Temporal patterns of motor behavioural improvements by MK-801 in Mongolian gerbils submitted to different duration of global cerebral ischemia

2008 ◽  
Vol 194 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Branka Janać ◽  
Vesna Selaković ◽  
Lidija Radenović
Keyword(s):  
Cerebral Ischemia ◽  
Temporal Patterns ◽  
Global Cerebral Ischemia ◽  
Mongolian Gerbils ◽  
Mk 801

scholarly journals Neuroprotectionby MK-801 following cerebral ischemia in Mongolian gerbils

2008 ◽  
Vol 60 (3) ◽  
pp. 341-346 ◽  
Author(s):  
Lidija Radenovic ◽  
Vesna Selakovic ◽  
P.R. Andjus
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Damage ◽  
Neuronal Loss ◽  
Brain Structures ◽  
Cell Loss ◽  
Global Cerebral Ischemia ◽  
Mongolian Gerbils ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Mk 801

Global cerebral ischemia in Mongolian gerbils is an established model in experimental research on cerebral ischemia, which is characterized morphologically by selective neuronal damage in the hippocampus, striatum, and cortex. Elevated glutamate levels are thought to be a primary cause of neuronal death after global cerebral ischemia. The purpose of this study was to investigate the potential neuroprotective effects of dizocilpine malate (MK-801), a non-competitive glutamate antagonist, in the model of 10-min gerbil cerebral ischemia. Gerbils were given MK-801(3 mg/kg i.p.)or saline immediately after the occlusion. On day 4 after reperfusion, neuronal damage was examined in the hippocampus (30 ?m)and striatum slices (5 ?m)stained with hematoxylin/eosin, fluorescent Nissl staining and membrane tracer DiI. The striatum and C3 regions of the hippocampus were analyzed by confocal microscopy. Neuroprotection was determined by quantifying the degree of cell loss, reduction of morphologically damaged cells, and the degree of preservation of recog?nizable neuroanatomical pathways after the ischemic insult. Our results demonstrate that the neuronal damage induced by sustained ischemia is related to abnormalities in glutamatergic function associated with NMDA receptors. MK-801significantly prevented neuronal loss in the tested brain structures. All of this contributes to a better understanding of the given pathophysiological process causing ischemic neuronal damage. <br><br><font color="red"><b> This article has been corrected. Link to the correction <u><a href="http://dx.doi.org/10.2298/ABS160524054E">10.2298/ABS160524054E</a><u></b></font>

scholarly journals Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils

2005 ◽  
Vol 144 (5) ◽  
pp. 727-735 ◽  
Author(s):  
Simona Pegorini ◽  
Daniela Braida ◽  
Chiara Verzoni ◽  
Chiara Guerini-Rocco ◽  
Gian Giacomo Consalez ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Mongolian Gerbils ◽  
Neuroprotective Effects ◽  
Transient Global Cerebral Ischemia

Validation of the effects of progesterone and MK-801 on acute phase changes induced by partial global cerebral ischemia in mice

2007 ◽  
Vol 172 ◽  
pp. S63
Author(s):  
Amitava Chakrabarti ◽  
Raman Aggarwal ◽  
Bikash Medhi ◽  
Ashis Pathak ◽  
Veena Dhawan
Keyword(s):  
Cerebral Ischemia ◽  
Acute Phase ◽  
Phase Changes ◽  
Global Cerebral Ischemia ◽  
Mk 801

Neuroprotective efficiency of tetanus toxin C fragment in model of global cerebral ischemia in Mongolian gerbils

2014 ◽  
Vol 101 ◽  
pp. 37-44 ◽  
Author(s):  
Lidija Radenovic ◽  
Vesna Selakovic ◽  
Sara Olivan ◽  
Ana Cristina Calvo ◽  
Amaya Rando ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Tetanus Toxin ◽  
Global Cerebral Ischemia ◽  
Mongolian Gerbils

scholarly journals MK-801 (Dizocilpine) Protects the Brain from Repeated Normothermic Global Ischemic Insults in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 925-932 ◽  
Author(s):  
Baowan Lin ◽  
W. Dalton Dietrich ◽  
Myron D. Ginsberg ◽  
Mordecai Y.-T. Globus ◽  
Raul Busto
Keyword(s):  
Cerebral Ischemia ◽  
Repeated Measures ◽  
Neuronal Damage ◽  
Brain Temperature ◽  
Global Cerebral Ischemia ◽  
Striatal Neurons ◽  
Ischemic Insult ◽  
Mk 801 ◽  
Bilateral Carotid ◽  
Ventrolateral Thalamus

