Acute Ethanol Inhibition of γ Oscillations Is Mediated by Akt and GSK3β.
- Authors
- Wang, JianGang; Zhao, JingXi; Liu, ZhiHua; Guo, FangLi; Wang, Yali; Wang, Xiaofang; Zhang, RuiLing; Vreugdenhil, Martin; Lu, Chengbiao
- Year
- 2016
- Journal
- Frontiers in cellular neuroscience
- PMID
- 27582689
- DOI
- 10.3389/fncel.2016.00189
- PMCID
- PMC4987361
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.
The effect of ethanol (ETOH) on kainate-induced γ oscillations. (A) Field potential recordings from the CA3 stratum pyramidale, before and after application of 50 mM ethanol (A1) or 100 mM ethanol (A2). (B) Power spectra corresponding to (A1,A2). (C) The time courses of γ power (normalized to the average γ power in the last 5 min before ethanol application (baseline) shows a reversible reduction of γ power. (D) γ power as % of baseline γ power for different concentrations of ethanol. (*P < 0.05; **P < 0.01; ***P < 0.001, compared with baseline, paired t-test, n = 12, 11, 8, 8, and 10 for 5, 10, 30, 50, and 100 mM ETOH, respectively). (E) Peak frequency of γ oscillations in control and for the different concentrations of ethanol (n = 8).
The effects of dopamine receptor antagonists on ethanol-induced suppression of γ oscillations. (A) Example of the time course of γ power, normalized to the γ power during the 5 min preceding application of the DR1/5 antagonist, SCH23390 (10 μM), with additional application of 50 mM ethanol followed by 100 mM ethanol. (B) γ power as % of baseline (γ power only in the presence of kainate as control, CTRL) after application of SCH23390, 50 and 100 mM ethanol (*P < 0.05; **P < 0.01; ***P < 0.001, compared with SCH23390 baseline, one-way repeated measures Analysis of Variance (RM ANOVA), n = 11; *P < 0.05 for comparison between ethanol effects in the presence and absence of SCH23390). (C) Example of the effect of ethanol on γ power, in the presence of the DR2/3/4 antagonist raclopride (10 μM) details as in (A). (D) γ power as % of baseline for 10 μM raclopride, 50 mM and 100 mM ethanol (n = 8). Details as in (B).
The effects of PKA inhibitor on ethanol-induced suppression of γ oscillations. (A) Example of the effect of ethanol on γ power in the presence of the PKA inhibitor H89 (10 μM). Details as in Figure 2A. (B) γ power as % of baseline for H89, 50 and 100 mM ethanol (n = 8). *P < 0.05; **P < 0.01. Details as in Figure 2B.
The effects of PI3-kinase and Akt inhibitors on ethanol-induced suppression of γ oscillations. (A) Example of the effect of ethanol on γ power in the presence of the PI3 kinase inhibitor wortmannin (200 nM). Details as in Figure 2A. (B) γ power as % of baseline for wortmannin (Wort), 50 mM ethanol (n = 16) and 100 mM ethanol (n = 11) Details as in Figure 2B. *P < 0.05; **P < 0.01. (C) Example of the effect of ethanol on γ power in the presence of the Akt inhibitor TCBN (5 μM). Details as in Figure 2A. (D) γ power as % of baseline for TCBN, 50 mM ethanol (n = 9) and 100 mM ethanol (n = 9). Details as in Figure 2B. *P < 0.05; **P < 0.01; ***P < 0.001.
The effects of GSK3β inhibitor on ethanol-induced suppression of γ oscillations. (A) Example of the effect of ethanol on γ power in the presence of the GSK3β inhibitor SB415286 (5 μM). Details as in Figure 2A. (B) γ power as % of baseline for SB415286, 50 and 100 mM ethanol (n = 9). Details as in Figure 2B. *P < 0.05.
The NMDA receptor antagonist and ERK inhibitor on ethanol-induced suppression of γ oscillations. (A) Example of the effect of ethanol on γ power in the presence of D-AP5 (10 μM). Details as in Figure 2A. (B) γ power as % of baseline for NMDAR antagonist D-AP5, 50 and 100 mM ethanol (n = 8). Details as in Figure 2B. *P < 0.05; **P < 0.01; ***P < 0.001. (C) Example of the effect of ethanol on γ power in the presence of ERK inhibitor U0126 (2.5 μM). Details as in Figure 2A. (D) γ power as % of baseline for U0126, 50 and 100 mM ethanol (n = 8). Details as in Figure 2B. *P < 0.05; ***P < 0.001.
Graphical representation of proposed ethanol-induced changes to the γ-generating network. Cellular excitability resulting from a tonic drive by intrinsic properties (blue arrow), NMDAR (orange arrow) and tonic δGABAR (purple arrow), is shaped by phasic GABAR (red arrows) and AMPAR (green arrows) activity in pyramidal neurons (green) and interneurons (red) in a simplified γ-generating network. At intoxicated concentrations, ethanol activates DR1-cAMP-PKA signaling, and causes Akt and GSK3β activation increase, which may increase phasic GABA release. On the other hand, ethanol inhibit NMDAR activity and increase δ GABAR activity, which can be mediated through activation of Akt and GSK3β activation, reducing the excitatory drive and phasic glutamate release, suppressing γ oscillations.
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In this knowledge base
| Title | Year | PMID |
|---|---|---|
| Using human stem cells as a model system to understand the neural mechanisms of alcohol use disorders: Current status and outlook. | 2019 | 30087005 |
External
| Title | Authors | Journal | Year | Link |
|---|---|---|---|---|
| Ethanol exposure alters Alzheimer's-related pathology, behavior, and metabolism in APP/PS1 mice. | Day SM et al. | — | 2023 | → |
| Oligomeric β-Amyloid Suppresses Hippocampal γ-Oscillations through Activation of the mTOR/S6K1 Pathway. | Wang YL et al. | — | 2023 | → |
| Isolation, Characterization and Neuroprotective Activity of Folecitin: An In Vivo Study. | Farooq U et al. | — | 2021 | → |
| The physiological modulation by intracellular kinases of hippocampal γ-oscillation in vitro. | Wang J et al. | — | 2020 | → |
| The Role of Gamma Oscillations in the Pathophysiology of Substance Use Disorders. | Ramlakhan JU et al. | — | 2020 | → |
| The Modulation of Gamma Oscillations by Methamphetamine in Rat Hippocampal Slices. | Li Y et al. | — | 2019 | → |
| Using human stem cells as a model system to understand the neural mechanisms of alcohol use disorders: Current status and outlook. | Scarnati MS et al. | — | 2019 | → |
| Acute Low Alcohol Disrupts Hippocampus-Striatum Neural Correlate of Learning Strategy by Inhibition of PKA/CREB Pathway in Rats. | Sun W et al. | — | 2018 | → |
| Multiple Kinases Involved in the Nicotinic Modulation of Gamma Oscillations in the Rat Hippocampal CA3 Area. | Wang J et al. | — | 2017 | → |
| Selective dopamine receptor 4 activation mediates the hippocampal neuronal calcium response via IP<sub>3</sub> and ryanodine receptors. | Wang YL et al. | — | 2017 | → |
| Strain-Dependent Effects of Acute Alcohol on Synaptic Vesicle Recycling and Post-Tetanic Potentiation in Medial Glutamate Inputs to the Mouse Basolateral Amygdala. | Gioia DA et al. | — | 2017 | → |