ArticleFrontiers in behavioral neuroscience2014
Astrocyte IP3R2-dependent Ca(2+) signaling is not a major modulator of neuronal pathways governing behavior.
Article in Frontiers in behavioral neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 110 citations in OpenAlex.
- Cocaine facilitates CaMolecular psychiatry · 2026Article
- Role of dysregulated calcium homeostasis in astrocytes in neurodegenerative disorders.Nature reviews. Neuroscience · 2026Review
- Constellations of Thought: Astrocytic Contributions to Cognition Across Rodent Models of Brain Dysfunction.Biomolecules · 2026Review
- Article
- Astrocyte Store-Released Calcium Modulates Visual Cortex Synapse Development and Circuit Function.Research square · 2025Article
- IP3R2-Mediated Astrocytic CaCells · 2025Article
- Astrocyte regulation of behavioral outputs: the versatile roles of calcium.Frontiers in cellular neuroscience · 2025Review
- Membrane Associated RNA-Containing Vesicles Regulate Cortical Astrocytic Microdomain Calcium Transients in Awake Ischemic Stroke Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Glial Control of Cortical Neuronal Circuit Maturation and Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- Graphene oxide electrodes enable electrical stimulation of distinct calcium signalling in brain astrocytes.Nature nanotechnology · 2024Article
- Astroglial Dysfunctions in Mood Disorders and Rodent Stress Models: Consequences on Behavior and Potential as Treatment Target.International journal of molecular sciences · 2024Review
- ITPR2 Mediated Calcium Homeostasis in Oligodendrocytes is Essential for Myelination and Involved in Depressive-Like Behavior in Adolescent Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Astrocyte's self-repairing characteristics improve working memory in spiking neuronal networks.iScience · 2023Article
- Exploring Astrocyte-Mediated Mechanisms in Sleep Disorders and Comorbidity.Biomedicines · 2023Review
- Genetic Ablation of Inositol 1,4,5-Trisphosphate Receptor Type 2 (IPInternational journal of molecular sciences · 2023Article
- Astrocytes: integrators of arousal state and sensory context.Trends in neurosciences · 2023Review
- Neuron-astrocyte omnidirectional signaling in neurological health and disease.Frontiers in molecular neuroscience · 2023Review
- Comparative assessment of the effects of DREADDs and endogenously expressed GPCRs in hippocampal astrocytes on synaptic activity and memory.Frontiers in cellular neuroscience · 2023Review
- Role of astrocytes in sleep deprivation: accomplices, resisters, or bystanders?Frontiers in cellular neuroscience · 2023Review
- Photonics tools begin to clarify astrocyte calcium transients.Neurophotonics · 2022Review
9 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-dependent release of gliotransmitters by astrocytes is reported to play a critical role in synaptic transmission and be necessary for long-term potentiation (LTP), long-term depression (LTD) and other forms of synaptic modulation that are correlates of learning and memory. Further, physiological processes reported to be dependent on Ca(2+) fluxes in astrocytes include functional hyperemia, sleep, and regulation of breathing. The preponderance of findings indicate that most, if not all, receptor dependent Ca(2+) fluxes within astrocytes are due to release of Ca(2+) through IP3 receptor/channels in the endoplasmic reticulum. Findings from several laboratories indicate that astrocytes only express IP3 receptor type 2 (IP3R2) and that a knockout of IP3R2 obliterates the GPCR-dependent astrocytic Ca(2+) responses. Assuming that astrocytic Ca(2+) fluxes play a critical role in synaptic physiology, it would be predicted that elimination of astrocytic Ca(2+) fluxes would lead to marked changes in behavioral tests. Here, we tested this hypothesis by conducting a broad series of behavioral tests that recruited multiple brain regions, on an IP3R2 conditional knockout mouse model. We present the novel finding that behavioral processes are unaffected by lack of astrocyte IP3R-mediated Ca(2+) signals. IP3R2 cKO animals display no change in anxiety or depressive behaviors, and no alteration to motor and sensory function. Morris water maze testing, a behavioral correlate of learning and memory, was unaffected by lack of astrocyte IP3R2-mediated Ca(2+)-signaling. Therefore, in contrast to the prevailing literature, we find that neither receptor-driven astrocyte Ca(2+) fluxes nor, by extension, gliotransmission is likely to be a major modulating force on the physiological processes underlying behavior.
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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.