We investigated the neuroprotective potential of MK-801 (dizocilpine), a noncompetitive N-methyl-d-aspartate (NMDA) antagonist, in the setting of three 5-min periods of global cerebral ischemia separated by 1-h intervals in halothane-anesthetized rats. Each ischemic insult was produced by bilateral carotid artery occlusions plus hypotension (50 mm Hg). Brain temperature was maintained at normothermic levels (36.5–37.0°C) throughout the experiment. MK-801 (3 mg/kg) (n = 6) or saline (n = 6) was injected intraperitoneally 45 min following the end of the first ischemic insult. Following 7-day survival, quantitative neuronal counts of perfusion-fixed brains revealed severe ischemic damage in hippocampal CA1 area, neocortex, ventrolateral thalamus, and striatum of untreated rats. By contrast, significant protection was observed in MK-801-treated rats. In area CA1 of the hippocampus, numbers of normal neurons were increased 11- to 14-fold by MK-801 treatment (p < 0.01). The ventrolateral thalamus of MK-801-treated rats showed almost complete histologic protection, and neocortical damage was reduced by 71% (p < 0.01). The degree of MK-801 protection of striatal neurons was less complete than that seen in other vulnerable structures, amounting to 63% for central striatum (p = 0.02, Mann–Whitney U test) and 48% in the dorsolateral striatum (NS). A repeated-measures analysis of variance demonstrated a highly significant overall protective effect of MK-801 treatment ( F1,10 = 37.2, p = 0.0001). These findings indicate that excitotoxic mechanisms play a major role in neuronal damage produced by repeated ischemic insults and that striking cerebroprotection is conferred by MK-801 administered following the first insult in animals with cerebral normothermia. NMDA antagonists may prove useful in patients at risk of repeated episodes of cerebral ischemia.

scholarly journals Corrigendum: Radenovic L, Selakovic V, Andjus P.R. Neuroprotection by MK-801 following cerebral ischemia in Mongolian gerbils. Arch Biol Sci. 2008;60(3):341-346. DOI: 10.2298/ABS0803341R

2016 ◽  
Vol 68 (3) ◽  
pp. 693-693
Author(s):  
E Editorial
Keyword(s):  
Biological Sciences ◽  
Cerebral Ischemia ◽  
Mongolian Gerbils ◽  
Mk 801 ◽  
Font Color

The corresponding author has informed the Editor-in-Chief that Fig. 2 in the article: Neuroprotection by MK-801 following cerebral ischemia in Mongolian gerbils, published in the Archives of Biological Sciences in 2008, Vol. 60, Issue 3, is incorrect due to submission of wrong figure. <br><br><font color="red"><b> Link to the corrected article <u><a href="http://dx.doi.org/10.2298/ABS0803341R">10.2298/ABS0803341R</a></b></u>

Alkalemia reduces recovery from global cerebral ischemia by NMDA receptor-mediated mechanism

1997 ◽  
Vol 272 (6) ◽  
pp. H2557-H2562
Author(s):  
P. D. Hurn ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Energy Metabolism ◽  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Nmda Receptor Antagonist ◽  
Global Cerebral Ischemia ◽  
Resonance Spectroscopy ◽  
Mk 801 ◽  
Sagittal Sinus

In vitro data suggest that low tissue pH reduces, whereas extracellular alkalosis potentiates, cerebral anoxic injury via excitotoxic mechanisms. We tested the hypothesis that in vivo metabolic alkalemia potentiates defects in energy metabolism after global incomplete cerebral ischemia (12 min) and reperfusion (180 min) by an N-methyl-D-aspartate (NMDA) receptor-mediated mechanism. Brain ATP, phosphocreatine, and intracellular pH (pHi) were measured by 31P magnetic resonance spectroscopy in anesthetized dogs treated with 1) preischemic intravenous carbicarb buffer (NaHCO3+Na2CO3, Carb, n = 7); 2) carbicarb infusion plus NMDA receptor antagonist MK-801 (MK-801 + Carb, n = 7); 3) an osmotically equivalent volume of 5% NaCl (NaCl, n = 8); or 4) equivalent volume of 0.9% NaCl (Sal, n = 3). Sagittal sinus pH was raised to 7.82 +/- 0.04 before and 7.65 +/- 0.03 during ischemia in Carb vs. 7.72 +/- 0.01 and 7.60 +/- 0.01 in MK-801+Carb, 7.25 +/- 0.02 and 7.15 +/- 0.03 in NaCl, and 7.31 +/- 0.00 and 7.26 +/- 0.01 in Sal, respectively. Ischemic cerebral blood flow (CBF, radiolabeled microspheres), pHi, and ATP reduction were similar among groups. By 180 min of reperfusion, recovery of ATP was greater in MK-801+Carb (104 +/- 6% of baseline), NaCl (93 +/- 6%), and Sal (94 +/- 6%) than in Carb (47 +/- 6%). Intraischemic pHi was similar among groups, and pHi recovery did not vary among groups despite differences in sagittal sinus pH. In Carb, CBF was restored but with delayed hypoperfusion. We conclude that extracellular alkalosis is deleterious to postischemic CBF and energy metabolism, acting by NMDA receptor-mediated mechanisms.

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