Mechanism of glutamate release from rat hippocampal slices during in vitro ischemia
References (38)
- et al.
l-trans-pyrrolidine-2,4-dicar☐ylate and cis-I-aminocyclobutane-1,3-dicar☐ylate behave as transportable, competitive inhibitors of the high-affinity glutamate transporters
Biochem. Pharmac.
(1994) - et al.
Extracellular accumulation of glutamate in the hippocampus induced by ischemia is not calcium dependent - in vitro and in vivo evidence
Neurosci. Lett.
(1989) - et al.
Sigma-ligands and non-competitive NMDA antagonists inhibit glutamate release during cerebral ischemia
Neurosci. Lett.
(1990) - et al.
Reduction of glutamate release and protection against ischemic brain damage by BW 1003C87
Brain Res.
(1992) - et al.
Origin of intracellular Ca++ elevation induced by in vitro ischemia-like condition in hippocampal slices
Brain Res.
(1993) - et al.
The release and uptake of excitatory amino acids
Trends pharmac. Sci.
(1990) - et al.
Characterization of glutamate, aspartate, and GABA release from ischemic rat cerebral cortex
Brain Res. Bull.
(1994) - et al.
HPLC-EC determination of free primary amino acid concentrations in cat cisternal cerebrospinal fluid
J. Neurosci. Meth.
(1991) - et al.
Extracellular potassium ion activity and electrophysiology in the hippocampal slice: paradoxical recovery of synaptic transmission during anoxia
Brain Res.
(1987) - et al.
Damage from oxygen + glucose deprivation in hippocampal slices is prevented by tetrodotoxin, lidocaine and phenytoin without blockade of action potentials
Brain Res.
(1994)
Differential modulation of human glutamate transporter subtypes by arachidonic acid
J. biol. Chem.
Functional comparisons of three glutamate transporter subtypes cloned from human motor cortex
J. Neurosci.
The structural specificity of the high affinity uptake of l-glutamate and l.-aspartate by rat brain slices
J. Neurochem.
Electrogenic glutamate uptake in glial cells is activated by intracellular potassium
Nature
Arachidonic acid induces a prolonged inhibition of glutamate uptake into glial cells
Nature
Ischemic damage in hippocampal CAI is dependent on glutmate release and intact innervation from CA3
J. cerebr Blood Flow Metab.
Hippocampal glutamate release during `in vitro ischemia' is calcium-independent and TTX-sensitive
Soc. Neurosci. Abstr.
The role of glutamate neurotoxicity in hypoxic/ischemic neuronal death
A. Rev. Neurosci.
An excitatory amino-acid transporter with properties of a ligand-gated chloride channel
Nature
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The role of inversely operating glutamate transporter in the paradoxical analgesia produced by glutamate transporter inhibitors
2016, European Journal of PharmacologyCitation Excerpt :We investigated whether the formalin-induced increase in extracellular glutamate was due to the glutamate transporter. For this purpose, a separate group of rats were pretreated with tPDC prior to induction of inflammatory pain, because once tPDC enters the cell, it is in a position to block carrier-mediated efflux of glutamate (Roettger and Lipton, 1996). Preloaded transportable inhibitor tPDC effectively blocked the formalin-induced glutamate increase in the dialysate when it was administered 30 min before formalin injection (Fig. 3).
BRAIN METABOLISM, THE PATHOPHYSIOLOGY OF BRAIN INJURY, AND POTENTIAL BENEFICIAL AGENTS AND TECHNIQUES
2010, Cottrell and Young's Neuroanesthesia: Fifth EditionElectrophysiology of cerebral ischemia
2008, NeuropharmacologyCitation Excerpt :According to Somjen (2001), this effect of high K+ is potentiated by the ongoing hypoxia. In addition, the depolarizing trend is probably quite early reinforced by glutamate release, both synaptic (Katayama et al., 1991; Katchman and Hershkowitz, 1993) and extrasynaptic (Sanchez-Prieto and Gonzalez, 1988; Katayama et al., 1991; Roettger and Lipton, 1996; Tanaka et al., 1997; Jabaudon et al., 2000). The gradually increasing inward current suddenly steps up to a much higher level, resulting in a large negative wave in external recordings (phase 2) and the near total depolarization and loss of membrane resistance seen intracelullarly (Bureš et al., 1974; Hansen, 1985; Tanaka et al., 1997; Hsu et al., 1994; Somjen, 2001; Tanaka et al., 2002).
Neuron is the primary target of Ca<sup>2+</sup> paradox-type insult-induced cell injury in neuron/astrocyte co-cultures
2008, Neurochemistry International
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