Abstract
Hippocampal network oscillations at gamma band frequency (γ, 30–80 Hz) are closely associated with higher brain functions such as learning and memory. Acute ethanol exposure at intoxicating concentrations (≥50 mM) impairs cognitive function. This study aimed to determine the effects and the mechanisms of acute ethanol exposure on γ oscillations in an in vitro model. Ethanol (25–100 mM) suppressed kainate-induced γ oscillations in CA3 area of the rat hippocampal slices, in a concentration-dependent, reversible manner. The ethanol-induced suppression was reduced by the D1R antagonist SCH23390 or the PKA inhibitor H89, was prevented by the Akt inhibitor triciribine or the GSk3β inhibitor SB415286, was enhanced by the NMDA receptor antagonist D-AP5, but was not affected by the MAPK inhibitor U0126 or PI3K inhibitor wortmanin. Our results indicate that the intracellular kinases Akt and GSk3β play a critical role in the ethanol-induced suppression of γ oscillations and reveal new cellular pathways involved in the ethanol-induced cognitive impairment.
Highlights
Gamma (γ) oscillations arise from rhythmic synchronized synaptic activity in the γ frequency band (30–80 Hz) and are associated with higher brain functions such as learning and memory (Howard et al, 2003). γ oscillations can be recorded in many brain regions including the hippocampus, olfactory bulb, thalamus and neocortex (Mainy et al, 2007)
We investigated the effect of acute ethanol exposure on kainate-induced γ oscillations and explored possible mechanisms for γ oscillation modulation related to membrane receptors and intracellular kinases
Application of 100 mM ethanol reduced γ power by 42.8 ± 4.9% (P < 0.01, n = 11). This reduction was not different from that of 100 mM ethanol alone. These results show that DR1/5 antagonist SCH23390 significantly reduced 50 mM but not 100 mM ethanol-induced suppression of γ oscillations
Summary
Gamma (γ) oscillations arise from rhythmic synchronized synaptic activity in the γ frequency band (30–80 Hz) and are associated with higher brain functions such as learning and memory (Howard et al, 2003). γ oscillations can be recorded in many brain regions including the hippocampus, olfactory bulb, thalamus and neocortex (Mainy et al, 2007). Gamma (γ) oscillations arise from rhythmic synchronized synaptic activity in the γ frequency band (30–80 Hz) and are associated with higher brain functions such as learning and memory (Howard et al, 2003). The most commonly abused drug in humans passes the blood-brain barrier and interferes with brain function and behavior. Ethanol Modulation of γ Oscillations properties such as γ oscillations. Ethanol withdrawal induces a rebound facilitation of γ oscillations in the rat cortex (Cheaha et al, 2014). It is not clear whether ethanol modulates γ oscillations at the local network level and, if so, by which the cellular mechanisms
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