scholarly journals NMDA Receptor Blockade and Spinal Cord Ischemia Due to Aortic Crossclamping in the Rat Model

1994 ◽  
Vol 21 (3) ◽  
pp. 227-232 ◽  
Author(s):  
F. Follis ◽  
K. Miller ◽  
O. U. Scremin ◽  
S. Pett ◽  
R. Kessler ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Brain Research ◽  
Spinal Cord Ischemia ◽  
Intrathecal Injection ◽  
Control Group ◽  
Receptor Subtype ◽  
Receptor Blockade ◽  
Mk 801 ◽  
Nmda Receptor Blockade

Abstract:Recent brain research proposes that, during ischemia, synaptically released excitatory amino acid neurotransmitters accumulate at toxic concentrations with ensuing neuronal death. Their action is mediated by the receptor subtype N-methyl-D-aspartate (NMDA). The protective effect of NMDA receptor blockade with intrathecal MgS04 and MK-801 was investigated during spinal cord ischemia induced by aortic occlusion of 12 minutes. Male Sprague-Dawley rats, 250-300g, underwent intrathecal administration of 20 μL of normal saline (SA n = 16), MgS04 1M (MG n = 16), or MK-801, 25 mM solutions (MK n = 16) in a randomized order. After 2 hours, the animals underwent occlusion of the thoracic aorta and subclavian arteries for 12 min. An additional control group (CO n = 16) underwent occlusion for 12 minutes, without intrathecal injection. The animals were scored according to their functional performance (LS = lesion score) each day for four days by a blinded observer. Mean LS were calculated for each group at a given day. Treatment and control groups were not different at day 1 (P = 0.302). Group MG was improved from groups SA (P = < 0.0039) and CO (P = < 0.0048) at day 4. This study demonstrates that although intrathecal NMDA receptor blockade with MgS04 or MK-801 does not prevent paraplegia due to spinal cord ischemia in the rat, it could however influence the rate of recovery after ischemic injury.

Intrathecal blockade of both NMDA and non-NMDA receptors attenuates the exercise pressor reflex in cats

1996 ◽  
Vol 80 (1) ◽  
pp. 315-322 ◽  
Author(s):  
C. M. Adreani ◽  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Nmda Receptors ◽  
Initial Phase ◽  
Intrathecal Injection ◽  
Secondary Phase ◽  
Receptor Blockade ◽  
Lumbosacral Spinal Cord ◽  
Ventilatory Responses ◽  
Nmda Receptor Blockade

In decerebrate unanesthetized cats we tested the hypothesis that glutamatergic-receptor blockade in the lumbosacral spinal cord attenuated the reflex increases in mean arterial pressure, inspired minute ventilation, and renal sympathetic nerve activity (RSNA) evoked by static contraction of the triceps surae muscles. Blockade of N-methyl-D-aspartate (NMDA) receptors by intrathecal injection of DL-2-amino-5-phosphonovaleric acid had no effect on the initial phase of the pressor, ventilatory, and RSNA responses to contraction but did attenuate the secondary phase of these responses. Subsequent blockade of non-NMDA receptors in the lumbosacral spinal cord by intrathecal injection of 6-cyano-7-nitroquinoxaline-2,3-dione attenuated both the initial phase of the pressor, RSNA, and ventilatory responses to contraction and the secondary phase of these responses. In addition, NMDA-receptor blockade had no effect on the pressor or RSNA responses to tendon stretch, whereas non-NMDA-receptor blockade abolished these responses. We confirmed that our results were not related to the order of the antagonists injected by performing a series of experiments in which a non-NMDA-receptor antagonist was injected first. Our findings suggest that non-NMDA receptors mediate the spinal transmission of the initial and secondary phases of the pressor, RSNA, and ventilatory responses to contraction and tendon stretch. Therefore, non-NMDA receptors in the dorsal horn appear to be involved in the spinal processing of input from mechanoreceptors and metaboreceptors. Our findings also suggest that NMDA receptors mediate the spinal transmission of the secondary phase of the pressor, RSNA, and ventilatory responses to contraction but do not mediate the spinal transmission of the responses to tendon stretch. Therefore, NMDA receptors in the dorsal horn appear to be involved in the spinal processing of input from metaboreceptors.

