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

Santos, Luiz Eduardo Canton; Rodrigues, Antônio Márcio; Lopes, Mariana Rodrigues; Costa, Victor Diego Cupertino; Scorza, Carla A.; Scorza, Fúlvio A.; Cavalheiro, Ésper A.; Almeida, Antônio-Carlos G. de

doi:10.1016/j.neuroscience.2016.11.015

Cited by 12 publications

(2 citation statements)

References 44 publications

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“…Loading control proteins were not used for normalization as surface protein isolation excludes antigens typically used as loading controls. Prior surface-expressed proteins used as controls (Na-K-ATPase) are well-known to be altered by ethanol exposure (Wang et al, 2009; Santos et al, 2017). Therefore, equal amounts of loaded protein samples were similarly quantified as elsewhere (Diaz et al, 2011; Centanni et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

Oxytocin and vasopressin modulation of social anxiety following adolescent intermittent ethanol exposure

et al. 2018

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These findings demonstrate that AIE induces changes in OXT-R and AVP-R surface expression in the hypothalamus along with social anxiety-like alterations in male rats. These social anxiety-like alterations can be reversed either by activation of the OXT system or by suppression of the AVP system, data that support the hypothesis that social anxiety-like alterations induced by adolescent alcohol exposure in male rats are associated at least in part with an OXT/AVP imbalance.

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Section: Methodsmentioning

confidence: 99%

Oxytocin and vasopressin modulation of social anxiety following adolescent intermittent ethanol exposure

et al. 2018

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“…Furthermore, topiramate, a drug used to treat seizures, psychiatric and neurological conditions is a CA inhibitor, and has shown beneficial effects in reducing craving and drinking obsessions in subjects with AUD [ 41 ]. Given that chronic ethanol experience results in epileptiform activity in the hippocampus [ 42 ], we tested the hypothesis that systemic administration of a novel CA inhibitor 4-fluoro-N-(4-sulfamoylphenyl)benzenesulfonamide (4-FS; CA II inhibitor [ 43 ]) will reduce physical withdrawal and unregulated drinking associated with alcohol dependence in CIE rats. We also tested the subhypothesis that the reduced behaviors by 4-FS will be associated with reduced expression of CA II and enhanced expression of GABA receptors in the hippocampus.…”

Section: Introductionmentioning

confidence: 99%

A Novel Sulfonamide, 4-FS, Reduces Ethanol Drinking and Physical Withdrawal Associated With Ethanol Dependence

Khan

Trenet

Xing

et al. 2020

IJMS

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Carbonic anhydrase (CA) is abundant in glial cells in the brain and CA type II isoform (CA II) activity in the hippocampus plays an important role in buffering extracellular pH transients produced by neural activity. Chronic ethanol exposure results in respiratory and metabolic acidosis, producing shifts in extracellular pH in the brain and body. These neurophysiological changes by ethanol are hypothesized to contribute to the continued drinking behavior and physical withdrawal behavior in subjects consuming ethanol chronically. We explored whether chronic ethanol self-administration (ethanol drinking, 10% v/v; ED) without or under the influence of chronic intermittent ethanol vapor (CIE-ED) experience alters the expression of CA II in the hippocampus. Postmortem hippocampal tissue analyses demonstrated that CA II levels were enhanced in the hilus region of the hippocampus in ED and CIE-ED rats. We used a novel molecule—4-fluoro-N-(4-sulfamoylphenyl) benzenesulfonamide (4-FS)—a selective CA II inhibitor, to determine whether CA II plays a role in ethanol self-administration in ED and CIE-ED rats and physical withdrawal behavior in CIE-ED rats. 4-FS (20 mg/kg, i.p.) reduced ethanol self-administration in ED rats and physical withdrawal behavior in CIE-ED rats. Postmortem hippocampal tissue analyses demonstrated that 4-FS reduced CA II expression in ED and CIE-ED rats to control levels. In parallel, 4-FS enhanced GABAA receptor expression, reduced ratio of glutamatergic GluN2A/2B receptors and enhanced the expression of Fos, a marker of neuronal activation in the ventral hippocampus in ED rats. These findings suggest that 4-FS enhanced GABAergic transmission and increased activity of neurons of inhibitory phenotypes. Taken together, these findings support the role of CA II in assisting with negative affective behaviors associated with moderate to severe alcohol use disorders (AUD) and that CA II inhibitors are a potential therapeutic target to reduce continued drinking and somatic withdrawal symptoms associated with moderate to severe AUD.

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Effect of the Combination of NKCC1 and KCC2 Cotransporter Blockades on Non-synaptic Epileptiform Activities

Cecílio

Santos

Rodrigues

et al. 2019

XXVI Brazilian Congress on Biomedical Engineering

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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

Cited by 12 publications

References 44 publications

Oxytocin and vasopressin modulation of social anxiety following adolescent intermittent ethanol exposure

Oxytocin and vasopressin modulation of social anxiety following adolescent intermittent ethanol exposure

A Novel Sulfonamide, 4-FS, Reduces Ethanol Drinking and Physical Withdrawal Associated With Ethanol Dependence

Effect of the Combination of NKCC1 and KCC2 Cotransporter Blockades on Non-synaptic Epileptiform Activities

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