NDLI: Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, Ca$^{2+}$-Activated K$^{+}$ Channels In Vitro

Please wait, while we are loading the content...

Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, Ca$^{2+}$-Activated K$^{+}$ Channels In Vitro

Pairwise Classifier Ensemble with Adaptive Sub-Classifiers for fMRI Pattern Analysis

Expression of SoxC Transcription Factors during Zebrafish Retinal and Optic Nerve Regeneration

A New Perspective for Parkinson’s Disease: Circadian Rhythm

A Review of the Functional and Anatomical Default Mode Network in Schizophrenia

Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity

Optical Brain Imaging: A Powerful Tool for Neuroscience

Intracellular TG2 Activity Increases Microtubule Stability but is not Sufficient to Prompt Neurite Growth

Associations Between PPP1R1B Gene Polymorphisms and Anxiety Levels in the Chinese Population

Neuroglial Crosstalk by Mitochondria

A Longer Siesta? DN1s in Control!

Finding the ‘Guilty’ Gene Variant of Sporadic Parkinson’s Disease Via CRISPR/Cas9

A New Link Between Insulin Signaling and Fragile X Syndrome

Glial Activation, A Common Mechanism Underlying Spinal Synaptic Plasticity?

Neuroscience Bulletin : Volume 32

Neuroscience Bulletin : Volume 31

Neuroscience Bulletin : Volume 30

Neuroscience Bulletin : Volume 29

Neuroscience Bulletin : Volume 28

Neuroscience Bulletin : Volume 27

Neuroscience Bulletin : Volume 26

Neuroscience Bulletin : Volume 25

Neuroscience Bulletin : Volume 24

Neuroscience Bulletin : Volume 23

Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, Ca$^{2+}$-Activated K$^{+}$ Channels In Vitro

Content Provider	Springer Nature Link
Author	Su, Fang Guo, An Chen Li, Wei Wei Zhao, Yi Long Qu, Zheng Yi Wang, Yong Jun Wang, Qun Zhu, Yu Lan
Copyright Year	2016
Abstract	Increasing evidence suggests that low to moderate ethanol ingestion protects against the deleterious effects of subsequent ischemia/reperfusion; however, the underlying mechanism has not been elucidated. In the present study, we showed that expression of the neuronal large-conductance, Ca$^{2+}$-activated K$^{+}$ channel (BK$_{Ca}$) α-subunit was upregulated in cultured neurons exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) compared with controls. Preconditioning with low-dose ethanol (10 mmol/L) increased cell survival rate in neurons subjected to OGD/R, attenuated the OGD/R-induced elevation of cytosolic Ca$^{2+}$ levels, and reduced the number of apoptotic neurons. Western blots revealed that ethanol preconditioning upregulated expression of the anti-apoptotic protein Bcl-2 and downregulated the pro-apoptotic protein Bax. The protective effect of ethanol preconditioning was antagonized by a BK$_{Ca}$ channel inhibitor, paxilline. Inside-out patches in primary neurons also demonstrated the direct activation of the BK$_{Ca}$ channel by 10 mmol/L ethanol. The above results indicated that low-dose ethanol preconditioning exerts its neuroprotective effects by attenuating the elevation of cytosolic Ca$^{2+}$ and preventing neuronal apoptosis, and this is mediated by BK$_{Ca}$ channel activation.
Starting Page	28
Ending Page	40
Page Count	13
File Format	PDF
ISSN	16737067
Journal	Neuroscience Bulletin
Volume Number	33
Issue Number	1
e-ISSN	19958218
Language	English
Publisher	Springer Singapore
Publisher Date	2016-11-16
Publisher Place	Singapore
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Oxygen-glucose deprivation/reoxygenation Ethanol preconditioning BK$_{Ca}$ channel Neuroprotection Apoptosis Neurosciences Human Physiology Anesthesiology Anatomy Neurology Pain Medicine
Content Type	Text
Resource Type	Article
Subject	Neuroscience Physiology Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Sulforaphane protects primary cultures of cortical neurons against injury induced by oxygen-glucose deprivation/reoxygenation via antiapoptosis

Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase

Mitochondrial BKCa Mediates the Protective Effect of Low-Dose Ethanol Preconditioning on Oxygen-Glucose Deprivation and Reperfusion-Induced Neuronal Apoptosis

Paeoniflorin protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced injury via activating JAK2/STAT3 signaling.

Activation of big conductance Ca2+-activated K+ channels (BK) protects the heart against ischemia–reperfusion injury

Scoparone protects neuronal cells from oxygen glucose deprivation/reoxygenation injury.

Dexmedetomidine protects against oxygen-glucose deprivation/reoxygenation injury-induced apoptosis via the p38 MAPK/ERK signalling pathway

Metformin Protects Neurons against Oxygen-Glucose Deprivation/Reoxygenation -Induced Injury by Down-Regulating MAD2B

A Novel Opener of Large-Conductance $Ca^{2+}-Activated$ $K^{+}$ (BK) Channel Reduces Ischemic Injury in Rat Cardiac Myocytes by Activating Mitochondrial $K_{Ca}$ Channel

Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, Ca$^{2+}$-Activated K$^{+}$ Channels In Vitro

Similar Documents

Sulforaphane protects primary cultures of cortical neurons against injury induced by oxygen-glucose deprivation/reoxygenation via antiapoptosis

Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase

Mitochondrial BKCa Mediates the Protective Effect of Low-Dose Ethanol Preconditioning on Oxygen-Glucose Deprivation and Reperfusion-Induced Neuronal Apoptosis

Paeoniflorin protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced injury via activating JAK2/STAT3 signaling.

Activation of big conductance Ca2+-activated K+ channels (BK) protects the heart against ischemia–reperfusion injury

Scoparone protects neuronal cells from oxygen glucose deprivation/reoxygenation injury.

Dexmedetomidine protects against oxygen-glucose deprivation/reoxygenation injury-induced apoptosis via the p38 MAPK/ERK signalling pathway

Metformin Protects Neurons against Oxygen-Glucose Deprivation/Reoxygenation -Induced Injury by Down-Regulating MAD2B

A Novel Opener of Large-Conductance $Ca^{2+}-Activated$ $K^{+}$ (BK) Channel Reduces Ischemic Injury in Rat Cardiac Myocytes by Activating Mitochondrial $K_{Ca}$ Channel

Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, Ca$^{2+}$-Activated K$^{+}$ Channels In Vitro