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

Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.

PLoS genetics - 1 Aug 2018

Brusich Douglas J, Spring Ashlyn M, James Thomas D, Yeates Catherine J, Helms Timothy H, Frank C Andrew

Abstract excerpt

Gain-of-function mutations in the human CaV2.1 gene CACNA1A cause familial hemiplegic migraine type 1 (FHM1). To characterize cellular problems potentially triggered by CaV2.1 gains of function, we engineered mutations encoding FHM1 amino-acid substitutions S218L (SL) and R192Q (RQ) into transgenes of Drosophila melanogaster CaV2/cacophony. We expressed the transgenes pan-neuronally. Phenotypes were mild for...

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, N-Type

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cerebellar Ataxia

Share to Migraine Disorders

Share to Neuromuscular Junction

Share to Synapses

Share to Synaptic Transmission

Share to Transgenes

Source

Open in PubMed Open full text

Identifiers

PMID: 30080864
DOI: 10.1371/journal.pgen.1007577
PMCID: PMC6095605

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.PMID 30080864Read ↗

Drosophila Ca <sub>V</sub> 2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca <sup>2+</sup> store release pathwaySemantic proximity Read ↗

Synaptic gain-of-function effects of mutant Cav2.1 channels in a mouse model of familial hemiplegic migraine are due to increased basal [Ca2+]i.Semantic proximity Read ↗

A hyperexcitability phenotype in mouse trigeminal sensory neurons expressing the R192Q Cacna1a missense mutation of familial hemiplegic migraine type-1.Semantic proximity Read ↗

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis.Semantic proximity Read ↗

Effects of familial hemiplegic migraine type 1 mutation T666M on voltage-gated calcium channel activities in trigeminal ganglion neurons.Semantic proximity Read ↗

Familial hemiplegic migraine.Semantic proximity Read ↗

Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraineSemantic proximity Read ↗

Abnormal synaptic Ca(2+) homeostasis and morphology in cortical neurons of familial hemiplegic migraine type 1 mutant mice.Semantic proximity Read ↗

Trigeminal ganglion neuron subtype-specific alterations of Ca(V)2.1 calcium current and excitability in a Cacna1a mouse model of migraine.Semantic proximity Read ↗

Biological science of headache channels.Semantic proximity Read ↗

Familial hemiplegic migraine type-1 mutated cav2.1 calcium channels alter inhibitory and excitatory synaptic transmission in the lateral superior olive of mice.Semantic proximity Read ↗

Familial hemiplegic migraine mutations increase Ca(2+) influx through single human CaV2.1 channels and decrease maximal CaV2.1 current density in neurons.Semantic proximity Read ↗

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