ArticleJournal of molecular neuroscience : MN2015
Calcium CaV1 channel subtype mRNA expression in Parkinson's disease examined by in situ hybridization.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Cinnarizine, a Calcium Channel Blocker, Partially Prevents the Striatal Dopamine Decline and Loss of Nigral Dopamine Neurons in the Lactacystin-Induced Rat Model of Parkinson's Disease.International journal of molecular sciences · 2025Article
- Monomeric α-synuclein activates the plasma membrane calcium pump.The EMBO journal · 2023Article
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- Alpha-synuclein aggregates activate calcium pump SERCA leading to calcium dysregulation.EMBO reports · 2018Article
- On Cell Loss and Selective Vulnerability of Neuronal Populations in Parkinson's Disease.Frontiers in neurology · 2018Review
- Calcium, mitochondrial dysfunction and slowing the progression of Parkinson's disease.Experimental neurology · 2017Review
- Parkinson's Disease Is Not Simply a Prion Disorder.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Review
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- Inhibition of L-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Selective neuronal vulnerability in Parkinson disease.Nature reviews. Neuroscience · 2017Review
- Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson's Disease: Therapeutic Rationale and Current Status.CNS drugs · 2016Review
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Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The factors which make some neurons vulnerable to neurodegeneration in Parkinson's disease while others remain resistant are not fully understood. Studies in animal models of Parkinson's disease suggest that preferential use of CaV1.3 subtypes by neurons may contribute to the neurodegenerative process by increasing mitochondrial oxidant stress. This study quantified the level of mRNA for the CaV1 subtypes found in the brain by in situ hybridization using CaV1 subtype-specific [(35)S]-radiolabelled oligonucleotide probes. In normal brain, the greatest amount of messenger RNA (mRNA) for each CaV1 subtype was found in the midbrain (substantia nigra), with a moderate level in the pons (locus coeruleus) and lower quantities in cerebral cortex (cingulate and primary motor). In Parkinson's disease, the level of CaV1 subtype mRNA was maintained in the midbrain and pons, despite cell loss in these areas. In cingulate cortex, CaV1.2 and CaV1.3 mRNA increased in cases with late-stage Parkinson's disease. In primary motor cortex, the level of CaV1.2 mRNA increased in late-stage Parkinson's disease. The level of CaV1.3 mRNA increased in primary motor cortex of cases with early-stage Parkinson's disease and normalized to near the control level in cases from late-stage Parkinson's disease. The finding of elevated CaV1 subtype expression in cortical brain regions supports the view that disturbed calcium homeostasis is a feature of Parkinson's disease throughout brain and not only a compensatory consequence to the neurodegenerative process in areas of cell loss.
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