ReviewCurrent molecular pharmacology2015
Regulation of Postsynaptic Stability by the L-type Calcium Channel CaV1.3 and its Interaction with PDZ Proteins.
Review in Current molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Deletion of the Voltage-Gated Calcium Channel Gene, CaCerebellum (London, England) · 2025Article
- CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023Review
- Neuronal deletion of CaScientific reports · 2022Article
- Ion Channel Partnerships: Odd and Not-So-Odd Couples Controlling Neuronal Ion Channel Function.International journal of molecular sciences · 2022Review
- Snapin Specifically Up-Regulates CaInternational journal of molecular sciences · 2021Article
- Role of densin-180 in mouse ventral hippocampal neurons in 24-hr retention of contextual fear conditioning.Brain and behavior · 2020Article
- Article
- NMDA receptors mediate synaptic depression, but not spine loss in the dentate gyrus of adult amyloid Beta (Aβ) overexpressing mice.Acta neuropathologica communications · 2018Article
- Modulation of CaBMC research notes · 2018Article
- Neurite Outgrowth Stimulated by Oxytocin Is Modulated by Inhibition of the Calcium Voltage-Gated Channels.Cellular and molecular neurobiology · 2018Article
- Enhancing VTA CaMolecular psychiatry · 2017Article
- Inflammation alters AMPA-stimulated calcium responses in dorsal striatal D2 but not D1 spiny projection neurons.The European journal of neuroscience · 2017Article
- Splice variants of the CaScientific reports · 2016Article
- Trafficking regulates the subcellular distribution of voltage-gated sodium channels in primary sensory neurons.Molecular pain · 2015Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alterations in dendritic spine morphology and postsynaptic structure are a hallmark of neurological disorders. Particularly spine pruning of striatal medium spiny neurons and aberrant rewiring of corticostriatal synapses have been associated with the pathology of Parkinson's disease and LDOPA induced dyskinesia, respectively. Owing to its low activation threshold the neuronal L-type calcium channel CaV1.3 is particularly critical in the control of neuronal excitability and thus in the calcium-dependent regulation of neuronal functions. CaV1.3 channels are located in dendritic spines and contain a C-terminal class 1 PDZ domain-binding sequence. Until today the postsynaptic PDZ domain proteins shank, densin-180, and erbin have been shown to interact with CaV1.3 channels and to modulate their current properties. Interestingly experimental evidence suggests an involvement of all three PDZ proteins as well as CaV1.3 itself in regulating dendritic and postsynaptic morphology. Here we briefly review the importance of CaV1.3 and its proposed interactions with PDZ proteins for the stability of dendritic spines. With a special focus on the pathology associated with Parkinson's disease, we discuss the hypothesis that CaV1.3 L-type calcium channels may be critical modulators of dendritic spine stability.
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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.