The Origin and Neuronal Function of In Vivo Nonsynaptic Glutamate

By D. Baker, Z. Xi, Hui Shen, C. Swanson, Peter W. Kalivas. Journal of Neuroscience, 2002

624 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/4542c3e7325589d702cf1db0549b95f39dc3e8c6

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Citations in the corpus

Uncovering the mechanism(s) of action of deep brain stimulation: activation, inhibition, or both. (2004, background): “However, it should be noted that the primary source of extracellular glutamate is non-vesicular glutamate release from cystineglutamate antiporter (Baker et al., 2002), so the actual contribution of synaptic release glutamate on the effects of Fig.”
The Cystine/Glutamate Antiporter System xc − in Health and Disease: From Molecular Mechanisms to Novel Therapeutic Opportunities (2013, positive): “Moreover, several groups demonstrated in microdialysis experiments in vivo that system xc - inhibitors reduced extrasynaptic glutamate concentrations in the striatum and hippocampus (9, 48).”
Neuroadaptations in cystine-glutamate exchange underlie cocaine relapse (2003, background): “In vivo basal levels of extrasynaptic glutamate are maintained primarily by Na + -independent anionic amino acid transporters that exchange extracellular cystine for intracellular glutamate, and the contribution by synaptically released glutamate is minima”
The glutamate homeostasis hypothesis of addiction (2009, background): “In the NAc core, ∼60% of the basal extracellular glutamate is derived from constitutive cystine–glutamate exchang”
Chronic Glutamate Toxicity in Neurodegenerative Diseases—What is the Evidence? (2015, result): “This is further supported by the observation that when measured by in vivomicrodialysis, the rise in extrasynaptic L-glu induced by EAAT inhibitors is neutralized by blocking system x−c while blocking neuronal vesicular L-glu release is ineffective (Baker et al., 2002; Melendez et al., 2005).”
Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders (2008, background): “Recent studies have also shown the importance of the cystine–glutamate antiporter in controlling extracellular glutamate conten”
Regulation of NMDA Receptor Subunit Expression and Its Implications for LTD, LTP, and Metaplasticity (2008, background): “Although microdialysis studies report that ambient glutamate concentrations in vivo are high enough to activate extrasynaptic NMDARs (Baker et al., 2002; Lerma et al., 1986; Nyitrai et al., 2006), a recent study suggests that glutamate transporters regulate ambient glutamate concentrations at a…”
Prefrontal Glutamate Release into the Core of the Nucleus Accumbens Mediates Cocaine-Induced Reinstatement of Drug-Seeking Behavior (2003, methodology): “For example, basal levels of extracellular glutamate have been shown in vivo to provide tone on group II mGluR autoreceptors (Baker et al., 2002; Xi et al., 2002), and the cocaine-induced reduction in basal glutamate combined with desensitization of group II mGluRs would be expected to promote incre”
The neural basis of addiction: a pathology of motivation and choice. (2005, background): “The cystine-glutamate exchanger is the rate-limiting step in glutathione synthesis (101) and is responsible for the majority of extracellular glutamate outside the synaptic cleft (102).”
Glutamate as a neurotransmitter in the healthy brain (2014, background): “A third reason for the interest in xCT is that xCT has been sug- gested to be a major source of extracellular glutamate (Baker et al. 2002).”
Astrocytes, from brain glue to communication elements: the revolution continues (2005, background): “Nevertheless, glutamate could be released by the CYSTINE/GLUTAMATE EXCHANGER”