• Korean Journal of Biological Psychiatry
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• v.20 no.2
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• pp.29-30
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• 2013

First-line therapy of depression is a pharmacological treatment. Many prescribed antidepressants modulate monoamine neurotransmitters including serotonin, norepinephrine and dopamine. Recently, Ketamine, an N-methyl-D-aspartate receptor antagonist, has received attention and has been investigated for clinical trials and neurobiological studies. Here, I introduce ketamine as a rapid-acting antidepressant.

• 대한예방의학회:학술대회논문집
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• 1995.10a
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• pp.263-264
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• 1995

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.92-92
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• 1997

Stereotaxic apparatus를 이용하여 흰쥐의 두개골을 천공하여 periaqueductal gray matter에 정확히 cannula를 삽입하여 1일 이상의 방치후 여기로 약물을 투여하여 일군의 동물들은 행동의 변화를 관찰하고, 일군의 동물들은 경동맥에서의 혈압과 심박수의 변화를 관찰한다. 결과: ET-1에 의해 유발된 barrel-rolling은 NMDA receptor-selective antagonist인 MK-801에 의해 유의성있게 억제되었으며, NOS antagonist인 L-NAME과 NO scavenger인 Hemoglobin에 의해서도 유의성 있게 억제되었다.

• 제어로봇시스템학회:학술대회논문집
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• 2002.10a
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• pp.39.1-39
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• 2002

We present nanoactuators and nanodetectors for high-precision Micro Electro Mechanical System (MEMS) applications. Major technical difficulties in the high-precision MEMS are arising from the fabrication uncertainty and electrical noise problems. In this paper, we present high-precision actuators and detectors, overcoming the technical limitations placed by the conventional MEMS technology. For the nano-precision actuation, we present a nonlinearly modulated digital actuator (NMDA). NMDA composed of a digital microactuator and a nonlinear micromechanical modulator. The nonlinear micromechanical modulator is intended to purify the actuation errors in the stroke of the digital a...

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.04a
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• pp.21-37
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• 2003

1. Stimulation of dopaminergic system by morphine was abolished in ${\mu}$-opioid receptor knockout mice. 2. Dopaminergic stimulation by opioid agonists, morphine, DPDPE, and U50488, acts independently. 3. Loss of ${\mu}$-opioid receptors is more sensitive to the response of NMDA-induced convulsion and increase in the expression of mRNA for NMDA receptors.

• Journal of Ginseng Research
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• v.44 no.3
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• pp.490-495
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• 2020

Background: Ginsenoside Rk1, a saponin component isolated from heat-processed Panax ginseng Meyer, has been implicated in the regulation of antitumor and anti-inflammatory activities. Although our previous studies have demonstrated that ginsenoside Rg3 significantly attenuated the activation of NMDA receptors (NMDARs) in hippocampal neurons, the effects of ginsenosides Rg5 and Rk1, which are derived from heat-mediated dehydration of ginsenoside Rg3, on neuronal NMDARs have not yet been elucidated. Methods: We examined the regulation of NMDARs by ginsenosides Rg5 and Rk1 in cultured rat hippocampal neurons using fura-2-based calcium imaging and whole-cell patch-clamp recordings. Results: The results from our investigation showed that ginsenosides Rg3 and Rg5 inhibited NMDARs with similar potencies. However, ginsenoside Rk1 inhibited NMDARs most effectively among the five compounds (Rg3, Rg5, Rk1, Rg5/Rk1 mixture, and protopanaxadiol) tested in cultured hippocampal neurons. Its inhibition is independent of the NMDA- and glycine-binding sites, and its action seems to involve in an interaction with the polyamine-binding site of the NMDAR channel complex. Conclusion: Taken together, our results suggest that ginsenoside Rk1 might be a novel component contributable to the development of ginseng-based therapeutic treatments for neurodegenerative diseases.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.156-161
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• 2001

We reported two cases of amantadine treatment in traumatic brain injury patients and reviewed the literature of amantadine treatment of those patients. Problems with short-term memory, attention, planning, problem solving, impulsivity, disinhibition, poor motivation, and other behavioral and cognitive deficit could occur following traumatic brain injury or other types of acquired brain injury. This report described results of amantadine using in two patients with this type of symptom profile. Patients received neuropsychiatric examination as well as BPRS and Barthel index. These patients were improved, respectively from 57 point to 82 point(case 1), from 85 to 94(case 2) in Barthel index, and from 66 point to 35 point(case 1), from 55 to 32 point(case 2) in BPRS. These two patients did not reveal any other adverse effect. The rationale for using amantadine were discussed.

