ArticleScientific reports2015
Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- α-Synuclein pathology differentially alters T-type calcium currents in vulnerable and resilient substantia nigra dopaminergic subpopulations.bioRxiv : the preprint server for biology · 2026Article
- Reinventing amlodipine.The Journal of pharmacology and experimental therapeutics · 2026Review
- Rebound Bursting Selectively Enables Fast Dynamics in Dopamine Midbrain Neurons Projecting to the Dorsolateral Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Muscarinic Receptor Activation Preferentially Inhibits Rebound in Vulnerable Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Muscarinic receptor activation preferentially inhibits rebound in vulnerable dopaminergic neurons.bioRxiv : the preprint server for biology · 2024Article
- Ion Channels and Metal Ions in Parkinson's Disease: Historical Perspective to the Current Scenario.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Exploring the role of mitochondrial uncoupling protein 4 in brain metabolism: implications for Alzheimer's disease.Frontiers in neuroscience · 2024Review
- The human channel gating-modifying A749G CACNA1D (Cav1.3) variant induces a neurodevelopmental syndrome-like phenotype in mice.JCI insight · 2023Article
- CaBritish journal of pharmacology · 2023Review
- Aberrant somatic calcium channel function in cNurr1 and LRRK2-G2019S mice.NPJ Parkinson's disease · 2023Article
- Article
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- Contributions of CaFrontiers in physiology · 2021Article
- Multi-Electrode Array Analysis Identifies Complex Dopamine Responses and Glucose Sensing Properties of Substantia Nigra Neurons in Mouse Brain Slices.Frontiers in synaptic neuroscience · 2021Article
- Functional Dissection of Basal Ganglia Inhibitory Inputs onto Substantia Nigra Dopaminergic Neurons.Cell reports · 2020Article
- Dopamine induces in vitro migration of synovial fibroblast from patients with rheumatoid arthritis.Scientific reports · 2020Article
- Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease.Nature communications · 2019Article
- Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019Review
- NCS-1 Deficiency Affects mRNA Levels of Genes Involved in Regulation of ATP Synthesis and Mitochondrial Stress in Highly VulnerableFrontiers in molecular neuroscience · 2019Article
- Calcium, Dopamine and Neuronal Calcium Sensor 1: Their Contribution to Parkinson's Disease.Frontiers in molecular neuroscience · 2019Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
The preferential degeneration of Substantia nigra dopamine midbrain neurons (SN DA) causes the motor-symptoms of Parkinson's disease (PD). Voltage-gated L-type calcium channels (LTCCs), especially the Cav1.3-subtype, generate an activity-related oscillatory Ca(2+) burden in SN DA neurons, contributing to their degeneration and PD. While LTCC-blockers are already in clinical trials as PD-therapy, age-dependent functional roles of Cav1.3 LTCCs in SN DA neurons remain unclear. Thus, we analysed juvenile and adult Cav1.3-deficient mice with electrophysiological and molecular techniques. To unmask compensatory effects, we compared Cav1.3 KO mice with pharmacological LTCC-inhibition. LTCC-function was not necessary for SN DA pacemaker-activity at either age, but rather contributed to their pacemaker-precision. Moreover, juvenile Cav1.3 KO but not WT mice displayed adult wildtype-like, sensitised inhibitory dopamine-D2-autoreceptor (D2-AR) responses that depended upon both, interaction of the neuronal calcium sensor NCS-1 with D2-ARs, and on voltage-gated T-type calcium channel (TTCC) activity. This functional KO-phenotype was accompanied by cell-specific up-regulation of NCS-1 and Cav3.1-TTCC mRNA. Furthermore, in wildtype we identified an age-dependent switch of TTCC-function from contributing to SN DA pacemaker-precision in juveniles to pacemaker-frequency in adults. This novel interplay of Cav1.3 L-type and Cav3.1 T-type channels, and their modulation of SN DA activity-pattern and D2-AR-sensitisation, provide new insights into flexible age- and calcium-dependent activity-control of SN DA neurons and its pharmacological modulation.
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