPM.
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