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

Wu, Mao-Cheng; Bing, Yan-Hua; Chu, Chun-Ping; Qiu, De-Lai

doi:10.1038/srep30857

Cited by 10 publications

(10 citation statements)

References 58 publications

(99 reference statements)

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“…Furthermore, we found that facial stimulation induced LTD at MLI-PC synapses (MLI-PC LTD), accompanied with a decrease in the stimulation-evoked pause of spike firing in PCs via activation of NMDA receptors in the mouse cerebellar cortex, suggesting that sensory stimulation evoked MLI-PC GABAergic synaptic plasticity may play a critical role in motor learning of living animals (Bing et al, 2015). Moreover, acute application of EtOH inhibits the facial stimulation evoked MLI-PC synaptic transmission (Cui et al, 2014), and significantly depresses the MLI-PC synaptic transmission by activating presynaptic cannabinoid receptors via the protein kinase signaling pathway, suggesting that EtOH modulates GABA release from MLIs onto PCs (Wu et al, 2016). Our previous studies suggest that the cerebellar MLI-PC synapse is a target of EtOH, and EtOH consumption may impair the MLI-PC synaptic plasticity.…”

Section: Introductionmentioning

confidence: 99%

Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

Bing

Chu

et al. 2019

Front. Cell. Neurosci.

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The cerebellum is sensitive to ethanol (EtOH) consumption. Chronic EtOH consumption impairs motor learning by modulating the cerebellar circuitry synaptic transmission and long-term plasticity. Under in vitro conditions, acute EtOH inhibits both parallel fiber (PF) and climbing fiber (CF) long-term depression (LTD). However, thus far it has not been investigated how chronic EtOH consumption affects sensory stimulation-evoked LTD at the molecular layer interneurons (MLIs) to the Purkinje cell (PC) synapses (MLI-PC LTD) in the cerebellar cortex of living animals. In this study, we investigated the effect of chronic EtOH consumption on facial stimulation-evoked MLI-PC LTD, using an electrophysiological technique as well as pharmacological methods, in urethane-anesthetized mice. Our results showed that facial stimulation induced MLI–PC LTD in the control mice, but it could not be induced in mice with chronic EtOH consumption (0.8 g/kg; 28 days). Blocking the cannabinoid type 1 (CB1) receptor activity with AM-251, prevented MLI-PC LTD in the control mice, but revealed a nitric oxide (NO)-dependent long-term potentiation (LTP) of MLI–PC synaptic transmission (MLI-PC LTP) in the EtOH consumption mice. Notably, with the application of a NO donor, S-nitroso-N-Acetyl-D, L-penicillamine (SNAP) alone prevented the induction of MLI–PC LTD, but a mixture of SNAP and AM-251 revealed an MLI-PC LTP in control mice. In contrast, inhibiting NO synthase (NOS) revealed the facial stimulation-induced MLI-PC LTD in EtOH consumption mice. These results indicate that long-term EtOH consumption can impair the sensory stimulation-induced MLI–PC LTD via the activation of a NO signaling pathway in the cerebellar cortex in vivo in mice. Our results suggest that the chronic EtOH exposure causes a deficit in the cerebellar motor learning function and may be involved in the impaired MLI–PC GABAergic synaptic plasticity.

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Section: Introductionmentioning

confidence: 99%

Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

Bing

Chu

et al. 2019

Front. Cell. Neurosci.

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“…In contrast to the inhibitory conductance, Palmer et al used two-photon uncaging of an intracellular NMDA receptor antagonist (tc-MK801) to locally manipulate NMDA receptors in single branches of tuft dendrites [ 164 ]. These studies with intracellular perfusion of antagonists precisely confirm the impact of specific channel conductance, whereas extracellular drug application enables us to activate/silence channel conductance in a wider range [ 165 , 166 , 167 , 168 ] (but see [ 169 ] for extracellular but greater local drug delivery to patched neurons).…”

Section: Hybrid Methodologies With In Vivo Whole-cell Recording Tementioning

confidence: 73%

In Vivo Whole-Cell Patch-Clamp Methods: Recent Technical Progress and Future Perspectives

Noguchi

Ikegaya

Matsumoto

2021

Sensors

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Brain functions are fundamental for the survival of organisms, and they are supported by neural circuits consisting of a variety of neurons. To investigate the function of neurons at the single-cell level, researchers often use whole-cell patch-clamp recording techniques. These techniques enable us to record membrane potentials (including action potentials) of individual neurons of not only anesthetized but also actively behaving animals. This whole-cell recording method enables us to reveal how neuronal activities support brain function at the single-cell level. In this review, we introduce previous studies using in vivo patch-clamp recording techniques and recent findings primarily regarding neuronal activities in the hippocampus for behavioral function. We further discuss how we can bridge the gap between electrophysiology and biochemistry.

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“…Paired-current pulses (0.2 ms, 10-100 µA; duration: 50 ms; 0.05 Hz) were used for parallel ber stimulation. For inhibiting postsynaptic PKA in some experiments, protein kinase inhibitor-(6-22) amide (PKI) was added in pipette internal solution [30]. Recordings of mEPSCs were performed in the presence of a mixture of gabazine (20 µM) and tetrodotoxin (TTX; 1 µM) [31].…”

Section: Electrophysiological Recordings [29]mentioning

confidence: 99%

GLP-1 facilitates cerebellar parallel fiber glutamate release through PKA cascade in vitro in mice

Wang

Liu

Cao

et al. 2023

Preprint

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Glucagon-like peptide-1 (GLP-1) is mainly secreted by preglucagon (PPG) neurons, which play important roles in modulation of neuronal activity and synaptic transmission through its receptors. In this study, we here studied the effect of GLP-1 on parallel fiber-Purkinje cell (PF-PC) synaptic transmission in mouse cerebellar slices, by whole-cell patch-clamp recording technique and pharmacology methods. In the presence of GABAA receptor antagonist, bath application of GLP-1 (100 nM) enhanced PF-PC synaptic transmission, which expressed an increase in amplitude of evoked excitatory postsynaptic synaptic currents (eEPSCs) and a decrease in paired-pulse ratio (PPR). GLP-1 induced enhancement of eEPSCs was abolished by a selective GLP-1 receptor antagonist, Exendin 9–39, as well as by extracellular application of a specific protein kinase A (PKA) inhibitor, KT5720. However, inhibition of postsynaptic PKA which PKI containing internal solution, failed to block GLP-1 induced enhancement of eEPSCs. In the presence of a mixture of gabazine (20 µM) and TTX (1 µM), GLP-1 receptor significantly increased the frequency of miniature excitatory postsynaptic synaptic currents (mEPSCs), but without change the amplitude of mEPSCs. The GLP-1 induced increase in the frequency of mEPSCs was blocked by Exendin 9–39, as well as by inhibition of PKA with KT5720. The results indicate that activation of GLP-1 receptor enhances glutamate release at PF-PC synapse via PKA signaling pathway, resulting in an enhancement of PF-PC synaptic transmission in vitro in mice. The finding suggests that GLP-1 plays critical role in modulation of cerebellar function by regulating the excitatory synaptic transmission at PF-PC synapses in living animals.

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

Cited by 10 publications

References 58 publications

Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

In Vivo Whole-Cell Patch-Clamp Methods: Recent Technical Progress and Future Perspectives

GLP-1 facilitates cerebellar parallel fiber glutamate release through PKA cascade in vitro in mice

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