ArticleProceedings of the National Academy of Sciences of the United States of America2010
Disruption of the olivo-cerebellar circuit by Purkinje neuron-specific ablation of BK channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed.
- LRRC55 modulates BK channels to support Purkinje cell plasticity and motor coordination.bioRxiv : the preprint server for biology · 2026Article
- BACE1 regulates sleep-wake cycle through both enzymatic and non-enzymatic actions.EMBO reports · 2026Article
- Homeostatic bidirectional plasticity in upbound and downbound micromodules in a model of the olivocerebellar loop.PLoS computational biology · 2025Article
- Increased intrinsic membrane excitability is associated with olivary hypertrophy in spinocerebellar ataxia type 1.Human molecular genetics · 2024Article
- BK channels promote action potential repolarization in skeletal muscle but contribute little to myotonia.Pflugers Archiv : European journal of physiology · 2024Article
- Climbing Fiber Activation Induced by Footshock in the Cerebellar Vermis Lobule IV/V of Freely Moving Mice.Physiological research · 2024Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- BK channels sustain neuronal CaCellular and molecular life sciences : CMLS · 2023Article
- Targeting Ion Channels and Purkinje Neuron Intrinsic Membrane Excitability as a Therapeutic Strategy for Cerebellar Ataxia.Life (Basel, Switzerland) · 2023Review
- Further Studies on the Role of BTBD9 in the Cerebellum, Sleep-like Behaviors and the Restless Legs Syndrome.Neuroscience · 2022Article
- Optical Fiber-Based Recording of Climbing Fiber CaBiology · 2022Article
- Neuronal mechanism of a BK channelopathy in absence epilepsy and dyskinesia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Protein kinase Cγ in cerebellar Purkinje cells regulates CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Non-invasive, opsin-free mid-infrared modulation activates cortical neurons and accelerates associative learning.Nature communications · 2021Article
- BK Channel Regulation of Afterpotentials and Burst Firing in Cerebellar Purkinje Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- In Vivo Whole-Cell Patch-Clamp Methods: Recent Technical Progress and Future Perspectives.Sensors (Basel, Switzerland) · 2021Review
- In vivo analysis of the spontaneous firing of cerebellar Purkinje cells in awake transgenic mice that model spinocerebellar ataxia type 2.Cell calcium · 2021Article
- Single-neuron representation of learned complex sounds in the auditory cortex.Nature communications · 2020Article
- Depressed neuromuscular transmission causes weakness in mice lacking BK potassium channels.The Journal of general physiology · 2020Article
- Differential Coding Strategies in Glutamatergic and GABAergic Neurons in the Medial Cerebellar Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
12 more citing papers are in PubMed but not listed here.
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9 authors.
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Abstract
The large-conductance voltage- and calcium-activated potassium (BK) channels are ubiquitously expressed in the brain and play an important role in the regulation of neuronal excitation. Previous work has shown that the total deletion of these channels causes an impaired motor behavior, consistent with a cerebellar dysfunction. Cellular analyses showed that a decrease in spike firing rate occurred in at least two types of cerebellar neurons, namely in Purkinje neurons (PNs) and in Golgi cells. To determine the relative role of PNs, we developed a cell-selective mouse mutant, which lacked functional BK channels exclusively in PNs. The behavioral analysis of these mice revealed clear symptoms of ataxia, indicating that the BK channels of PNs are of major importance for normal motor coordination. By using combined two-photon imaging and patch-clamp recordings in these mutant mice, we observed a unique type of synaptic dysfunction in vivo, namely a severe silencing of the climbing fiber-evoked complex spike activity. By performing targeted pharmacological manipulations combined with simultaneous patch-clamp recordings in PNs, we obtained direct evidence that this silencing of climbing fiber activity is due to a malfunction of the tripartite olivo-cerebellar feedback loop, consisting of the inhibitory synaptic connection of PNs to the deep cerebellar nuclei (DCN), followed by a projection of inhibitory DCN afferents to the inferior olive, the origin of climbing fibers. Taken together, our results establish an essential role of BK channels of PNs for both cerebellar motor coordination and feedback regulation in the olivo-cerebellar loop.
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