ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Calmodulin kinase pathway mediates the K+-induced increase in Gap junctional communication between mouse spinal cord astrocytes.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 104 citations in OpenAlex.
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- The Astroglia Syncytial Theory of Consciousness.International journal of molecular sciences · 2025Review
- Astroglial Connexins Inactivation Increases Relapse of Depressive-like Phenotype after Antidepressant Withdrawal.International journal of molecular sciences · 2022Article
- Review
- Exacerbation of Epilepsy by Astrocyte Alkalization and Gap Junction Uncoupling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Heterogeneity of Astrocytes in Grey and White Matter.Neurochemical research · 2021Review
- Calmodulin-Cork Model of Gap Junction Channel Gating-One Molecule, Two Mechanisms.International journal of molecular sciences · 2020Review
- Calmodulin-Mediated Regulation of Gap Junction Channels.International journal of molecular sciences · 2020Review
- Gap junctions, pannexins and pain.Neuroscience letters · 2019Review
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Connexin 43-Mediated Astroglial Metabolic Networks Contribute to the Regulation of the Sleep-Wake Cycle.Neuron · 2017Article
- Connexin-Dependent Neuroglial Networking as a New Therapeutic Target.Frontiers in cellular neuroscience · 2017Review
- Connexin 43 contributes to ectopic orofacial pain following inferior alveolar nerve injury.Molecular pain · 2016Article
- The central role of aquaporins in the pathophysiology of ischemic stroke.Frontiers in cellular neuroscience · 2015Review
- A novel role of spinal astrocytic connexin 43: mediating morphine antinociceptive tolerance by activation of NMDA receptors and inhibition of glutamate transporter-1 in rats.CNS neuroscience & therapeutics · 2014Article
- Sparse short-distance connections enhance calcium wave propagation in a 3D model of astrocyte networks.Frontiers in computational neuroscience · 2014Article
- How do astrocytes shape synaptic transmission? Insights from electrophysiology.Frontiers in cellular neuroscience · 2013Review
- Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis?Neurochemistry international · 2013Review
- Astroglial networking contributes to neurometabolic coupling.Frontiers in neuroenergetics · 2013Article
- Calmodulin dependent protein kinase increases conductance at gap junctions formed by the neuronal gap junction protein connexin36.Brain research · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Astrocytes are coupled to one another by gap junction channels that allow the diffusion of ions and small molecules throughout the interconnected syncytium. In astrocytes, gap junctions are believed to participate in spatial buffering removing the focal excess of potassium resultant from intense neuronal activity by current loops through the syncytium and are also implicated in the propagation of astrocytic calcium waves, a form of extraneuronal signaling. Gap junctions can be modulated by several factors, including elevation of extracellular potassium concentration. Because K(+) elevation is a component of spinal cord injury, we evaluated the extent to which cultured spinal cord astrocytes is affected by K(+) levels and obtained evidence suggesting that a Ca(2+)-calmodulin (CaM) protein kinase is involved in the K(+)-induced increased coupling. Exposure of astrocytes to high K(+) solutions induced a dose-dependent increase in dye coupling; such increased coupling was greatly attenuated by reducing extracellular Ca(2+) concentration, prevented by nifedipine, and potentiated by Bay-K-8644. These results indicate that K(+)-induced increased coupling is mediated by a signaling pathway that is dependent on the influx of Ca(2+) through L-type Ca(2+) channels. Evidence supporting the participation of the CaM kinase pathway on K(+)-induced increased coupling was obtained in experiments showing that calmidazolium and KN-93 totally prevented the increase in dye and electrical coupling induced by high K(+) solutions. Because no changes in connexin43 expression levels or distribution were observed in astrocytes exposed to high K(+) solutions, we propose that the increased junctional communication is related to an increased number of active channels within gap junction plaques.
Indexed as
Identifiers
11517253PMC1513544W2151305004What OpenQuestion holds
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.