ArticleMolecular neurodegeneration2009
Neuroprotective effects of blockers for T-type calcium channels.
Article in Molecular neurodegeneration, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 44 citations in OpenAlex.
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- Calcium: Alpha-Synuclein Interactions in Alpha-Synucleinopathies.Frontiers in neuroscience · 2016Review
- Simvastatin potently induces calcium-dependent apoptosis of human leiomyoma cells.The Journal of biological chemistry · 2014Article
- T-type calcium channel blockers as neuroprotective agents.Pflugers Archiv : European journal of physiology · 2014Review
- Potassium depolarization and raised calcium induces α-synuclein aggregates.Neurotoxicity research · 2013Article
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- Antihypertensives for combating dementia? A perspective on candidate molecular mechanisms and population-based prevention.Translational psychiatry · 2012Review
- Anti-epileptic drugs delay age-related loss of spiral ganglion neurons via T-type calcium channel.Hearing research · 2011Article
- Why do hair cells and spiral ganglion neurons in the cochlea die during aging?Aging and disease · 2011Article
- Kv7-type channel currents in spiral ganglion neurons: involvement in sensorineural hearing loss.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cognitive and functional decline with age is correlated with deregulation of intracellular calcium, which can lead to neuronal death in the brain. Previous studies have found protective effects of various calcium channel blockers in pathological conditions. However, little has been done to explore possible protective effects of blockers for T-type calcium channels, which forms a family of FDA approved anti-epileptic drugs. In this study, we found that neurons showed an increase in viability after treatment with either L-type or T-type calcium channel antagonists. The family of low-voltage activated, or T-type calcium channels, comprise of three members (Cav3.1, Cav3.2, and Cav3.3) based on their respective main pore-forming alpha subunits: alpha1G, alpha1H, and alpha1I. Among these three subunits, alpha1H is highly expressed in hippocampus and certain cortical regions. However, T-type calcium channel blockers can protect neurons derived from alpha1H-/- mice, suggesting that neuroprotection demonstrated by these drugs is not through the alpha1H subunit. In addition, blockers for T-type calcium channels were not able to confer any protection to neurons in long-term cultures, while blockers of L-type calcium channels could protect neurons. These data indicate a new function of blockers for T-type calcium channels, and also suggest different mechanisms to regulate neuronal survival by calcium signaling pathways. Thus, our findings have important implications in the development of new treatment for age-related neurodegenerative disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.