Long-term alcohol exposure elicits hippocampal nonsynaptic epileptiform activity changes associated with expression and functional changes in NKCC1, KCC2 co-transporters and Na+ /K+ -ATPase

Highlights • Nonsynaptic effects of long-term alcohol exposure (3 months) on the hippocampus were investigated. • Alcohol exposure changed NKCC1, KCC2 and Na-K-ATPase expressions. • NEA enhanced due to alcohol exposure. • Increase in DC shift is due to NKCC1 action. • Neurodegeneration observed in t...

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Veröffentlicht in:	Neuroscience 2017-01, Vol.340, p.530-541
Hauptverfasser:	Santos, Luiz E.C, Rodrigues, Antônio M, Lopes, Mariana R, Costa, Victor D.C, Scorza, Carla A, Scorza, Fulvio A, Cavalheiro, Esper A, Almeida, Antônio-Carlos G
Format:	Artikel
Sprache:	eng
Schlagworte:	Alcohol-Related Disorders - complications Alcohol-Related Disorders - metabolism Alcohol-Related Disorders - pathology Animals Bumetanide - pharmacology Central Nervous System Depressants - toxicity dentate gyrus Dose-Response Relationship, Drug electrophysiology epilepsy Epilepsy - etiology Epilepsy - metabolism Epilepsy - pathology ethanol Ethanol - toxicity Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology immunohistochemistry K Cl- Cotransporters Male Membrane Potentials - drug effects Membrane Potentials - physiology Neurodegenerative Diseases - etiology Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - pathology Neurology Rats, Wistar Receptors, GABA-A - metabolism Sodium Potassium Chloride Symporter Inhibitors - pharmacology Sodium-Potassium-Exchanging ATPase - metabolism Solute Carrier Family 12, Member 2 - metabolism Symporters - metabolism Tissue Culture Techniques
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Zusammenfassung:	Highlights • Nonsynaptic effects of long-term alcohol exposure (3 months) on the hippocampus were investigated. • Alcohol exposure changed NKCC1, KCC2 and Na-K-ATPase expressions. • NEA enhanced due to alcohol exposure. • Increase in DC shift is due to NKCC1 action. • Neurodegeneration observed in the treated groups diminished with NKCC1 blockage.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2016.11.015