Small conductance Ca 2+ -activated K + channels in the plasma membrane, mitochondria and the ER: Pharmacology and implications in neuronal diseases

Honrath, Birgit; Krabbendam, Inge; Culmsee, Carsten; Dolga, Amalia M.

doi:10.1016/j.neuint.2017.05.005

Cited by 36 publications

(25 citation statements)

References 146 publications

(157 reference statements)

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“…Another important finding of the present work is that sevoflurane impaired hippocampal plasticity and hippocampus‐dependent learning and memory through promoting surface expression of SK2 channels. SK channels are a subpopulation of calcium‐activated potassium channels, including three isoforms (SK1–3) with distinct expression profiles and pharmacological features . The SK2 channels, primarily expressed in the ganglionic layer of the cortex and the hippocampus, contribute to the ionic homeostasis by carrying out potassium efflux and regulating calcium homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane anesthesia impairs metabotropic glutamate receptor‐dependent long‐term depression and cognitive functions in senile mice

Zhang

Shi

2019

Geriatrics Gerontology Int

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Aim Postoperative cognitive dysfunction is often observed in older patients. Previous reports described the link between postoperative cognitive dysfunction and general anesthetics, such as sevoflurane, but the exact mechanism remains unclear. We therefore sought to characterize the effects of sevoflurane on hippocampal‐dependent cognitive functions, as well as hippocampal plasticity, and to delineate the underlying mechanisms. Methods Behavioral assays including the novel object recognition test and the Morris water maze test were carried out to assess the cognitive performance of control and sevoflurane‐exposed mice. Electrophysiological recordings were carried out to evaluate the sevoflurane‐induced changes of synaptic plasticity in the hippocampus. Furthermore, western blot assay was utilized to quantitatively assess the altered protein expression resulting from sevoflurane exposure. Results Sevoflurane anesthesia impaired cognitive functions, as well as metabotropic glutamate receptor‐dependent long‐term depression, through elevated surface expression of small conductance calcium‐activated potassium type 2 channels. Blockage of calcium‐activated potassium type 2 channels reversed the sevoflurane‐induced deficits at both cellular and behavioral levels. Conclusions Sevoflurane anesthesia impaired metabotropic glutamate receptor‐dependent long‐term depression and thereby affected cognitive functions in old mice. Inhibitory modulators of calcium‐activated potassium type 2 channels might prevent cognitive decline elicited by sevoflurane. Geriatr Gerontol Int 2019; 19: 357–362.

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Section: Discussionmentioning

confidence: 99%

Sevoflurane anesthesia impairs metabotropic glutamate receptor‐dependent long‐term depression and cognitive functions in senile mice

Zhang

Shi

2019

Geriatrics Gerontology Int

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“…The smallconductance calcium-dependent potassium channels (Sah, 1996) are highly calcium-dependent and are quite sensitive to transient increases of cytosolic calcium (Blatz and Magleby, 1987). The small-conductance channels mediate the shift of the excitotoxic calcium mobilization into a protective, hyperpolarizing signal (Madison and Nicoll, 1984;Lancaster and Adams, 1986;Sah, 1996;Honrath et al, 2017). Other key potassium channels are the ATP-dependent potassium channels, whose conductance is enhanced by ATP depletion (Politi and Rogawski, 1991;Riepe et al, 1992), particularly following excitotoxic insults (Trapp and Ballanyi, 1995).…”

Section: Saving Private Neuron: Cellular Defenses Against Excitotoxicitymentioning

confidence: 99%

Going the Extra (Synaptic) Mile: Excitotoxicity as the Road Toward Neurodegenerative Diseases

Armada‐Moreira

Gomes

Pina

et al. 2020

Front. Cell. Neurosci.

