Tolerance to a suprathreshold dose of L-Dopa in MPTP mice: effects of glutamate antagonists

1999 ◽  
Vol 106 (3-4) ◽  
pp. 283-300 ◽  
Author(s):  
A. Fredriksson ◽  
T. Palomo ◽  
T. Chase ◽  
T. Archer
Keyword(s):  
Glutamate Antagonists ◽  
Suprathreshold Dose

Neuroprotective effects of glutamate antagonists and extracellular acidity

Science ◽  
1993 ◽  
Vol 260 (5113) ◽  
pp. 1516-1518 ◽  
Author(s):  
D. Kaku ◽  
R. Giffard ◽  
D. Choi
Keyword(s):  
Neuroprotective Effects ◽  
Glutamate Antagonists

Differential Contribution of Reticulospinal Cells to the Control of Locomotion Induced By the Mesencephalic Locomotor Region

2003 ◽  
Vol 90 (3) ◽  
pp. 1714-1727 ◽  
Author(s):  
Frédéric Brocard ◽  
Réjean Dubuc
Keyword(s):  
Discharge Rate ◽  
Recruitment Pattern ◽  
Glutamate Antagonists ◽  
Locomotor Rhythm ◽  
Mesencephalic Locomotor Region ◽  
Relative Contribution ◽  
Excitatory Responses ◽  
Reticular Nuclei ◽  
Differential Contribution ◽  
Maximal Discharge

In lampreys as in other vertebrates, the reticulospinal (RS) system relays inputs from the mesencephalic locomotor region (MLR) to the spinal locomotor networks. Semi-intact preparations of larval sea lamprey were used to determine the relative contribution of the middle (MRRN) and the posterior (PRRN) rhombencephalic reticular nuclei to swimming controlled by the MLR. Intracellular recordings were performed to examine the inputs from the MLR to RS neurons. Stimulation of the MLR elicited monosynaptic excitatory responses of a higher magnitude in the MRRN than in the PRRN. This differential effect was not attributed to intrinsic properties of RS neurons. Paired recordings showed that at threshold intensity for swimming, spiking activity was primarily elicited in RS cells of the MRRN. Interestingly, cells of the PRRN began to discharge at higher stimulation intensities only when MRRN cells had reached their maximal discharge rate. Glutamate antagonists were ejected in either nucleus to reduce their activity. Ejections over the MRRN increased the stimulation threshold for evoking locomotion and resulted in a marked decrease in the swimming frequency and the strength of the muscle contractions. Ejections over the PRRN decreased the frequency of swimming. This study provides support for the concept that RS cells show a specific recruitment pattern during MLR-induced locomotion. RS cells in the MRRN are primarily involved in initiation and maintenance of low-intensity swimming. At higher frequency locomotor rhythm, RS cells in both the MRRN and the PRRN are recruited.

INVERTEBRATE PHARMACOLOGICAL ASSAY OF NOVEL, POTENT GLUTAMATE ANTAGONISTS: ACYLATED SPERMINES

1990 ◽  
Vol 42 (S1) ◽  
pp. 168P-168P
Author(s):  
Ian S. Blagbrough ◽  
Mary Bruce ◽  
Barrie W. Bycroft ◽  
Alan J. Mather ◽  
Peter N.R. Usherwood
Keyword(s):  
Glutamate Antagonists

scholarly journals Mitochondrial superoxide production and MnSOD activity following exposure to an agonist and antagonists of ionotropic receptors in rat brain

2005 ◽  
Vol 57 (1) ◽  
pp. 1-10
Author(s):  
Lidija Radenovic ◽  
Vesna Selakovic
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Rat Brain ◽  
Nmda Receptor Antagonist ◽  
Superoxide Production ◽  
Kainate Receptors ◽  
Glutamate Antagonists ◽  
Time Dynamics ◽  
Mitochondrial Superoxide ◽  
Intrahippocampal Injection

