Astrocyte control of synaptic transmission and neurovascular coupling.
By Philip Haydon, Giorgio Carmignoto. Physiological Reviews, 2006
1,351 citations recorded by the source corpus.
Subfields: Biochemistry, Cellular and Molecular Neuroscience, Physiology
View Paper: https://www.semanticscholar.org/paper/cede4ce09ab1663a87f072b79923ab28d3f68ffd
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Citations in the corpus
- The role of glutamate transporters in neurodegenerative diseases and potential opportunities for intervention. (2007, background): “In addition, there is now pretty clear evidence that excitatory cell-to-cell signaling is not restricted to that observed between neurons; astrocytes release glutamate and express glutamate receptors (for reviews, see Carmignoto, 2000, Haydon and Carmignoto, 2006).”
- Astroglial networks: a step further in neuroglial and gliovascular interactions (2010, background): “Astrocytic networks regulate neuronal function Astrocytes are now considered to be active elements of the brain circuitry: they integrate neuronal signals, exhibit Ca 2+ excitability and process informatio”
- Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “Of particular concern, excessive release of glutamate by astrocytes can access extrasynaptic NMDA receptors, which mediate excitotoxicity and decreased production of trophic factors including brain derived neurotrophic factor (BDNF) (Hardingham et al., 2002; Haydon and Carmignoto, 2006).”
- Regional blood flow in the normal and ischemic brain is controlled by arteriolar smooth muscle cell contractility and not by capillary pericytes (2015, positive): “…the mechanisms controlling neurovascular coupling are not well understood, previous work demonstrates the involvement of complex interactions between neurons, glia, and vascular cells (Haydon and Carmignoto, 2006; Iadecola and Nedergaard, 2007; Kety and Schmidt, 1948; Roy and Sherrington , 1890).”
- Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders (2008, background): “This, in turn, leads to selective stimulation of extrasynaptic NMDA receptor”
- Conditional Knock-Out of Kir4.1 Leads to Glial Membrane Depolarization, Inhibition of Potassium and Glutamate Uptake, and Enhanced Short-Term Synaptic Potentiation (2007, background): “…synaptic levels of neurotransmitters, in particular glutamate, buffering of extracellular K , and release of neuroactive substances or gliotransmitters, all of which have been shown to directly modulate neuronal excitability and transmission (Fiacco and McCarthy, 2006; Haydon and Carmignoto, 2006).”
- Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024, background): “161 The blood-brain barrier (BBB) consists of endothelial cells tight junctions, a continuous basement membrane and astrocytic end-feet.”
- How widespread is adult neurogenesis in mammals? (2007, background): “Although receiving synaptic input, vesicular release of transmitters and voltage-gated ion channels are features of both neurons and gli”
- Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, neutral): “N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript Table 1 Potential Translational Targets for Inflammation-Induced Depression Immune System Cytokines (e.g., TNF-alpha, IL-1, IL-6) Cy”