Activation of mitochondrial KATP channels mediates neuroprotection induced by chronic morphine preconditioning in hippocampal CA-1 neurons following cerebral ischemia

Arabian, Maedeh; Aboutaleb, Nahid; Soleimani, Mansoureh; Ajami, Marjan; Habibey, Rouhollah; Pazoki‐Toroudi, Hamidreza

doi:10.1016/j.advms.2017.11.003

Cited by 19 publications

(6 citation statements)

References 42 publications

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“…Neuroprotection via mitochondrial ATP-sensitive potassium channels enhance cell survival against oxidative stress (Yang et al, 2016). In a chronic morphine (CM) preconditioning study of ischemia/reperfusion hippocampal CA1 neurons, inhibition of mKATP channels with 5-hydroxydecanoate (5-HD) significantly increased apoptosis, suggesting that CM preconditioning obstructs apoptosis via activation of mKATP channels (Arabian et al, 2018). Various studies have suggested that the protection afforded by the activation of potassium channels may be due to membrane potential hyperpolarization, and/or increased repolarization speed effectively reducing the level of calcium entry and ATP consumption; both considered pro-apoptotic events.…”

Section: Neuronal Cells and Cell Deathmentioning

confidence: 99%

Ions, the Movement of Water and the Apoptotic Volume Decrease

Bortner

Cidlowski

2020

Front. Cell Dev. Biol.

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The movement of water across the cell membrane is a natural biological process that occurs during growth, cell division, and cell death. Many cells are known to regulate changes in their cell volume through inherent compensatory regulatory mechanisms. Cells can sense an increase or decrease in their cell volume, and compensate through mechanisms known as a regulatory volume increase (RVI) or decrease (RVD) response, respectively. The transport of sodium, potassium along with other ions and osmolytes allows the movement of water in and out of the cell. These compensatory volume regulatory mechanisms maintain a cell at near constant volume. A hallmark of the physiological cell death process known as apoptosis is the loss of cell volume or cell shrinkage. This loss of cell volume is in stark contrast to what occurs during the accidental cell death process known as necrosis. During necrosis, cells swell or gain water, eventually resulting in cell lysis. Thus, whether a cell gains or loses water after injury is a defining feature of the specific mode of cell death. Cell shrinkage or the loss of cell volume during apoptosis has been termed apoptotic volume decrease or AVD. Over the years, this distinguishing feature of apoptosis has been largely ignored and thought to be a passive occurrence or simply a consequence of the cell death process. However, studies on AVD have defined an underlying movement of ions that result in not only the loss of cell volume, but also the activation and execution of the apoptotic process. This review explores the role ions play in controlling not only the movement of water, but the regulation of apoptosis. We will focus on what is known about specific ion channels and transporters identified to be involved in AVD, and how the movement of ions and water change the intracellular environment leading to stages of cell shrinkage and associated apoptotic characteristics. Finally, we will discuss these concepts as they apply to different cell types such as neurons, cardiomyocytes, and corneal epithelial cells.

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Section: Neuronal Cells and Cell Deathmentioning

confidence: 99%

Ions, the Movement of Water and the Apoptotic Volume Decrease

Bortner

Cidlowski

2020

Front. Cell Dev. Biol.

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“…In addition, acupuncture is widely used as a traditional medical treatment in our country to help eliminate drug addiction. Studies have shown that heroin-dependent patients can effectively reduce withdrawal symptoms with the help of acupuncture [ 10 ]. Some researchers have proposed that PHC is a new class of drugs that can interact with cholinergic receptors (M receptors) independently developed by our country.…”

Section: Introductionsmentioning

confidence: 99%

Experimental Study on the Central Mechanism of Penehyclidine Hydrochloride against Relapse Behavior in Morphine-Dependent Rats

Yufeng

Jin

et al. 2022

Applied Bionics and Biomechanics

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Objective. This article is mainly to study the central mechanism of penehyclidine hydrochloride against relapse behavior in morphine-dependent rats. Methods. The rats were randomly divided into the blank control group (k), PHC low-dose group (LP according to a body weight of 0.22 mg/kg), middle-dose group (MP according to a body weight of 0.55 mg/kg), high-dose group (HP according to a body weight of 1.38 mg/kg), and administration group, with 40 rats in each group. Each group was randomly divided into 5 subgroups ( n = 10 ): 4 h after administration, 7 h after administration, 13 h after administration, 25 h after administration (K48, LP48, MP48, and HP48), and 37 h after administration, and then, Morris water maze experiment and immunohistochemical detection of the rat brain hippocampus were carried out. Results. 4 and 7 hours after administration, compared with group 1, the TchE activity increased and Ach level decreased in groups 2, 3, and 4 and the difference was significant ( P < 0.05 ), so the principle of penehyclidine hydrochloride against morphine-dependent rats is that penehyclidine hydrochloride causes cognitive impairment in the brain of mice, thereby achieving antimorphine effects.

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“…In addition, morphine protected PC12 cells against the cytotoxicity of 1-methyl-4phenylpyridinium through activating phosphatidylinositol 3-kinase (PI3K)/Akt pathway (Fan et al, 2019). Some groups demonstrated that preconditioning with morphine alleviated cerebral ischemia injury through activating the mTOR pathway (Arabian et al, 2018b) or mitochondrial KATP channels (Arabian et al, 2018a). However, repeated use of morphine will lead to various sideeffects, such as antinociceptive tolerance, dependence, and addiction.…”

Section: Introductionmentioning

confidence: 99%

Morphine Addiction and Oxidative Stress: The Potential Effects of Thioredoxin-1

2020

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Long-term administration of morphine for the management of chronic pain will result in tolerance to its analgesic effect and could even cause drug dependence. Numerous studies have demonstrated significant redox alteration in morphine dependence and addiction. Thioredoxin-1 (Trx-1) play important roles in controlling the cellular redox balance. In recent years, several recent studies have demonstrated that Trx-1 may be a promising novel therapeutic target for morphine addiction. In this article, we firstly review the redox alteration in morphine addiction. We also summarize the expression and the protective roles of Trx-1 in morphine dependence. We further highlight the protection of geranylgeranylacetone (GGA), a noncytotoxic pharmacological inducer of Trx-1, in morphine-induced conditioned place preference. In conclusion, Trx-1 may be very promising for clinical therapy of morphine addiction in the future.

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Activation of mitochondrial KATP channels mediates neuroprotection induced by chronic morphine preconditioning in hippocampal CA-1 neurons following cerebral ischemia

Cited by 19 publications

References 42 publications

Ions, the Movement of Water and the Apoptotic Volume Decrease

Ions, the Movement of Water and the Apoptotic Volume Decrease

Experimental Study on the Central Mechanism of Penehyclidine Hydrochloride against Relapse Behavior in Morphine-Dependent Rats

Morphine Addiction and Oxidative Stress: The Potential Effects of Thioredoxin-1

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