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      Cortical spreading depression-induced preconditioning in the brain

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          Abstract

          Cortical spreading depression is a technique used to depolarize neurons. During focal or global ischemia, cortical spreading depression-induced preconditioning can enhance tolerance of further injury. However, the underlying mechanism for this phenomenon remains relatively unclear. To date, numerous issues exist regarding the experimental model used to precondition the brain with cortical spreading depression, such as the administration route, concentration of potassium chloride, induction time, duration of the protection provided by the treatment, the regional distribution of the protective effect, and the types of neurons responsible for the greater tolerance. In this review, we focus on the mechanisms underlying cortical spreading depression-induced tolerance in the brain, considering excitatory neurotransmission and metabolism, nitric oxide, genomic reprogramming, inflammation, neurotropic factors, and cellular stress response. Specifically, we clarify the procedures and detailed information regarding cortical spreading depression-induced preconditioning and build a foundation for more comprehensive investigations in the field of neural regeneration and clinical application in the future.

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          Most cited references86

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          The function of heat-shock proteins in stress tolerance: degradation and reactivation of damaged proteins.

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            Mechanisms of spreading depression and hypoxic spreading depression-like depolarization.

            G Somjen (2001)
            Spreading depression (SD) and the related hypoxic SD-like depolarization (HSD) are characterized by rapid and nearly complete depolarization of a sizable population of brain cells with massive redistribution of ions between intracellular and extracellular compartments, that evolves as a regenerative, "all-or-none" type process, and propagates slowly as a wave in brain tissue. This article reviews the characteristics of SD and HSD and the main hypotheses that have been proposed to explain them. Both SD and HSD are composites of concurrent processes. Antagonists of N-methyl-D-aspartate (NMDA) channels or voltage-gated Na(+) or certain types of Ca(2+) channels can postpone or mitigate SD or HSD, but it takes a combination of drugs blocking all known major inward currents to effectively prevent HSD. Recent computer simulation confirmed that SD can be produced by positive feedback achieved by increase of extracellular K(+) concentration that activates persistent inward currents which then activate K(+) channels and release more K(+). Any slowly inactivating voltage and/or K(+)-dependent inward current could generate SD-like depolarization, but ordinarily, it is brought about by the cooperative action of the persistent Na(+) current I(Na,P) plus NMDA receptor-controlled current. SD is ignited when the sum of persistent inward currents exceeds persistent outward currents so that total membrane current turns inward. The degree of depolarization is not determined by the number of channels available, but by the feedback that governs the SD process. Short bouts of SD and HSD are well tolerated, but prolonged depolarization results in lasting loss of neuron function. Irreversible damage can, however, be avoided if Ca(2+) influx into neurons is prevented.
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              Cellular distribution and functions of P2 receptor subtypes in different systems.

              This review is aimed at providing readers with a comprehensive reference article about the distribution and function of P2 receptors in all the organs, tissues, and cells in the body. Each section provides an account of the early history of purinergic signaling in the organ?cell up to 1994, then summarizes subsequent evidence for the presence of P2X and P2Y receptor subtype mRNA and proteins as well as functional data, all fully referenced. A section is included describing the plasticity of expression of P2 receptors during development and aging as well as in various pathophysiological conditions. Finally, there is some discussion of possible future developments in the purinergic signaling field.
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                Author and article information

                Journal
                Neural Regen Res
                Neural Regen Res
                NRR
                Neural Regeneration Research
                Medknow Publications & Media Pvt Ltd (India )
                1673-5374
                1876-7958
                November 2016
                : 11
                : 11
                : 1857-1864
                Affiliations
                [1]Institute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China
                Author notes
                [* ] Correspondence to: Li Cui or Jia-chun Feng, chuili1967@ 123456126.com or fengjcfrank@ 123456qq.com .

                Author contributions: PPS, LC and JCF conceived and designed the work. SH, DM, MMZ, JDZ and LSF prepared and edited the paper. MQZ reviewed the paper. All authors approved the final version of the paper.

                Author information
                http://orcid.org/0000-0002-5999-2492
                Article
                NRR-11-1857
                10.4103/1673-5374.194759
                5204245
                28123433
                a74280e6-4a63-40c3-a4d8-2ec8c43c5d30
                Copyright: © Neural Regeneration Research

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                : 09 October 2016
                Categories
                Review

                nerve regeneration,cortical spreading depression,neuronal depolarization,ischemic tolerance,peri-infarct depolarization,excitatory neurotransmission,nitric oxide,genomic reprogramming,inflammation,neurotropic factors,cellular stress response,neural regeneration

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