Enhanced G protein-dependent modulation of excitatory synaptic transmission in the cerebellum of the Ca2+ channel-mutant mouse, tottering.
about
Effects of familial hemiplegic migraine type 1 mutations on neuronal P/Q-type Ca2+ channel activity and inhibitory synaptic transmissionGenetic enhancement of thalamocortical network activity by elevating alpha 1g-mediated low-voltage-activated calcium current induces pure absence epilepsy.Noradrenergic control of associative synaptic plasticity by selective modulation of instructive signalsAnimal models of generalized dystonia.Contribution of calcium-dependent facilitation to synaptic plasticity revealed by migraine mutations in the P/Q-type calcium channel.Flocculus Purkinje cell signals in mouse Cacna1a calcium channel mutants of escalating severity: an investigation of the role of firing irregularity in ataxia.Abnormal excitability and episodic low-frequency oscillations in the cerebral cortex of the tottering mouse.Effects of familial hemiplegic migraine type 1 mutation T666M on voltage-gated calcium channel activities in trigeminal ganglion neuronsPurkinje cell-specific ablation of Cav2.1 channels is sufficient to cause cerebellar ataxia in mice.Stargazer--a mouse to seize!Altered functional expression of Purkinje cell calcium channels precedes motor dysfunction in tottering mice.Low-frequency oscillations in the cerebellar cortex of the tottering mouse.Different relationship of N- and P/Q-type Ca2+ channels to channel-interacting slots in controlling neurotransmission at cultured hippocampal synapses.STD-dependent and independent encoding of input irregularity as spike rate in a computational model of a cerebellar nucleus neuron.Enhanced synaptic inhibition disrupts the efferent code of cerebellar Purkinje neurons in leaner Cav2.1 Ca 2+ channel mutant mice.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.Does modulation of the endocannabinoid system have potential therapeutic utility in cerebellar ataxia?Eye movements of the murine P/Q calcium channel mutant tottering, and the impact of aging.The du(2J) mouse model of ataxia and absence epilepsy has deficient cannabinoid CB₁ receptor-mediated signalling.
P2860
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P2860
Enhanced G protein-dependent modulation of excitatory synaptic transmission in the cerebellum of the Ca2+ channel-mutant mouse, tottering.
description
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name
Enhanced G protein-dependent m ...... annel-mutant mouse, tottering.
@en
Enhanced G protein-dependent m ...... annel-mutant mouse, tottering.
@nl
type
label
Enhanced G protein-dependent m ...... annel-mutant mouse, tottering.
@en
Enhanced G protein-dependent m ...... annel-mutant mouse, tottering.
@nl
prefLabel
Enhanced G protein-dependent m ...... annel-mutant mouse, tottering.
@en
Enhanced G protein-dependent m ...... annel-mutant mouse, tottering.
@nl
P2860
P1476
Enhanced G protein-dependent m ...... hannel-mutant mouse, tottering
@en
P2093
Kathleen Dunlap
P2860
P304
P356
10.1113/JPHYSIOL.2002.033415
P407
P577
2003-01-24T00:00:00Z