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

The weaver mouse gain-of-function phenotype of dopaminergic midbrain neurons is determined by coactivation of wvGirk2 and K-ATP channels.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 15 Oct 1999

Liss B, Neu A, Roeper J

Abstract excerpt

The phenotype of substantia nigra (SN) neurons in homozygous weaver (wv/wv) mice was studied by combining patch-clamp and single-cell RT-multiplex PCR techniques in midbrain slices of 14-d-old mice. In contrast to GABAergic SN neurons, which were unaffected in homozygous weaver mice (wv/wv), dopaminergic SN neurons possessed a dramatically altered phenotype with a depolarized membrane potential and complete loss...

Read the complete abstract on PubMed

Topics

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

Share to Adenosine Triphosphate
Share to Dopamine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to G Protein-Coupled Inwardly-Rectifying Potassium Channels

Share to Mesencephalon

Share to Mice, Neurologic Mutants

Share to Patch-Clamp Techniques

Share to Potassium Channels

Share to Potassium Channels, Inwardly Rectifying

Source

Open in PubMed Open full text

Identifiers

PMID: 10516303
PMCID: PMC6782762

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

The weaver mouse gain-of-function phenotype of dopaminergic midbrain neurons is determined by coactivation of wvGirk2 and K-ATP channels.PMID 10516303Read ↗

Cell death in weaver mouse cerebellum.Semantic proximity Read ↗

The weaver mutation of GIRK2 results in a loss of inwardly rectifying K+ current in cerebellar granule cells.Semantic proximity Read ↗

Girk2 expression in the ventral midbrain, cerebellum, and olfactory bulb and its relationship to the murine mutation weaver.Semantic proximity Read ↗

K-ATP channels promote the differential degeneration of dopaminergic midbrain neurons.Semantic proximity Read ↗

Nigrostriatal Dopaminergic Neurodegeneration in theWeaverMouse Is Mediated via Neuroinflammation and Alleviated by Minocycline AdministrationSemantic proximity Read ↗

Cell specific single viral vector CRISPR/Cas9 editing and genetically encoded tool delivery in the central and peripheral nervous systemsSemantic proximity Read ↗

Conditional Knockout of Striatal Gnal Produces Dystonia-like Motor PhenotypesSemantic proximity Read ↗

Generation of knock-in Cre and FlpO mouse lines for precise targeting of striatal projection neurons and dopaminergic neuronsSemantic proximity Read ↗

Neuron-specific Kv1.1 deficiency is sufficient to cause epilepsy, premature death, and cardiorespiratory dysregulationSemantic proximity Read ↗

Impaired striatal dopamine release in homozygous Vps35 D620N knock-in mice.Semantic proximity Read ↗

Assessment of a mutation in the H5 domain of Girk2 as a candidate for the weaver mutation.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 ↗

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