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

K-ATP channels promote the differential degeneration of dopaminergic midbrain neurons.

Nature neuroscience - 1 Dec 2005

Liss Birgit, Haeckel Olga, Wildmann Johannes, Miki Takashi, Seino Susumu, Roeper Jochen

Abstract excerpt

The selective degeneration of dopaminergic (DA) midbrain neurons in the substantia nigra (SN) is a hallmark of Parkinson disease. DA neurons in the neighboring ventral tegmental area (VTA) are significantly less affected. The mechanisms for this differential vulnerability of DA neurons are unknown. We identified selective activation of ATP-sensitive potassium (K-ATP) channels as a potential mechanism. We show...

Read the complete abstract on PubMed

Topics

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

Share to Electron Transport Complex I
Share to Mice, Neurologic Mutants

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Neurotoxins

Share to Organ Culture Techniques

Share to Parkinsonian Disorders

Share to Potassium Channels, Inwardly Rectifying

Share to Substantia Nigra

Share to Ventral Tegmental Area

Source

Identifiers

PMID: 16299504
DOI: 10.1038/nn1570

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

K-ATP channels promote the differential degeneration of dopaminergic midbrain neurons.PMID 16299504Read ↗

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

Calcium, bioenergetics, and neuronal vulnerability in Parkinson's disease.Semantic proximity Read ↗

Physiological phenotype and vulnerability in Parkinson's disease.Semantic proximity Read ↗

Preserved striatal innervation maintains motor function despite severe loss of nigral dopaminergic neurons.Semantic proximity Read ↗

Preserved striatal innervation and motor function despite severe loss of nigral dopamine neurons following mitochondrial dysfunction induced by mtDNA mutationsSemantic proximity Read ↗

Impaired nigrostriatal function precedes behavioral deficits in a genetic mitochondrial model of Parkinson's diseaseSemantic proximity Read ↗

Neuronal vulnerability following inhibition of mitochondrial complex II: a possible ionic mechanism for Huntington's disease.Semantic proximity Read ↗

SK channel function regulates the dopamine phenotype of neurons in the substantia nigra pars compacta.Semantic proximity Read ↗

Reduced synaptic activity and dysregulated extracellular matrix pathways are common phenotypes in midbrain neurons derived from sporadic and mutation-associated Parkinson’s disease patientsSemantic proximity Read ↗

Mutant Twinkle increases dopaminergic neurodegeneration, mtDNA deletions and modulates Parkin expression.Semantic proximity Read ↗

4-Aminopyridine Induced Activity Rescues Hypoexcitable Motor Neurons from Amyotrophic Lateral Sclerosis Patient-Derived Induced Pluripotent Stem Cells.Semantic proximity Read ↗

Glutamate, excitotoxicity, and programmed cell death in Parkinson disease.Semantic proximity Read ↗

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