ReviewNeurochemical research2015
Excitable Astrocytes: Ca(2+)- and cAMP-Regulated Exocytosis.
Review in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 67 citations in OpenAlex.
- Crosstalk of noradrenergic CaCell communication and signaling : CCS · 2026Article
- Article
- Photoactivated adenylyl cyclase in cortical astrocytes promotes synaptic potentiation and reveals alterations in Huntington's disease.iScience · 2025Article
- The Role of Neuroglia in Cognitive Longevity.Neurochemical research · 2025Review
- DYRK1A in the physiology and pathology of the neuron-astrocyte axis.Frontiers in neuroscience · 2025Review
- AFrontiers in immunology · 2023Article
- Astrocyte arborization enhances CaGlia · 2021Article
- Endocytic BDNF secretion regulated by Vamp3 in astrocytes.Scientific reports · 2021Article
- Bupivacaine in combination with sildenafil (Viagra) and vitamin D3 have anti-inflammatory effects in osteoarthritic chondrocytes.Current research in pharmacology and drug discovery · 2021Article
- Lactate as an Astroglial Signal Augmenting Aerobic Glycolysis and Lipid Metabolism.Frontiers in physiology · 2021Review
- Astrocytes, Noradrenaline, α1-Adrenoreceptors, and Neuromodulation: Evidence and Unanswered Questions.Frontiers in cellular neuroscience · 2021Review
- A Mechanistic Rationale for PDE-4 Inhibitors to Treat Residual Cognitive Deficits in Acquired Brain Injury.Current neuropharmacology · 2020Review
- Astroglial Mechanisms of Ketamine Action Include Reduced Mobility of Kir4.1-Carrying Vesicles.Neurochemical research · 2020Review
- Gliocrine System: Astroglia as Secretory Cells of the CNS.Advances in experimental medicine and biology · 2019Review
- Article
- Anti-inflammatory effects induced by pharmaceutical substances on inflammatory active brain astrocytes-promising treatment of neuroinflammation.Journal of neuroinflammation · 2018Article
- Astroglial vesicular network: evolutionary trends, physiology and pathophysiology.Acta physiologica (Oxford, England) · 2018Review
- Physiology of Astroglia.Physiological reviews · 2018Review
- Noradrenergic Hypothesis Linking Neurodegeneration-Based Cognitive Decline and Astroglia.Frontiers in molecular neuroscience · 2018Review
- Stratification of astrocytes in healthy and diseased brain.Brain pathology (Zurich, Switzerland) · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During neural activity, neurotransmitters released at synapses reach neighbouring cells, such as astrocytes. These get excited via numerous mechanisms, including the G protein coupled receptors that regulate the cytosolic concentration of second messengers, such as Ca(2+) and cAMP. The stimulation of these pathways leads to feedback modulation of neuronal activity and the activity of other cells by the release of diverse substances, gliosignals that include classical neurotransmitters such as glutamate, ATP, or neuropeptides. Gliosignal molecules are released from astrocytes through several distinct molecular mechanisms, for example, by diffusion through membrane channels, by translocation via plasmalemmal transporters, or by vesicular exocytosis. Vesicular release regulated by a stimulus-mediated increase in cytosolic second messengers involves a SNARE-dependent merger of the vesicle membrane with the plasmalemma. The coupling between the stimulus and vesicular secretion of gliosignals in astrocytes is not as tight as in neurones. This is considered an adaptation to regulate homeostatic processes in a slow time domain as is the case in the endocrine system (slower than the nervous system), hence glial functions constitute the gliocrine system. This article provides an overview of the mechanisms of excitability, involving Ca(2+) and cAMP, where the former mediates phasic signalling and the latter tonic signalling. The molecular, anatomic, and physiologic properties of the vesicular apparatus mediating the release of gliosignals is presented.
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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.