scholarly journals Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.

Stroke ◽  
1992 ◽  
Vol 23 (8) ◽  
pp. 1125-1130 ◽  
Author(s):  
Y Ueda ◽  
T P Obrenovitch ◽  
S Y Lok ◽  
G S Sarna ◽  
L Symon
Keyword(s):  
Rat Striatum ◽  
Extracellular Glutamate ◽  
Glutamate Concentration ◽  
Repeated Ischemia

Changes in rat brain extracellular glutamate concentration during seizures induced by systemic picrotoxin or focal bicuculline injection: an in vivo dialysis study with on-line enzymatic detection

1991 ◽  
Vol 9 (2) ◽  
pp. 86-91 ◽  
Author(s):  
Maria H. Millan ◽  
Tihomir P. Obrenovitch ◽  
Gurcharan S. Sarna ◽  
She Yen Lok ◽  
Lindsay Symon ◽  
...  
Keyword(s):  
Rat Brain ◽  
Extracellular Glutamate ◽  
Glutamate Concentration ◽  
On Line ◽  
Enzymatic Detection

Receptor binding properties of di (1,N6-ethenoadenosine) 5′, 5′′′-P1, P4-tetraphosphate and its modulatory effect on extracellular glutamate levels in rat striatum

2001 ◽  
Vol 309 (3) ◽  
pp. 177-180 ◽  
Author(s):  
Sol Oaknin ◽  
Carmen Rosa Rodrı́guez-Ferrer ◽  
José Santiago Aguilar ◽  
Antonio Ramos ◽  
Pedro Rotllán
Keyword(s):  
Receptor Binding ◽  
Rat Striatum ◽  
Extracellular Glutamate ◽  
Binding Properties

A use-dependent sodium channel antagonist, 619C89, in reduction of ischemic brain damage and glutamate release after acute subdural hematoma in the rat

1996 ◽  
Vol 85 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Eiji Tsuchida ◽  
John F. Harms ◽  
John J. Woodward ◽  
Ross Bullock
Keyword(s):  
Sodium Channel ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Glutamate Release ◽  
Acute Subdural Hematoma ◽  
Extracellular Glutamate ◽  
Ischemic Brain ◽  
Content Type ◽  
Glutamate Concentration ◽  
Fine Print

✓ Acute subdural hematoma kills or disables more severely head injured patients than any other complication of cranial trauma. The main pathological factor involved is ischemic neuronal damage, which is caused by raised intracranial pressure and local effect. The authors have evaluated the hypothesis that a novel use-dependent sodium channel antagonist, 619C89, could reduce ischemic brain damage in the rat subdural hematoma model. Because previous studies have shown that focal neuronal damage may be mediated by “excitotoxic” mechanisms, and because excitatory amino acid levels have been shown to be markedly elevated after brain trauma in humans, the authors have measured levels of glutamate, aspartate, and threonine within the cortex underneath the hematoma, using in vivo microdialysis before and after induction of hematoma, in both vehicle- and drug-treated rats. Postinjury treatment with 619C89 (30 mg/kg) significantly reduced the volume of hemispheric ischemic damage produced by subdural hematoma, from 99.77 ± 7.51 mm3 in vehicle-treated control rats to 46.07 ± 11.06 mm3 (p = 0.0007) in drug-treated animals. In the vehicle-treated animals, induction of subdural hematoma led to a fourfold increase in glutamate in the first 30 minutes after subdural hematoma occurred. The mean extracellular glutamate concentration in these animals remained 2- to 2.6-fold increased over the following 2.5 hours. In the 619C89-treated animals, the release of glutamate from the cortex underneath the hematoma was significantly attenuated. In these rats, induction of subdural hematoma led to a 2.7-fold increase in the first 30-minute sample, but extracellular glutamate concentration returned to near-basal levels thereafter, compared with vehicle-treated animals (p < 0.05). These results show that 619C89 is highly neuroprotective in this model and that its effects may, in part, be mediated by the inhibiton of glutamate release from the ischemic cortex underneath the hematoma.

Extracellular glutamate and dopamine measured by microdialysis in the rat striatum during blockade of synaptic transmission in anesthetized and awake rats

1997 ◽  
Vol 759 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Masaharu Shiraishi ◽  
Yoishiro Kamiyama ◽  
Peter Christian Hüttemeier ◽  
Helene Benveniste
Keyword(s):  
Synaptic Transmission ◽  
Rat Striatum ◽  
Extracellular Glutamate ◽  
Awake Rats

scholarly journals Extracellular Glutamate Concentration in Hippocampal Slice

2007 ◽  
Vol 27 (36) ◽  
pp. 9736-9741 ◽  
Author(s):  
M. A. Herman ◽  
C. E. Jahr
Keyword(s):  
Hippocampal Slice ◽  
Extracellular Glutamate ◽  
Glutamate Concentration

Long-Term Potentiation in the Dentate Gyrus Is Not Linked to Increased Extracellular Glutamate Concentration

1999 ◽  
Vol 81 (4) ◽  
pp. 1741-1748 ◽  
Author(s):  
T. M. Jay ◽  
E. Zilkha ◽  
T. P. Obrenovitch
Keyword(s):  
Dentate Gyrus ◽  
Synaptic Cleft ◽  
Long Term Potentiation ◽  
Perforant Path ◽  
Mammalian Brain ◽  
Excitatory Postsynaptic Potential ◽  
Extracellular Glutamate ◽  
Glutamate Concentration ◽  
Term Potentiation

Long-term potentiation in the dentate gyrus is not linked to increased extracellular glutamate concentration. Long-term potentiation (LTP) of excitatory transmission is a likely candidate for the encoding and storage of information in the mammalian brain. There is a general agreement that LTP involves an increase in synaptic strength, but the mechanisms underlying this persistent change are unclear and controversial. Synaptic efficacy may be enhanced because more transmitter glutamate is released or because postsynaptic responsiveness increases or both. The purpose of this study was to examine whether increased extracellular glutamate concentration was associated with the robust and well-characterized LTP that can be induced in the rat dentate gyrus. To favor the detection of any putative change in extracellular glutamate associated with LTP, our experimental strategy included the following features. 1) Two separate series of experiments were carried out with animals under pentobarbital or urethan anesthesia; 2) changes in extracellular concentration of glutamate were monitored continuously by microdialysis coupled to enzyme amperometry; and 3) dialysate glutamate levels and changes in the slope of excitatory postsynaptic potential evoked by activation of the perforant path were recorded precisely at the same site. Tetanic stimulation of the perforant path increased persistently test-evoked responses in the dentate gyrus (by 19 and 14% in barbiturate and urethan group, respectively), but there was no glutamate change either during or after LTP induction and no indication of increased glutamate efflux when low-frequency stimulation was applied. The results do not rule out a possible contribution of enhanced glutamate exocytosis to LTP induction and/or maintenance because such a presynaptic change may not be detectable extracellularly. However, our findings and other data supporting the notion that neurotransmitter glutamate may hardly leak out of the synaptic cleft conflict with the hypothesis that LTP could also involve a broad synaptic spillover of glutamate.

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