182

128

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Excitotoxicity is a phenomenon that describes the toxic actions of excitatory neurotransmitters, primarily glutamate, where the exacerbated or prolonged activation of glutamate receptors starts a cascade of neurotoxicity that ultimately leads to the loss of neuronal function and cell death. In this process, the shift between normal physiological function and excitotoxicity is largely controlled by astrocytes since they can control the levels of glutamate on the synaptic cleft. This control is achieved through glutamate clearance from the synaptic cleft and its underlying recycling through the glutamate-glutamine cycle. The molecular mechanism that triggers excitotoxicity involves alterations in glutamate and calcium metabolism, dysfunction of glutamate transporters, and malfunction of glutamate receptors, particularly N-methyl-D-aspartic acid receptors (NMDAR). On the other hand, excitotoxicity can be regarded as a consequence of other cellular phenomena, such as mitochondrial dysfunction, physical neuronal damage, and oxidative stress. Regardless, it is known that the excessive activation of NMDAR results in the sustained influx of calcium into neurons and leads to several deleterious consequences, including mitochondrial dysfunction, reactive oxygen species (ROS) overproduction, impairment of calcium buffering, the release of pro-apoptotic factors, among others, that inevitably contribute to neuronal loss. A large body of evidence implicates NMDAR-mediated excitotoxicity as a central mechanism in the pathogenesis of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and epilepsy. In this review article, we explore different causes and consequences of excitotoxicity, discuss the involvement of NMDAR-mediated

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“…The following potassium channels, similar to plasma membrane potassium channels, have been identified in the inner mitochondrial membrane: mitochondrial (a) ATP‐regulated potassium channels (mitoK ATP channels), (b) small‐, intermediate‐ and large‐conductance calcium‐activated potassium channels, (c) voltage‐dependent potassium Kv1.3/Kv7.1 channels (mitoKv channels) and (d) twin‐pore TASK‐3 potassium channels (mitoTASK) . Potassium ion transport through the inner mitochondrial membrane regulates mitochondrial metabolism, primarily via the regulation of mitochondrial membrane potential, respiration and mitochondrial reactive oxygen species (ROS) synthesis …”

Section: Introductionmentioning

confidence: 99%

Naringenin as an opener of mitochondrial potassium channels in dermal fibroblasts

Kampa

Kicińska

Jarmuszkiewicz

et al. 2019

Experimental Dermatology

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Flavonoids belong to a large group of polyphenolic compounds that are widely present in plants. Certain flavonoids, including naringenin, have cytoprotective properties. Although the antioxidant effect has long been thought to be a crucial factor accounting for the cellular effects of flavonoids, mitochondrial channels have emerged recently as targets for cytoprotective strategies. In the present study, we characterized interactions between naringenin and the mitochondrial potassium (mitoBKCa and mitoKATP) channels recently described in dermal fibroblasts. With the use of the patch‐clamp technique and mitoplasts isolated from primary human dermal fibroblast cells, our study shows that naringenin in micromolar concentrations leads to an increase in mitoBKCa channel activity. The opening probability of the channel decreased from 0.97 in the control conditions (200 μmol/L Ca2+) to 0.06 at a low Ca2+ level (1 μmol/L) and increased to 0.85 after the application of 10 μmol/L naringenin. Additionally, the activity of the mitoKATP channel increased following the application of 10 μmol/L naringenin. To investigate the effects of naringenin on mitochondrial function, the oxygen consumption of dermal fibroblast cells was measured in potassium‐containing media. The addition of naringenin significantly and dose‐dependently increased the respiratory rate from 5.8 ± 0.2 to 14.0 ± 0.6 nmol O2 × min−1 × mg protein−1. Additionally, a Raman spectroscopy analysis of skin penetration indicated that the naringenin was distributed in all skin layers, including the epidermis and dermis. In this study, we demonstrated that a flavonoid, naringenin, can activate two potassium channels present in the inner mitochondrial membrane of dermal fibroblasts.

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Small conductance Ca 2+ -activated K + channels in the plasma membrane, mitochondria and the ER: Pharmacology and implications in neuronal diseases

Cited by 36 publications

References 146 publications

Sevoflurane anesthesia impairs metabotropic glutamate receptor‐dependent long‐term depression and cognitive functions in senile mice

Sevoflurane anesthesia impairs metabotropic glutamate receptor‐dependent long‐term depression and cognitive functions in senile mice

Going the Extra (Synaptic) Mile: Excitotoxicity as the Road Toward Neurodegenerative Diseases

Naringenin as an opener of mitochondrial potassium channels in dermal fibroblasts

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