Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Altered functional expression of Purkinje cell calcium channels precedes motor dysfunction in tottering mice.

Neuroscience - 12 Dec 2007

Erickson M A, Haburćák M, Smukler L, Dunlap K

Abstract excerpt

In tottering mice, a point mutation in the gene encoding P-type (Ca(v)2.1) voltage-gated calcium channels results in ataxia, absence epilepsy, and motor dystonia that appear 3-4 weeks postnatally. The aberrant motor behaviors have been linked to cerebellar dysfunction, and adult Purkinje cells (PCs) of tottering mice exhibit calcium-dependent changes in gene transcription suggestive of altered calcium...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Calcium
Share to Calcium Channels
Share to Channelopathies

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Electrophysiology

Share to Gait Disorders, Neurologic

Share to Homeostasis

Share to Mice, Neurologic Mutants

Share to Purkinje Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 18023294
DOI: 10.1016/j.neuroscience.2007.09.052
PMCID: PMC2203215

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Altered functional expression of Purkinje cell calcium channels precedes motor dysfunction in tottering mice.PMID 18023294Read ↗

L-type calcium channels contribute to the tottering mouse dystonic episodes.Semantic proximity Read ↗

Single tottering mutations responsible for the neuropathic phenotype of the P-type calcium channel.Semantic proximity Read ↗

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.Semantic proximity Read ↗

Delayed postnatal loss of P/Q-type calcium channels recapitulates the absence epilepsy, dyskinesia, and ataxia phenotypes of genomic Cacna1a mutations.Semantic proximity Read ↗

Enhanced G protein-dependent modulation of excitatory synaptic transmission in the cerebellum of the Ca2+ channel-mutant mouse, tottering.Semantic proximity Read ↗

Aberrant cerebellar granule cell-specific GABAA receptor expression in the epileptic and ataxic mouse mutant, Tottering.Semantic proximity Read ↗

Disrupted Calcium Signaling in Animal Models of Human Spinocerebellar Ataxia (SCA)Semantic proximity Read ↗

Alterations in intracellular calcium ion concentrations in cerebellar granule cells of the CACNA1A mutant mouse, leaner, during postnatal development.Semantic proximity Read ↗

Differential expression of T-type calcium channels in P/Q-type calcium channel mutant mice with ataxia and absence epilepsy.Semantic proximity Read ↗

Reduced immunoreactivity to calcium-binding proteins in Purkinje cells precedes onset of ataxia in spinocerebellar ataxia-1 transgenic mice.Semantic proximity Read ↗

Altered calcium homeostasis in cerebellar Purkinje cells of leaner mutant mice.Semantic proximity Read ↗

Functional compensation by other voltage-gated Ca2+ channels in mouse basal forebrain neurons with Ca(V)2.1 mutations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.