No abstract available.
Dizocilpine Maleate* ; Dopamine* ; Methamphetamine*

No abstract available.
Animals ; Dizocilpine Maleate ; Rats ; Spinal Cord

No abstract available.
6-Cyano-7-nitroquinoxaline-2,3-dione ; Cycloheximide ; Dizocilpine Maleate

The anti-allodynic effect of NMDA receptor antagonist and acupuncture treatments were explored through spinal p35 regulation of diabetic neuropathic rat. We evaluated the change over time of p35/p25 protein levels in the spinal cord compared with behavioral responses to thermal and mechanical stimulation in streptozotocin (STZ)-induced diabetic rats. Additionally, we studied p35 expression when electroacupuncture (EA) and a sub-effective dose of NMDA (N-methyl-D-aspartate) receptor antagonist (MK-801) were used to treat hyperalgesia in the diabetic neuropathic pain (DNP). Thermal paw withdrawal latency (PWL) and mechanical paw withdrawal threshold (PWT) were significantly decreased in the early stage of diabetes in rats. p35 expression after STZ injection gradually decreased from 1 week to 4 weeks compared to normal controls. p25 expression in 4-week diabetic rats was significantly higher than that of 2-week diabetic rats, and thermal PWL in 4-week diabetic rats showed delayed responses to painful thermal stimulation compared with those at 2 weeks. EA applied to the SP-9 point (2 Hz frequency) significantly prevented the thermal and mechanical hyperalgesia in the DNP rat. Additionally, EA combined with MK-801 prolonged anti-hyperalgesia, increased p35 expression, and decreased the cleavage of p35 to p25 during diabetic neuropathic pain. In this study we show EA combined with a sub-effective dose of MK-801 treatment in DNP induced by STZ that is related to p35/p25 expression in spinal cord.
Acupuncture ; Animals ; Diabetic Neuropathies ; Dizocilpine Maleate ; Electroacupuncture ; Hyperalgesia ; N-Methylaspartate ; Neuralgia ; Rats ; Spinal Cord ; Streptozocin

OBJECTIVE: Early maternal separation (EMS) during the development has been known to influence the alteration of behavior in adulthood. Nitric oxide (NO) may have been implicated to play a crucial role in the neurodevelopment as an intracellular and intercellular messenger. This study was designed to investigate the neurochemical mechanism of the behavioral changes resulting from EMS during the development in juvenile rats. METHODS: Experimental group consisted of subjects that were removed and weaned from the day on postnatal day 15. Control group were the litters that experienced no EMS until postnatal day 21. On postnatal day 15 and 36, the locomotor activity (LA) was measured. On postnatal day 36 the behavioral changes in the forced swimming test (FST) were also measured. Test drugs were intraperitoneally injected including MK-801 (0.5 mg/kg), N omega-nitro-L-arginine (L-NA, 20 mg/kg), paroxetine (20 mg/kg), and bupropion (150 mg/kg). RESULTS:EMS produced the decrease of LA significantly in juvenile rats (p<0.001). Both MK-801 and L-NA increased LA in experimental group (p<0.001) and control group (p<0.05). The degree of increase was higher in experimental group than in control group. However, both paroxetine and bupropion increased LA in experimental group (p<0.001, p<0.05), but not in control group. In the FST, immobility was significantly increased in experimental group compared with control group (p<0.001). The increases of immobility in experimental group were abolished after injecting MK-801, L-NA, paroxetine, and bupropion, respectively. CONCLUSION: These results indicate that EMS during the development can lead to behavioral abnormalities in juvenile rats. The underlying neurochemical mechanism of this behavioral changes may be, in part, related to the glutamatergic NMDA-NO pathway. This suggests that glutamatergic NMDA-NO pathway vulnerable to stress may predispose to depression.
Animals ; Bupropion ; Depression ; Dizocilpine Maleate ; Motor Activity ; Nitric Oxide ; Nitroarginine ; Paroxetine ; Rats ; Swimming

