http://www.cnr.it/ontology/cnr/individuo/prodotto/ID38182
Acute retinal ganglion cell injury caused by intraocular pressure spikes is mediated by endogenous extracellular ATP. (Articolo in rivista)
- Type
- Label
- Acute retinal ganglion cell injury caused by intraocular pressure spikes is mediated by endogenous extracellular ATP. (Articolo in rivista) (literal)
- Anno
- 2007-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1242/dev.01855 (literal)
- Alternative label
Resta V, Novelli E, Vozzi G, Scarpa C, Caleo M, Ahluwalia A, Solini A, Santini E, Parisi V, Di Virgilio F, Galli-Resta L. (2007)
Acute retinal ganglion cell injury caused by intraocular pressure spikes is mediated by endogenous extracellular ATP.
in European journal of neuroscience (Print)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Resta V, Novelli E, Vozzi G, Scarpa C, Caleo M, Ahluwalia A, Solini A, Santini E, Parisi V, Di Virgilio F, Galli-Resta L. (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Istituto di Neuroscienze CNR PISA (literal)
- Titolo
- Acute retinal ganglion cell injury caused by intraocular pressure spikes is mediated by endogenous extracellular ATP. (literal)
- Abstract
- Elevated intraocular pressure may lead to retinal ganglion cell injury and consequent visual deficits. Chronic intraocular pressure
increase is a major risk factor for glaucoma, a leading blinding disease, and permanent visual deficits can also occur following acute
pressure increments due to trauma, acute glaucoma or refractive surgery. How pressure affects retinal neurons is not firmly
established. Mechanical damage at the optic nerve head, reduced blood supply, inflammation and cytotoxic factors have all been
called into play. Reasoning that the analysis of retinal neurons soon after pressure elevation would provide useful cues, we imaged
individual ganglion cells in isolated rat retinas before and after short hydrostatic pressure increments. We found that slowly rising
pressure to peaks observed in trauma, acute glaucoma or refractive surgery (50-90 mmHg) did not damage ganglion cells, whereas
a rapid 1 min pulse to 50 mmHg injured 30% of these cells within 1 h. The severity of damage and the number of affected cells
increased with stronger or repeated insults. Degrading extracellular ATP or blocking the P2X receptors for ATP prevented acute
pressure-induced damage in ganglion cells. Similar effects were observed in vivo. A short intraocular pressure transient increased
extracellular ATP levels in the eye fluids and damaged ganglion cells within 1 h. Reducing extracellular ATP in the eye prevented
damage to ganglion cells and accelerated recovery of their response to light. These data show that rapid pressure transients induce
acute ganglion cell injury and unveil the causal role of extracellular ATP elevation in such injury. (literal)
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