Oral ethanol self-administration in rats is reduced by the administration of dopamine and glutamate receptor antagonists into the nucleus accumbens

1992 ◽  
Vol 109 (1-2) ◽  
pp. 92-98 ◽  
Author(s):  
Stefanie Rassnick ◽  
Luigi Pulvirenti ◽  
George F. Koob
Keyword(s):  
Nucleus Accumbens ◽  
Glutamate Receptor ◽  
Self Administration ◽  
Receptor Antagonists ◽  
Glutamate Receptor Antagonists

The Analgesic Interaction Between Intrathecal Clonidine and Glutamate Receptor Antagonists on Thermal and Formalin-Induced Pain in Rats

2001 ◽  
pp. 725-732 ◽  
Author(s):  
Tomoki Nishiyama ◽  
Laszlo Gyermek ◽  
Chingmuh Lee ◽  
Sachiko Kawasaki-Yatsugi ◽  
Tokio Yamaguchi ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Receptor Antagonists ◽  
Glutamate Receptor Antagonists ◽  
Intrathecal Clonidine

Imaging Anoxic Depolarization During Ischemia-Like Conditions in the Mouse Hemi-Brain Slice

2001 ◽  
Vol 85 (1) ◽  
pp. 414-424 ◽  
Author(s):  
I. Joshi ◽  
R. D. Andrew
Keyword(s):  
Glutamate Receptor ◽  
Brain Slice ◽  
Neuronal Damage ◽  
Glucose Deprivation ◽  
Light Transmittance ◽  
Cell Swelling ◽  
Receptor Antagonists ◽  
Anoxic Depolarization ◽  
Glutamate Receptor Antagonists ◽  
Ischemic Core

Focal ischemia evokes a sudden loss of membrane potential in neurons and glia of the ischemic core termed the anoxic depolarization (AD). In metabolically compromised regions with partial blood flow, peri-infarct depolarizations (PIDs) further drain energy reserves, promoting acute and delayed neuronal damage. Visualizing and quantifying the AD and PIDs and their acute deleterious effects are difficult in the intact animal. In the present study, we imaged intrinsic optical signals to measure changes in light transmittance in the mouse coronal hemi-brain slice during AD generation. The AD was induced by oxygen/glucose deprivation (OGD) or by ouabain exposure. Potential neuroprotective strategies using glutamate receptor antagonists or reduced temperature were tested. Eight minutes of OGD ( n = 18 slices) or 4 min of 100 μM ouabain ( n = 14) induced a focal increase of increased light transmittance (LT) in neocortical layers II/III that expanded concentrically to form a wave front coursing through neocortex and independently through striatum. The front was coincident with a negative voltage shift in extracellular potential. Wherever the LT front (denoting cell swelling) propagated, a decrease in LT (denoting dendritic beading) followed in its wake. In addition the evoked field potential was permanently lost, indicating neuronal damage. Glutamate receptor antagonists did not block the onset and propagation of AD or the extent of irreversible damage post-AD. Lowering temperature to 25–30°C protected the tissue from OGD damage by inhibiting AD onset. This study shows that anoxic depolarization evoked by global ischemia-like conditions is a spreading process that is focally initiated at multiple sites in cortical and subcortical gray. The combined energy demands of O2/glucose deprivation and the AD greatly exacerbate neuronal damage. Glutamate receptor antagonists neither block the AD in the ischemic core nor, we propose, block recurrent PID arising close to the core.

Glutamate receptor antagonists inhibit calpain-mediated cytoskeletal proteolysis in focal cerebral ischemia

1998 ◽  
Vol 810 (1-2) ◽  
pp. 181-199 ◽  
Author(s):  
Stephen L Minger ◽  
James W Geddes ◽  
Mary L Holtz ◽  
Susan D Craddock ◽  
Sidney W Whiteheart ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Glutamate Receptor ◽  
Focal Cerebral Ischemia ◽  
Receptor Antagonists ◽  
Glutamate Receptor Antagonists
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