The effects of NMDA-receptor antagonist (MK-801) were assessed for the oxygen free radical mediated brain (hippocampus) injury with eighty rats which were exposed to carbon monoxide (CO) followed by hyperbaric oxygen (HBO) treatment. Superoxide dismutase (SOD) and malondialdehyde (MDA) were used as parameters of the oxygen free radical reaction. Experimental groups consisted of (1) control group (=breathing with air), (2) CO group (=exposed to CO after air breath), (3) CO-air group(exposed to CO after air breath followed by air breath), and (4) CO-HBO group (=exposed to CO after air breath followed by 3 ATA HBO). Each group was divided two subgroup according to the pretreatment (normal saline or MK-801). CO, CO-air and HBO groups increased in SOD activity as compared with control group. And CO-air and HBO groups increased in MDA as compared with control and CO group. Pretreatment of MK-801 decreased SOD activities significantly (p-value<.05) , but MDA amount not significantly (p-value=.107). These results suggest a useful protective effect of NMDA-receptor antagonist (MK-801) in CO induced hippocampal injury mediated by oxygen free radicals.
Animals ; Brain Injuries* ; Brain* ; Carbon Monoxide ; Dizocilpine Maleate ; Free Radicals ; Malondialdehyde ; Oxygen* ; Rats* ; Superoxide Dismutase

BACKGROUND: There has been much interest in the involvement of wind-up in the hyperalgesia and allodynia of chronic pain syndrome. To investigate the behavioral parallels of this wind-up phenomenon, we evaluated the effects of intrathecal morphine, clonidine and MK801 on the formalin test in the rats. METHOD: All experimental animals were divided randomly into six groups. In group 1(n=7), normal saline 50 l was administered through the intrathecal catheter(PE10, 8 cm in length). In group 2(n=7), morphine 10 g was administered through the catheter. In group 3(n=7), group 4(n=7), group 5(n=7) and group 6(n=7), clonidine 10 g, clonidine 20 g, MK801 1 g, MK801 10 g was administered in same manner, respectively. Thirty min after recoverying from anesthesia, 50 l 5% formalin was injected in the hind paw. To quantify the formalin response, we counted the number of spontaneous flinching for 60 min. RESULT: Intrathecal morphine(group 2) decreased the number of paw flinches in both phases 1 and 2 readily compared to control(p<0.05). In the clonidine(group 3 and 4), both groups decreased the number of flinching in both phases 1 and 2, but there was no significant difference between two groups. In group 5, intrathecal MK-801 decreased the number of paw flinches in phase 2. In group 6, intrathecal MK-801 decreased the number of paw flinches in both phases 1 and 2. CONCLUSION: This study suggest that wind-up is readily blocked by pretreatment of morphine, clonidine and MK801.
Analgesics ; Anesthesia ; Animals ; Catheters ; Chronic Pain ; Clonidine* ; Dizocilpine Maleate* ; Formaldehyde* ; Hyperalgesia ; Morphine* ; Pain Measurement* ; Rats*

To examine the effect of biflorin, a component of Syzygium aromaticum, on memory deficit, we introduced a scopolamine-induced cognitive deficit mouse model. A single administration of biflorin increased latency time in the passive avoidance task, ameliorated alternation behavior in the Y-maze, and increased exploration time in the Morris water maze task, indicating the improvement of cognitive behaviors against cholinergic dysfunction. The biflorin-induced reverse of latency in the scopolamine-treated group was attenuated by MK-801, an NMDA receptor antagonist. Biflorin also enhanced cognitive function in a naïve mouse model. To understand the mechanism of biflorin for memory amelioration, we performed Western blot. Biflorin increased the activation of protein kinase C-ζ and its downstream signaling molecules in the hippocampus. These results suggest that biflorin ameliorates drug-induced memory impairment by modulation of protein kinase C-ζ signaling in mice, implying that biflorin could function as a possible therapeutic agent for the treatment of cognitive problems.
Animals ; Blotting, Western ; Cognition ; Cognition Disorders ; Dizocilpine Maleate ; Hippocampus ; Memory Disorders ; Memory* ; Mice* ; N-Methylaspartate ; Protein Kinases ; Syzygium ; Water

