Glutamate release in severe brain ischaemia is mainly by reversed uptake

By D. Rossi, T. Oshima, David Attwell. Nature, 2000

1,170 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/cbeadaf540fb35a6da07efdb9f028bff37ac8328

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Hilmar Bading
2. G. Hardingham
3. Yun Zhou
4. N. Danbolt
5. Andrea Volterra
6. Jie Zheng
7. N. Hamilton
8. David Attwell

In Molecular Biology

1. Jie Zheng
2. Hilmar Bading
3. R. Swanson
4. Yun Zhou
5. Yongmei Chen
6. David Attwell
7. N. Danbolt
8. G. Hardingham

Citations in the corpus

• Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways (2002, background): “These pathological conditions are characterized by glutamate transporters operating in reverse (pumping glutamate out of the cells”
• Glutamate as a neurotransmitter in the healthy brain (2014, background): “2013) and another is via reversed operation of the glutamate transporting proteins at the plasma membrane (e.g. Levi and Raiteri 1993; Longuemare and Swanson 1995; Roettger and Lipton 1996; Jensen et al. 2000; Rossi et al. 2000; Jabaudon et al. 2000; Sontheimer 2008).”
• Astrocytes and Brain Injury (2003, background): “Glutamate efflux from neurons is also likely to occur during ATP depletion, and this may be a quantitatively greater than release from astrocytes in many brain regions (Rossi et al., 2000).”
• Handbook of ion channels (2015, background): “During brain injuries such as stroke, glutamate is released by reversed uptake (Rossi et al., 2000), because ion gradients driving glutamate transporters collapse.”
• Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders (2010, neutral): “During an ischaemic episode, extracellular glutamate accumulates owing to synaptic release and impairment or reversal of uptake mechanism”
• Excitotoxicity: bridge to various triggers in neurodegenerative disorders. (2013, background): “This intense exposure to NO/O(2) with resultant ONOO formation has been demonstrated to result in neuronal necrosis because of energy failure, while mild insults lead to apoptosis (Rossi et al., 2001).”
• Do astrocytes really exocytose neurotransmitters? (2010, background): “In pathological conditions such as ischaemia, in which the ion gradients that power glutamate uptake run down, these transporters can reverse and release glutamat”
• Synaptic energy use and supply. (2012, neutral): “However, if ischemia is prolonged, the rundown of ion gradients that results from inhibition of mitochondrial function leads to a reversal of glutamate transporters and a rise of extracellular glutamate concentration to 200 mM (Rossi et al., 2000).”
• Excitotoxicity and stroke: identifying novel targets for neuroprotection. (2014, neutral): “released is likely multi-factorial and depends on the severity of stroke and the ischemic model used (Dawson et al., 2000; Drejer et al., 1985; Rossi et al., 2000).”
• Astrocytes, from brain glue to communication elements: the revolution continues (2005, background): “Reversal of HIGH-AFFINITY GLUTAMATE TRANSPORTERS is unlikely to occur during normal brain functio”