Effects of ethanol on sensory stimulus-evoked responses in the cerebellar molecular layer in vivo in mice

Cui, Song-Biao; Cui, Bai-Ri; Liu, Heng; Wu, Mao-Cheng; Xu, Yaolin; Bian, Jin-Hua; Chu, Chun-Ping; Qiu, De-Lai

doi:10.1016/j.neulet.2014.05.037

Cited by 9 publications

(8 citation statements)

References 26 publications

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“…High concentrations of ethanol have been shown to increase the spontaneous release of GABA from MLI axonal terminals onto PCs 14 29 30 , which can be elicited by increasing the intrinsic firing rate of MLIs through the enhancement of hyperpolarization-activated cationic currents 18 . However, we recently found that high concentrations of ethanol significantly inhibit the GABAergic response, suggesting that ethanol inhibits GABAergic sensory responses in the cerebellar molecular layer 20 .…”

Section: Discussionmentioning

confidence: 95%

“…The alcohol produces significant reductions in the amplitude, the area under the curve, the rise time constant and the decay constant of the inhibitory response. Blockade of GABA A receptor activity abolishes these effects of ethanol on the sensory stimulation-evoked inhibitory responses 20 . We previously showed that ethanol affects sensory stimulation-evoked inhibitory responses in the cerebellar cortical molecular layer via the modulation of GABA release from MLIs onto PCs.…”

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confidence: 99%

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Ethanol modulates facial stimulation-evoked outward currents in cerebellar Purkinje cells in vivo in mice

Bing

Chu

et al. 2016

Sci Rep

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Acute ethanol overdose can induce dysfunction of cerebellar motor regulation and cerebellar ataxia. In this study, we investigated the effect of ethanol on facial stimulation-evoked inhibitory synaptic responses in cerebellar Purkinje cells (PCs) in urethane-anesthetized mice, using in vivo patch-clamp recordings. Under voltage-clamp conditions, ethanol (300 mM) decreased the amplitude, half-width, rise time and decay time of facial stimulation-evoked outward currents in PCs. The ethanol-induced inhibition of facial stimulation-evoked outward currents was dose-dependent, with an IC50 of 148.5 mM. Notably, the ethanol-induced inhibition of facial stimulation-evoked outward currents were significantly abrogated by cannabinoid receptor 1 (CB1) antagonists, AM251 and O-2050, as well as by the CB1 agonist WIN55212-2. Moreover, the ethanol-induced inhibition of facial stimulation-evoked outward currents was prevented by cerebellar surface perfusion of the PKA inhibitors H-89 and Rp-cAMP, but not by intracellular administration of the PKA inhibitor PKI. Our present results indicate that ethanol inhibits the facial stimulation-evoked outward currents by activating presynaptic CB1 receptors via the PKA signaling pathway. These findings suggest that ethanol overdose impairs sensory information processing, at least in part, by inhibiting GABA release from molecular layer interneurons onto PCs.

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Section: Discussionmentioning

confidence: 95%

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confidence: 99%

Ethanol modulates facial stimulation-evoked outward currents in cerebellar Purkinje cells in vivo in mice

Bing

Chu

et al. 2016

Sci Rep

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“…Local field potential recordings have shown that sensory stimulation evokes a field potential in the ML that expresses a GABA A receptor-mediated inhibitory component [8,9,22], suggesting that activation of MLIs occurs in clusters in response to the sensory stimulation. Our results showed that the stimulation-off response evoked in the ML required a longer duration of stimulation, and was weaker than that in the GCL, indicating that high-fidelity sensory information coming from the GCL was modified by the MLI network.…”

Section: Discussionmentioning

confidence: 99%

Dynamic properties of sensory stimulation evoked responses in mouse cerebellar granule cell layer and molecular layer

Bing

Zhang

Sun

et al. 2015

Neuroscience Letters

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“…We previously reported that high concentrations of ethanol significantly inhibit sensory stimulation-evoked responses in the cerebellar molecular (Cui et al, 2014 ) and granule cell (Wu et al, 2014 ) layers via activation of GABA A receptors in urethane anesthetized mice, suggesting that high concentrations of ethanol impair sensory information processing in the cerebellar cortex. More recently, we found that ethanol dose-dependently inhibits facial stimulation-evoked outward currents by activating presynaptic cannabinoid receptor 1 (CB1) receptors via the PKA signaling pathway.…”

Section: Introductionmentioning

confidence: 96%

Ethanol Modulates the Spontaneous Complex Spike Waveform of Cerebellar Purkinje Cells Recorded in vivo in Mice

Zhang

Jin

et al. 2017

Front. Cell. Neurosci.

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Cerebellar Purkinje cells (PCs) are sensitive to ethanol, but the effect of ethanol on spontaneous complex spike (CS) activity in these cells in vivo is currently unknown. Here, we investigated the effect of ethanol on spontaneous CS activity in PCs in urethane-anesthetized mice using in vivo patch-clamp recordings and pharmacological manipulation. Ethanol (300 mM) induced a decrease in the CS-evoked pause in simple spike (SS) firing and in the amplitude of the afterhyperpolarization (AHP) under current clamp conditions. Under voltage-clamp conditions, ethanol significantly decreased the area under the curve (AUC) and the number of CS spikelets, without changing the spontaneous frequency of the CSs or the instantaneous frequency of the CS spikelets. Ethanol-induced a decrease in the AUC of spontaneous CSs was concentration dependent. The EC50 of ethanol for decreasing the AUC of spontaneous CSs was 168.5 mM. Blocking N-methyl-D-aspartate receptors (NMDARs) failed to prevent the ethanol-induced decreases in the CS waveform parameters. However, blockade of cannabinoid receptor 1 (CB1) significantly suppressed the ethanol-induced effects on the CS-evoked pause in SS firing, amplitude of the AHP, spikelet number and the AUC of CSs. Moreover, a CB1 receptor agonist not only reduced the number of spikelets and the AUC of CSs, but also prevented the ethanol-induced inhibition of CS activity. Our results indicate that ethanol inhibits CS activity via activation of the CB1 receptor in vivo in mice, suggesting that excessive ethanol intake inhibits climbing fiber (CF)–PC synaptic transmission by modulating CB1 receptors in the cerebellar cortex.

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Effects of ethanol on sensory stimulus-evoked responses in the cerebellar molecular layer in vivo in mice

Cited by 9 publications

References 26 publications

Ethanol modulates facial stimulation-evoked outward currents in cerebellar Purkinje cells in vivo in mice

Ethanol modulates facial stimulation-evoked outward currents in cerebellar Purkinje cells in vivo in mice

Dynamic properties of sensory stimulation evoked responses in mouse cerebellar granule cell layer and molecular layer

Ethanol Modulates the Spontaneous Complex Spike Waveform of Cerebellar Purkinje Cells Recorded in vivo in Mice

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