BACKGROUND AND OBJECTIVES: Several lines of evidence suggest that recovery of symptoms following unilateral labyrinthectomy (ULX) is due to the restoration of neuronal activity in the ipsilateral vestibular nuclei, leading to the reestablishment of bilateral symmetry in the resting neuronal activity. Effects of dizocilpine maleate (MK801), a non-competitive NMDA receptor antagonist, on vestibular compensation following unilateral labyrinthectomy (ULX) were investigated in adult Sprague-Dawley rats. MAERIAL AND METHODS: Responses of spontaneous nystagmus and neuronal activity of the contralateral medial vestibular nuclei (MVN) to labyrinthectomy were recorded in course of time after intraperitoneal injection of MK801. RESULT: Spontaneous nystagmus decreased gradually with time, but recovery of the nystagmus was aggravated 2 to 4 hours after administration of MK801 (p<0.05). In the labyrinthine intact rats, MK801 treatment significantly increased resting activity of type I and II in MVN compared with non-treated rats, and the effect of MK801 on neuronal activity was more prominent in the type I neurons than in the type II neurons. After 6 hours of ULX, the activities of type I and II neurons were decreased compared with labyrinthine intact rats, and type II neurons showed higher activity than the type I neurons. MK801 treated ULX rats showed higher resting activity in the type I and II neurons than in the labyrinthine intact rats or ULX rats, but lower resting activity than the MK801 treated labyrinthine intact rats. In the neuronal activity induced by sinusoidal rotation, gain was the highest in the MK801 treated ULX rats among the 4 experimental groups, and sensitivity was decreased in the type I & II neurons by treatment of MK801. CONCLUSION: These results suggest that MK801 deteriorates asymmetry of the resting activity in the bilateral MVN by inhibition of cerebellar Purkinje system inhibiting the intact MVN, which results in decompensation of the vestibular function following ULX.
Adult ; Animals ; Compensation and Redress ; Dizocilpine Maleate* ; Humans ; Injections, Intraperitoneal ; N-Methylaspartate ; Neurons* ; Rats* ; Rats, Sprague-Dawley ; Vestibular Nuclei*

OBJECTIVE: The interaction between MK-801, a model of psychosis and KCl-induced depolarization or electroconvulsive shock (ECS), a therapeutic model of electroconvulsive therapy (ECT), was investigated in SH-SY5Y cells and the rat frontal cortex. METHODS: SH-SY5Y cells were pretreated with 1 microM MK-801 for 15 min, followed by cotreatment with 100 mM KCl for 5 min. MK-801 was reintroduced after the KCl was washed out, and the samples were incubated before harvesting. For the experiments in rats, male Sprague-Dawley rats were treated with MK-801 followed by ECS. Immunoblot analyses of glycogen synthase kinase 3beta (GSK3beta) (Ser9), AKT (Ser473) and extracellular legulated kinase (ERK)1/2 in SH-SY5Y cells and the rat frontal cortex were performed. RESULTS: KCl-induced neuronal depolarization resulted in the transient dephosphorylation of AKT (Ser473) and GSK3beta (Ser9), followed by increased phosphorylation of the enzymes in SH-SY5Y cells. Cotreatment with MK-801 and KCl inhibited the initial dephosphorylation of AKT and GSK3beta produced by KCl-induced neuronal depolarization. Similarly, ECS resulted in the transient dephosphorylation of AKT (Ser473) and GSK3beta (Ser9), whereas cotreatment with MK-801 inhibited the initial dephosphorylation of AKT (Ser473) and GSK3beta (Ser9) produced by ECS in the rat frontal cortex. No significant interaction was observed between MK-801 and KCl in the dephosphorylation of ERK1/2. CONCLUSION: These results suggest that an antagonistic interplay between MK-801 and neuronal depolarization by KCl or ECS is involved the regulation of AKT (Ser473) and GSK3beta (Ser9) phosphorylation.
Animals ; Dizocilpine Maleate* ; Electroconvulsive Therapy ; Electroshock ; Glycogen Synthase Kinases ; Humans ; Male ; Neurons* ; Phosphorylation ; Phosphotransferases ; Psychotic Disorders ; Rats* ; Rats, Sprague-Dawley