• Journal of Preventive Medicine and Public Health
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• v.32 no.4
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• pp.459-466
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• 1999

Objectives:eurotoxicity is mediated by nitric oxide(NO) in the rat primary neuronal cultures and assess the effect of $Mn^{2+}$ on the N-methyl-D aspartate(NMDA) receptors. Methods: We have used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)assay to examine the effect of cytotoxicity of $MnCl_2$ in neuronal cells , NO production was determined by measuring nirites, a stable oxidation product of NO. The neurons in the rat that contains neuronal nitric oxide synthase(nNOS) were examined by immunofluorescence and confocal microscopy. The effects of $Mn^{2+}$ on the NMDA receptors was assesed by the whole cell voltage clamp technique. Results: We showed that the NO release and NOS expression was increased with 500uM $MnCl_2$ treatment and an NOS inhibitors, $N^G-nitro-L-arginine$, prevented neurotoxicity elicited by manganese. In the electrophysiological study, $Mn^{2+}$ does not block or activate the NMDA receptors and not pass through the NMDA receptors in a neurons of basal ganglia. Conclusions: It is concluded that manganese neurotoxicity in basal ganglia was partially mediated by nitric oxide in the cell culture model.

• The Korean Journal of Pain
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• v.13 no.1
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• pp.31-37
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• 2000

Background: Recent studies suggested that a preoperative block of N-methyl-D-aspartate (NMDA) receptors with NMDA antagonists may reduce postoperative pain. In this double-blind study, magnesium sulfate, a natural NMDA receptor antagonist, was administered preoperatively to investigate the effects of magnesium sulfate on postoperative pain and pulmonary function. Methods: Seventy patients who were to undergo gastrectomy under general anesthesia were randomly assigned to one of three groups. Groups 2 and 3 received intravenous magnesium, preoperatively (Group 2: 50 mg/kg bolus, 7.5 mg/kg/hr for 20 hr, Group 3: 50 mg/kg bolus, 15 mg/kg/hr for 20 hr). Group 1 received normal saline as the control group. Visual analog scale (VAS) for postoperative pain and mood, cumulative analgesic consumption, recovery of pulmonary function and side effects were evaluated at 6, 24, 48 and 72 hours after the operation. Results: In Groups 2 and 3, plasma concentration of magnesium were significantly higher than in Group 1 at 6 and 20 hours after infusion (P<0.05). There were no significant differences in the analgesic consumption, and recovery of pulmonary function and the incidence of side effects at 6, 24, 48 and 72 hours after the operation among the three groups. In Group 3, pain scores at rest measured 24 and 48 hours after operation were lower than the control group, and pain scores when deep breathing were significantly lower than the control group at postoperative 6, 24, 48, and 72 hours. Conclusions: We conclude that intravenous infusion of greater amount of magnesium has little effectiveness in reducing postoperative pain. However, further studies are needed to characterize the clinical significance of these effects on postoperative pain.

• The Korean Journal of Pain
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• v.21 no.3
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• pp.173-178
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• 2008

Background: The intrathecal (IT) $GABA_A$ receptor antagonist, bicuculline (BIC), results in tactile allodynia (TA) through disinhibition in the spinal cord. Such disinhibition is considered to be an important mechanism for neuropathic pain. Agmatine, an endogenous polyamine, has a neuro-protective effect in the central nervous system. We investigated the analgesic effects and mechanisms of agmatine action on BIC-induced TA. Methods: Male Sprague-Dawley rats, weighting 250-300 g, were subjected to implantations of PE-10 into the lumbar subarachnoid space for IT drug injection. Five days after surgery, either $10{\mu}l$ of normal saline (NS) or agmatine ($30{\mu}g$ or $10{\mu}g$) in $10{\mu}l$ NS were injected 10 min prior to BIC ($10{\mu}g$) or NMDA ($5{\mu}g$). We assessed the degree of TA (graded 0: no response, 1: mild response, 2: moderate response, 3: strong response) every 5 min for 30 min. Areas under curves and degree of TA were expressed as mean ${\pm}$ SEM. Results were analyzed using one-way ANOVA followed by a Tukey test for multiple comparisons. P < 0.05 was considered significant. Results: IT BIC-induced strong TA reached its peak and plateaued between 10 to 15 min. IT NS-NMDA induced mild transient TA for up to 15 min. Preemptive IT AG attenuated IT BIC-induced TA dose dependently and preemptive IT AG10 completely abolished the IT NMDA-induced TA. Conclusions: Preemptive IT AG attenuated the IT BIC-induced TA through inhibitory actions on postsynaptic NMDA receptor activation. AG might be a viable therapeutic option in the treatment of neuropathic pain.