Increased cholesterol content of erythrocyte and brain membranes in ethanol-tolerant mice

Chin, Jane H.; Parsons, Linda M.; Goldstein, Dora B.

doi:10.1016/0005-2736(78)90204-3

Cited by 245 publications

(50 citation statements)

References 20 publications

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“…In both cell culture and animal models of chronic EtOH exposure, alterations in both content (Chin et al, 1978;Omodeo-Sale et al, 1995) and distribution (Wood et al, 1990) of membrane CHS have been reported. These alterations might represent a compensatory response (i.e., "tolerance") to counteract the effects of EtOH on relevant targets, such as defined ion channel populations.…”

Section: Discussionmentioning

confidence: 99%

“…Modulation of membrane CHS content and distribution may play a role in cellular adaptation to ethanol (EtOH) (Wood et al, 1990). Increased content (Chin et al, 1978;Omodeo-Sale et al, 1995) and altered distribution of CHS between membrane leaflets (Wood et al, 1990) are observed in response to EtOH exposure in both animal and cell culture models. Ethanol differentially increases the diffusion of various lipid probes in Aplysia californica neurons, suggesting that its actions on ion channels might depend upon the existence of dissimilar lateral domains (Treistman et al, 1987).…”

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confidence: 99%

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Cholesterol Antagonizes Ethanol Potentiation of Human Brain BK_Ca Channels Reconstituted into Phospholipid Bilayers

Crowley

Treistman²,

Dopico³

2003

Mol Pharmacol

107

148

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The activity of large conductance, Ca 2ϩ -sensitive K ϩ (BK Ca ) channels, known to control neuronal excitability, is increased by ethanol (EtOH) exposure. Moreover, brain cholesterol (CHS) is elevated after chronic exposure to EtOH, suggesting that membrane CHS may play a role in drug tolerance. Here, we use BK Ca channels from human brain (hslo subunits), reconstituted into 1-palmitoyl-2-oleoyl phosphatidylethanolamine/1-palmitoyl-2-oleoyl phosphatidylserine (POPS) bilayers, to examine CHS modulation of EtOH sensitivity. Acute exposure to clinically relevant EtOH levels increases channel activity without modifying conductance. In this minimal system, increases in CHS content within the range found in neuronal membranes lead to progressive antagonism of EtOH action. Furthermore, CHS inhibits basal channel activity with an affinity similar to that of CHS blunting of the alcohol effect. Modification of channel gating by either EtOH or CHS is reduced dramatically by removal of POPS from the bilayer, suggesting a common mechanism(s) of action. Indeed, channel dwell-time analysis indicates that CHS and EtOH exert opposite actions on the stability of channel closed states. However, each agent also acts on distinct dwell states not mirrored by the other, which contribute to the opposite effects of CHS and EtOH on channel gating.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BK_Ca Channels Reconstituted into Phospholipid Bilayers

Crowley

Treistman²,

Dopico³

2003

Mol Pharmacol

107

148

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“…Membranes isolated from chronically ethanol-treated mice proved resistant to the fluidizing effect of ethanol (Chin and Goldstein 1977), and in parallel, the cholesterol content of the membranes was increased (Chin et al 1978). Chronic ethanol treatment also induced a significantly increased cholesterol level in microsomes isolated from chicken brain and liver (Sanchez-Amate et al 1991).…”

Section: Heat Shock Proteins and Their Roles In Membrane Protectionmentioning

confidence: 93%

Alcohol stress, membranes, and chaperones

Tóth

Vı́gh

Sántha

2014

Cell Stress and Chaperones

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Ethanol, which affects all body organs, exerts a number of cytotoxic effects, most of them independent of cell type. Ethanol treatment leads to increased membrane fluidity and to changes in membrane protein composition. It can also interact directly with membrane proteins, causing conformational changes and thereby influencing their function. The cytotoxic action may include an increased level of oxidative stress. Heat shock protein molecular chaperones are ubiquitously expressed evolutionarily conserved proteins which serve as critical regulators of cellular homeostasis. Heat shock proteins can be induced by various forms of stresses such as elevated temperature, alcohol treatment, or ischemia, and they are also upregulated in certain pathological conditions. As heat shock and ethanol stress provoke similar responses, it is likely that heat shock protein activation also has a role in the protection of membranes and other cellular components during alcohol stress.

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“…Furthermore, the effect of ethanol as well as cholesterol was greatly reduced in the absence of phosphatidylserine in the bilayer membrane stressing the complexity of lipid impact on BK channel activity. This is of special interest since brain cholesterol in mice (Chin et al 1978) or cerebellar granula cells is elevated after exposure to alcohol (Omodeo-Salé et al, 1995). Ethanol also reduced the asymmetric distribution of cholesterol between the cytofacial (higher cholesterol) and exofacial leaflet of the lipid bilayer (Wood et al, 1990).…”

Section: Ethanol -And Membrane Lipidsmentioning

confidence: 99%

BK Channels – Focus on Polyamines, Ethanol/Acetaldehyde and Hydrogen Sulfide (H2S)

Hermann¹,

Ситдикова²,

Weiger³

2012

Patch Clamp Technique

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Increased cholesterol content of erythrocyte and brain membranes in ethanol-tolerant mice

Cited by 245 publications

References 20 publications

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BK_Ca Channels Reconstituted into Phospholipid Bilayers

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BK_Ca Channels Reconstituted into Phospholipid Bilayers

Alcohol stress, membranes, and chaperones

BK Channels – Focus on Polyamines, Ethanol/Acetaldehyde and Hydrogen Sulfide (H2S)

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Increased cholesterol content of erythrocyte and brain membranes in ethanol-tolerant mice

Cited by 245 publications

References 20 publications

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BKCa Channels Reconstituted into Phospholipid Bilayers

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BKCa Channels Reconstituted into Phospholipid Bilayers

Alcohol stress, membranes, and chaperones

BK Channels – Focus on Polyamines, Ethanol/Acetaldehyde and Hydrogen Sulfide (H2S)

Contact Info

Product

Resources

About

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BK_Ca Channels Reconstituted into Phospholipid Bilayers

Cholesterol Antagonizes Ethanol Potentiation of Human Brain BK_Ca Channels Reconstituted into Phospholipid Bilayers