NMDA receptor blockade attenuates CCK-induced reduction of real feeding but not sham feeding

2004 ◽  
Vol 286 (5) ◽  
pp. R826-R831 ◽  
Author(s):  
Mihai Covasa ◽  
Robert C. Ritter ◽  
Gilbert A. Burns
Keyword(s):  
Gastric Emptying ◽  
Ion Channels ◽  
Nmda Receptor ◽  
Food Intake ◽  
Receptor Blockade ◽  
Sham Feeding ◽  
Systemic Injection ◽  
Mk 801 ◽  
Nmda Receptor Blockade ◽  
Series Of Experiments

Systemic injection of MK-801, a noncompetitive antagonist of N-methyl-d-aspartate (NMDA) receptor ion channels, increases meal size and delays satiation. We examined whether MK-801 increases food intake by directly interfering with actions of cholecystokinin (CCK). Prior administration of MK-801 (100 μg/kg ip) reversed the inhibitory effects of CCK-8 (2 and 4 μg/kg ip) on real feeding of both liquid and solid foods. MK-801 alone did not alter 30-min sham intake of 15% sucrose compared with intake after saline. Furthermore, while CCK-8 (2 or 4 μg/kg ip) reduced sham intake, this reduction was not attenuated by MK-801 pretreatment. To ascertain whether MK-801 attenuation of CCK-induced reduction of real feeding was associated with attenuated inhibition of gastric emptying, we tested the effect of MK-801 pretreatment on CCK-induced inhibition of gastric emptying of 5-ml saline loads. Ten-minute gastric emptying was accelerated after MK-801 (3.9 ± 0.2 ml) compared with saline vehicle (2.72 ± 0.2 ml). CCK-8 (0.5 μg/kg ip) reduced 10-min emptying to 1.36 ± 0.3 ml. Pretreatment with MK-801 did not significantly attenuate CCK-8-induced reduction of gastric emptying (0.9 ± 0.4 ml). This series of experiments demonstrates that blockade of NMDA ion channels reverses inhibition of real feeding by CCK. However, neither inhibition of sham feeding nor inhibition of gastric emptying by CCK is attenuated by MK-801. Therefore, increased food intake after NMDA receptor blockade is not caused by a direct interference with CCK-induced satiation. Rather, increased real feeding, either in the presence or absence of CCK, depends on blockade of NMDA receptor participation in other postoral feedback signals such as gastric sensation or gastric tone.

NMDA receptor blockade retards axonal growth in the transected spinal cord

Neuroreport ◽  
2004 ◽  
Vol 15 (15) ◽  
pp. 2361-2364 ◽  
Author(s):  
Louise M. F. Doyle ◽  
Barry L. Roberts
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Axonal Growth ◽  
Receptor Blockade ◽  
Nmda Receptor Blockade

Chronic neonatal NMDA receptor blockade with MK-801 alters monoamine metabolism in the adult rat

1992 ◽  
Vol 137 (1) ◽  
pp. 97-100 ◽  
Author(s):  
Jan A. Gorter ◽  
Margriet H.A. Botterblom ◽  
Matthijs G.P. Feenstra ◽  
Gerard J. Boer
Keyword(s):  
Nmda Receptor ◽  
Receptor Blockade ◽  
Monoamine Metabolism ◽  
Mk 801 ◽  
Adult Rat ◽  
Nmda Receptor Blockade

scholarly journals Behavioral Consequences of a Combination of Gad1 Haplodeficiency and Adolescent Exposure to an NMDA Receptor Antagonist in Long-Evans Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Kazuyuki Fujihara ◽  
Takumi Sato ◽  
Kazuya Higeta ◽  
Yoshiki Miyasaka ◽  
Tomoji Mashimo ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Forced Swim Test ◽  
Nmda Receptor Antagonist ◽  
Receptor Blockade ◽  
Novelty Preference ◽  
Behavioral Consequences ◽  
Mk 801 ◽  
Model Studies ◽  
Affective Symptoms ◽  
Nmda Receptor Blockade

