A pharmaco-EEG study of the interaction between ethanol and retigabine in rabbits

Zwierzyńska, Ewa; Krupa, Agata; Pietrzak, Bogusława

doi:10.3109/00952990.2014.987349

Cited by 6 publications

(1 citation statement)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast to RTG, high doses of ethanol increase dopaminergic neurotransmission [ 232 ]. Repeated administration of RTG significantly reduces neurological changes in the hippocampus caused by long-term administration of ethanol [ 233 ]. RTG also reduces NMDA-induced cell apoptosis in organotypic hippocampal cultures and in models of hypoxia and hypoglycemia [ 234 ].…”

Section: Mitochondrial Voltage-dependent Potassium Channelsmentioning

confidence: 99%

Alternative Targets for Modulators of Mitochondrial Potassium Channels

et al. 2022

View full text Add to dashboard Cite

Mitochondrial potassium channels control potassium influx into the mitochondrial matrix and thus regulate mitochondrial membrane potential, volume, respiration, and synthesis of reactive oxygen species (ROS). It has been found that pharmacological activation of mitochondrial potassium channels during ischemia/reperfusion (I/R) injury activates cytoprotective mechanisms resulting in increased cell survival. In cancer cells, the inhibition of these channels leads to increased cell death. Therefore, mitochondrial potassium channels are intriguing targets for the development of new pharmacological strategies. In most cases, however, the substances that modulate the mitochondrial potassium channels have a few alternative targets in the cell. This may result in unexpected or unwanted effects induced by these compounds. In our review, we briefly present the various classes of mitochondrial potassium (mitoK) channels and describe the chemical compounds that modulate their activity. We also describe examples of the multidirectional activity of the activators and inhibitors of mitochondrial potassium channels.

show abstract

Section: Mitochondrial Voltage-dependent Potassium Channelsmentioning

confidence: 99%

Alternative Targets for Modulators of Mitochondrial Potassium Channels

et al. 2022

View full text Add to dashboard Cite

show abstract

Chronic Alcohol, Intrinsic Excitability, and Potassium Channels: Neuroadaptations and Drinking Behavior

Cannady

Rinker

Nimitvilai

et al. 2018

Handbook of Experimental Pharmacology

View full text Add to dashboard Cite

Neural mechanisms underlying alcohol use disorder remain elusive, and this lack of understanding has slowed the development of efficacious treatment strategies for reducing relapse rates and prolonging abstinence. While synaptic adaptations produced by chronic alcohol exposure have been extensively characterized in a variety of brain regions, changes in intrinsic excitability of critical projection neurons are understudied. Accumulating evidence suggests that prolonged alcohol drinking and alcohol dependence produce plasticity of intrinsic excitability as measured by changes in evoked action potential firing and after-hyperpolarization amplitude. In this chapter, we describe functional changes in cell firing of projection neurons after long-term alcohol exposure that occur across species and in multiple brain regions. Adaptations in calcium-activated (K2), voltage-dependent (K7), and G protein-coupled inwardly rectifying (K3 or GIRK) potassium channels that regulate the evoked firing and after-hyperpolarization parallel functional changes in intrinsic excitability induced by chronic alcohol. Moreover, there are strong genetic links between alcohol-related behaviors and genes encoding K2, K7, and GIRK channels, and pharmacologically targeting these channels reduces alcohol consumption and alcohol-related behaviors. Together, these studies demonstrate that chronic alcohol drinking produces adaptations in K2, K7, and GIRK channels leading to impaired regulation of the after-hyperpolarization and aberrant cell firing. Correcting the deficit in the after-hyperpolarization with positive modulators of K2 and K7 channels and altering the GIRK channel binding pocket to block the access of alcohol represent a potentially highly effective pharmacological approach that can restore changes in intrinsic excitability and reduce alcohol consumption in affected individuals.

show abstract

Transcranial low-level infrared laser irradiation ameliorates depression induced by reserpine in rats

Mohammed

2016

Lasers Med Sci

View full text Add to dashboard Cite

Transcranial low-level infrared laser is a modality of therapy based on the principle of photons delivered in a non-invasive manner through the skull for the treatment of some neurological conditions such as psychological disorders, traumatic brain injuries, and neurodegenerative diseases among others. In the present study, effects of low-level infrared laser irradiation with different radiation powers (80, 200, and 400 mW, continuous wave) were investigated on normal animals subjected to forced swimming test (FST). Results indicated that there are changes in FST parameters in animals irradiated with laser; the lowest dose provoked a significant increase in animal activity (swimming and climbing) and a significant decrease in animal's immobility, while the highest laser dose resulted in a complete inverse action by significantly increasing animal immobility and significantly decreasing animal activity with respect to control animals. The lowest dose (80 mW) of transcranial laser irradiation has then utilized on animals injected with a chronic dose of reserpine (0.2 mg/kg i.p. for 14 days) served as an animal model of depression. Laser irradiation has successfully ameliorated depression induced by reserpine as indicated by FST parameters and electrocorticography (ECoG) spectral analysis in irradiated animals. The findings of the present study emphasized the beneficial effects of low-level infrared laser irradiation on normal and healthy animals. Additionally, it indicated the potential antidepressant activity of the low dose of infrared laser irradiation.

show abstract

A pharmaco-EEG study of the interaction between ethanol and retigabine in rabbits

Abstract: Retigabine in multiple doses decreases the sensitivity of the hippocampus to an acute dose of ethanol in rabbits. Given the role of hippocampal-related memory processes to addiction, retigabine may have therapeutic potential.

Cited by 6 publications

References 40 publications

Alternative Targets for Modulators of Mitochondrial Potassium Channels

Alternative Targets for Modulators of Mitochondrial Potassium Channels

Chronic Alcohol, Intrinsic Excitability, and Potassium Channels: Neuroadaptations and Drinking Behavior

Transcranial low-level infrared laser irradiation ameliorates depression induced by reserpine in rats

Contact Info

Product

Resources

About