The involvement of NMDA and AMPA/kainate receptors in the induction of superoxide production in the rat brain was examined after intrahippocampal injection of kainate, a non-NMDA receptor agonist; kainate plus CNQX, a selective AMPA/kainate receptor antagonist; or kainate plus APV, a selective NMDA receptor antagonist. The measurements took place at different times in the ipsi- and contralateral hippocampus, forebrain cortex, striatum, and cerebellum homogenates. The used glutamate antagonists both ensured sufficient neuroprotection in the sense of lowering superoxide production and raising MnSOD levels, but in the mechanisms and time dynamics of their effects were different. Our findings suggest that NMDA and AMPA/kainate receptors are differentially involved in superoxide production. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href="http://dx.doi.org/10.2298/ABS150318026E">10.2298/ABS150318026E</a><u></b></font>

Acidotoxicity in brain ischaemia

2006 ◽  
Vol 34 (6) ◽  
pp. 1356-1361 ◽  
Author(s):  
R. Simon ◽  
Z. Xiong
Keyword(s):  
Time Window ◽  
Calcium Entry ◽  
Calcium Flux ◽  
Central Feature ◽  
Brain Ischaemia ◽  
Ischaemic Injury ◽  
Glutamate Antagonists ◽  
Acid Sensing Ion Channels ◽  
Pharmacological Blockade ◽  
Therapeutic Time Window

Intracellular calcium toxicity remains the central feature in the pathophysiology of ischaemic cell death in brain. Glutamate-gated channels have been thought to be the major sites of ischaemia-induced toxic calcium entry, but the failure of glutamate antagonists in clinical trials has suggested that glutamate-independent mechanisms of calcium entry during ischaemia must exist and may prove central to ischaemic injury. We have shown that ASICs (acid-sensing ion channels) in brain are glutamate-independent vehicles of calcium flux and transport calcium in greater measure in the setting of the two major neurochemical components of ischaemia: acidosis and substrate depletion. Pharmacological blockade of ASICs markedly attenuates stroke injury with a robust therapeutic time window of 5 h following stroke onset. Here, we describe this new mechanism of calcium toxicity in brain ischaemia and offer a potential new therapy for stroke.

Stroke Management

1993 ◽  
Vol 6 (6) ◽  
pp. 297-303
Author(s):  
Susan C. Fagan
Keyword(s):  
Cerebral Ischemia ◽  
Antiplatelet Agent ◽  
The United States ◽  
Minor Stroke ◽  
Future Research ◽  
Stroke Management ◽  
Pharmacological Agents ◽  
Glutamate Antagonists ◽  
First Line Therapy ◽  
Patients At Risk

With as many as 500,000 new strokes per year in the United States, the need for safe and effective therapy of these patients is evident. The area in which the greatest impact has been made is in the development of prophylactic treatments for patients at risk of stroke. Aspirin, long the mainstay of stroke management, has repeatedly been shown to reduce the risk of cerebral ischemia in patients who have had a transient ischemic attack (TIA) or minor stroke and is first-line therapy for these patients. Either 325 mg or 975 mg of aspirin may be used. Ticlopidine (250 mg twice daily) is a new antiplatelet agent that is recommended for the prophylaxis of stroke in patients who cannot tolerate or who are resistant to aspirin therapy. The surgical procedure, carotid endarterectomy, has been shown to reduce the stroke rate in symptomatic patients, with between 70% to 99% stenosis of a carotid artery. The use of warfarin has been shown to be extremely useful in patients with atrial fibrillation for prevention of recurrent embolic events. The use of pharmacological agents in the acute treatment of the ischemic stroke patient has not yet been proven successful. It is hoped that with the trend towards hyperacute (less than 6 hours) intervention, investigators may be successful in finding an agent to decrease the ultimate neurological deficit due to stroke. Some of the more promising agents are thrombolytics, glutamate antagonists, and aminosteroids. Future research in cerebral ischemia will undoubtedly improve the prognosis of stroke patients.

Glutamate Antagonists for Parkinson??s Disease

CNS Drugs ◽  
1998 ◽  
Vol 9 (6) ◽  
pp. 421-429 ◽  
Author(s):  
Alison J. Cooper ◽  
Camille B. Carroll ◽  
Ian J. Mitchell
Keyword(s):  
Glutamate Antagonists
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