Glutamate decarboxylase 67-kDa isoform (GAD67), which is encoded by the GAD1 gene, is one of the key enzymes that produce GABA. The reduced expression of GAD67 has been linked to the pathophysiology of schizophrenia. Additionally, the excitatory glutamatergic system plays an important role in the development of this disorder. Animal model studies have revealed that chronic blockade of NMDA-type glutamate receptors can cause GABAergic dysfunction and long-lasting behavioral abnormalities. Based on these findings, we speculated that Gad1 haplodeficiency combined with chronic NMDA receptor blockade would lead to larger behavioral consequences relevant to schizophrenia in a rat model. In this study, we administered an NMDAR antagonist, MK-801 (0.2 mg/kg), to CRISPR/Cas9-generated Gad1+/− rats during adolescence to test this hypothesis. The MK-801 treated Gad1+/− rats showed a shorter duration in each rearing episode in the open field test than the saline-treated Gad1+/+ rats. In contrast, immobility in the forced swim test was increased and fear extinction was impaired in Gad1+/− rats irrespective of MK-801 treatment. Interestingly, the time spent in the center region of the elevated plus-maze was significantly affected only in the saline-treated Gad1+/− rats. Additionally, the MK-801-induced impairment of the social novelty preference was not observed in Gad1+/− rats. These results suggest that the synergistic and additive effects of Gad1 haplodeficiency and NMDA receptor blockade during adolescence on the pathogenesis of schizophrenia may be more limited than expected. Findings from this study also imply that these two factors mainly affect negative or affective symptoms, rather than positive symptoms.

Reduction of food intake by intestinal macronutrient infusion is not reversed by NMDA receptor blockade

2000 ◽  
Vol 278 (2) ◽  
pp. R345-R351 ◽  
Author(s):  
M. Covasa ◽  
R. C. Ritter ◽  
G. A. Burns
Keyword(s):  
Oleic Acid ◽  
Nmda Receptor ◽  
Food Intake ◽  
Intraperitoneal Injection ◽  
Receptor Blockade ◽  
Sucrose Intake ◽  
Sham Feeding ◽  
Mk 801 ◽  
Intraduodenal Infusion ◽  
Nmda Receptor Blockade

Rats increase their intake of food, but not water, after intraperitoneal injection of MK-801, a noncompetitive antagonist of N-methyl-d-aspartate-activated ion channels. We hypothesized that MK-801 might enhance intake by interfering with intestinal chemosensory signals. To test this hypothesis, we examined the effect of the antagonist on 15% sucrose intake after an intraduodenal infusion of maltotriose, oleic acid, or phenylalanine in both real- and sham-feeding paradigms. MK-801 (100 μg/kg) significantly increased sucrose intake regardless of the composition of the infusate during real feeding. Furthermore, MK-801 had no effect on reduction of sucrose intake by intestinal nutrient infusions in sham-feeding rats. These results indicate that MK-801 does not increase meal size and duration by interfering with signals activated by intestinal macronutrients.

The effect of hippocampal NMDA receptor blockade by MK-801 on cued fear extinction

2017 ◽  
Vol 332 ◽  
pp. 200-203 ◽  
Author(s):  
Bo Zhang ◽  
Chuan-Yu Li ◽  
Xiu-Song Wang
Keyword(s):  
Nmda Receptor ◽  
Fear Extinction ◽  
Receptor Blockade ◽  
Mk 801 ◽  
Nmda Receptor Blockade

Maslinic acid ameliorates NMDA receptor blockade-induced schizophrenia-like behaviors in mice

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381 ◽  
Author(s):  
H Kim ◽  
SJ Jeon ◽  
E Kim ◽  
J Zhang ◽  
Y Gwon ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Receptor Blockade ◽  
Maslinic Acid ◽  
Nmda Receptor Blockade

NMDA receptor blockade by memantine increases hormonal counterregulation during hypoglycaemia

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
I Pais ◽  
C Hubold ◽  
M Hallschmid ◽  
KM Oltmanns ◽  
B Schultes ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Receptor Blockade ◽  
Nmda Receptor Blockade
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