ArticleThe Journal of physiology2003
Enhanced G protein-dependent modulation of excitatory synaptic transmission in the cerebellum of the Ca2+ channel-mutant mouse, tottering.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 58 citations in OpenAlex.
- Cerebellar α1Cellular and molecular life sciences : CMLS · 2025Article
- GABAMedComm · 2025Review
- Does modulation of the endocannabinoid system have potential therapeutic utility in cerebellar ataxia?The Journal of physiology · 2016Review
- Abnormal excitability and episodic low-frequency oscillations in the cerebral cortex of the tottering mouse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Flocculus Purkinje cell signals in mouse Cacna1a calcium channel mutants of escalating severity: an investigation of the role of firing irregularity in ataxia.Journal of neurophysiology · 2014Article
- The du(2J) mouse model of ataxia and absence epilepsy has deficient cannabinoid CB₁ receptor-mediated signalling.The Journal of physiology · 2013Article
- Postnatal loss of P/Q-type channels confined to rhombic-lip-derived neurons alters synaptic transmission at the parallel fiber to purkinje cell synapse and replicates genomic Cacna1a mutation phenotype of ataxia and seizures in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Cerebellar ataxia by enhanced Ca(V)2.1 currents is alleviated by Ca2+-dependent K+-channel activators in Cacna1a(S218L) mutant mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Enhanced synaptic inhibition disrupts the efferent code of cerebellar Purkinje neurons in leaner Cav2.1 Ca 2+ channel mutant mice.Cerebellum (London, England) · 2012Article
- Effects of familial hemiplegic migraine type 1 mutation T666M on voltage-gated calcium channel activities in trigeminal ganglion neurons.Journal of neurophysiology · 2012Article
- Purkinje cell-specific ablation of Cav2.1 channels is sufficient to cause cerebellar ataxia in mice.Cerebellum (London, England) · 2012Article
- STD-dependent and independent encoding of input irregularity as spike rate in a computational model of a cerebellar nucleus neuron.Cerebellum (London, England) · 2011Article
- Spatiotemporal firing patterns in the cerebellum.Nature reviews. Neuroscience · 2011Review
- Contribution of calcium-dependent facilitation to synaptic plasticity revealed by migraine mutations in the P/Q-type calcium channel.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- CaV2.1 channelopathies.Pflugers Archiv : European journal of physiology · 2010Review
- Different relationship of N- and P/Q-type Ca2+ channels to channel-interacting slots in controlling neurotransmission at cultured hippocampal synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Noradrenergic control of associative synaptic plasticity by selective modulation of instructive signals.Neuron · 2009Article
- Genetic enhancement of thalamocortical network activity by elevating alpha 1g-mediated low-voltage-activated calcium current induces pure absence epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Low-frequency oscillations in the cerebellar cortex of the tottering mouse.Journal of neurophysiology · 2009Article
- Altered functional expression of Purkinje cell calcium channels precedes motor dysfunction in tottering mice.Neuroscience · 2007Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tottering, a mouse model for absence epilepsy and cerebellar ataxia, carries a mutation in the gene encoding class A (P/Q-type) Ca2+ channels, the dominant exocytotic Ca2+ channel at most synapses in the mammalian central nervous system. Comparing tottering to wild-type mice, we have studied glutamatergic transmission between parallel fibres and Purkinje cells in cerebellar slices. Results from biochemical assays and electrical field recordings demonstrate that glutamate release from parallel fibre terminals of the tottering mouse is controlled largely by class B Ca2+ channels (N-type), in contrast to the P/Q-channels that dominate release from wild-type terminals. Since N-channels, in a variety of assays, are more effectively inhibited by G proteins than are P/Q-channels, we tested whether synaptic transmission between parallel fibres and Purkinje cells in tottering mice was more susceptible to inhibitory modulation by G protein-coupled receptors than in their wild-type counterparts. GABAB receptors and alpha2-adrenergic receptors (activated by bath application of transmitters) produced a three- to fivefold more potent inhibition of transmission in tottering than in wild-type synapses. This increased modulation is likely to be important for cerebellar transmission in vivo, since heterosynaptic depression, produced by activating GABAergic interneurones, greatly prolonged GABAB receptor-mediated presynaptic inhibition in tottering as compared to wild-type slices. We propose that this enhanced modulation shifts the balance of synaptic input to Purkinje cells in favour of inhibition, reducing Purkinje cell output from the cerebellum, and may contribute to the aberrant motor phenotype that is characteristic of this mutant animal.
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