ArticleBiological psychiatry2011
Small conductance calcium-activated potassium type 2 channels regulate alcohol-associated plasticity of glutamatergic synapses.
Article in Biological psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 69 citations in OpenAlex.
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- MPP2 interacts with SK2 to rescue the excitability of glutamatergic neurons in the BLA and facilitate the extinction of conditioned fear in mice.CNS neuroscience & therapeutics · 2024Article
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- Chronic intermittent ethanol exposure differentially alters the excitability of neurons in the orbitofrontal cortex and basolateral amygdala that project to the dorsal striatum.Neuropharmacology · 2023Article
- Tauopathy and alcohol consumption interact to alter locus coeruleus excitatory transmission and excitability in male and female mice.Alcohol (Fayetteville, N.Y.) · 2023Article
- Modulation of neuronal excitability by binge alcohol drinking.Frontiers in molecular neuroscience · 2023Review
- Alcohol Use Disorder: Neurobiology and Therapeutics.Biomedicines · 2022Review
- Chronic ethanol exposure differentially alters neuronal function in the medial prefrontal cortex and dentate gyrus.Neuropharmacology · 2021Article
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- SK2 channel regulation of neuronal excitability, synaptic transmission, and brain rhythmic activity in health and diseases.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Bioinformatics identification and pharmacological validation of Kcnn3/KTranslational psychiatry · 2020Article
- The role of intrinsic excitability in the evolution of memory: Significance in memory allocation, consolidation, and updating.Neurobiology of learning and memory · 2020Review
- A Single Prior Injection of Methamphetamine Enhances Methamphetamine Self-Administration (SA) and Blocks SA-Induced Changes in DNA Methylation and mRNA Expression of Potassium Channels in the Rat Nucleus Accumbens.Molecular neurobiology · 2020Article
- Activation of small conductance calcium-activated potassium channels suppresses seizure susceptibility in the genetically epilepsy-prone rats.Neuropharmacology · 2020Article
- Nucleus accumbens shell small conductance potassium channels underlie adolescent ethanol exposure-induced anxiety.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Chronic Intermittent Ethanol Exposure Selectively Increases Synaptic Excitability in the Ventral Domain of the Rat Hippocampus.Neuroscience · 2019Article
- Calcium chloride mimics the effects of acamprosate on cognitive deficits in chronic alcohol-exposed mice.Psychopharmacology · 2018Article
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Abstract
backgroundSmall conductance calcium-activated potassium type 2 channels (SK2) control excitability and contribute to plasticity by reducing excitatory postsynaptic potentials. Recent evidence suggests that SK2 channels form a calcium-dependent negative-feedback loop with synaptic N-methyl-D-aspartate (NMDA) receptors. Addiction to alcohol and other drugs of abuse induces plastic changes in glutamatergic synapses that include the targeting of NMDA receptors to synaptic sites; however, the role of SK2 channels in alcohol-associated homeostatic plasticity is unknown.
methodsElectrophysiology, Western blot, and behavioral analyses were used to quantify changes in hippocampal small conductance calcium-activated potassium (SK) channel function and expression using well-characterized in vitro and in vivo models of chronic alcohol exposure.
resultsChronic ethanol reduced apamin-sensitive SK currents in cornu ammonis 1 pyramidal neurons that were associated with a downregulation of surface SK2 channels. Blocking SK channels with apamin potentiated excitatory postsynaptic potentials in control but not ethanol-treated cornu ammonis 1 pyramidal neurons, suggesting that chronic ethanol disrupts the SK channel-NMDA receptor feedback loop. Alcohol reduced expression of SK2 channels and increased expression of NMDA receptors at synaptic sites in a mouse model. Positive modulation of SK function by 1-EBIO decreased alcohol withdrawal hyperexcitability and attenuated ethanol withdrawal neurotoxicity in hippocampus. The 1-EBIO also reduced seizure activity in mice undergoing withdrawal.
conclusionsThese results provide evidence that SK2 channels contribute to alcohol-associated adaptive plasticity of glutamatergic synapses and that positive modulation of SK channels reduces the severity of withdrawal-related hyperexcitability. Therefore, SK2 channels appear to be critical regulators of alcohol-associated plasticity and may be novel therapeutic targets for the treatment of addiction.
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