• The Journal of Korean Physical Therapy
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• v.22 no.4
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• pp.97-101
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• 2010

Purpose: Sensory input is very important for proper performance of human. Two-point discrimination is the most widely used tactile sensory test. The purpose of this study was to find the changes in cortical activation patterns between tactile stimulation and two-point discrimination. Methods: Two healthy subjects participated in our study. fMRI scanning was done during 4 repeated blocks of tactile stimulation and two point discrimination of the right index finger tip. In one block, stimuli were repeated 10 times every three seconds. To determine the changes of cortical neurons during sensory input, intensity index was analyzed. Results: When tactile stimulation of the right index finger tip was completed, only contralateral primary somatosensory area was activated. In contrast, during two-point discrimination, both the primary somatosensory area and ipsilateral supplementary sensory area were activated. Conclusion: During two point discrimination, both primary somatosensory area and ipsilateral supplementary sensory area were activated. Therefore, two-point discrimination is required more complex and conscious activity than tactile stimulation.

• Archives of Pharmacal Research
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• v.17 no.5
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• pp.343-347
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• 1994

Effects of betaine on glutamate-induced neurotoxicity were examined on primary culturs of chicken embryonic brain cells and on rat cortical cultures. Betaine was found to attenuate glutamate-induced neurotoxicity both morphologically and biochemically. A 30 min exposure of chicken embryonic brain cells cultured for 12 days to 500 .mu.M glutamate produced wide-spread acute neuronal swelling and neurtic fragmentation. A 2-h pretreatment of cultured chicken embryonic brain cells with i mM betaine prior to a 30 min exposure to 500 , mu, M glutamate significantly raised the survival rate of neurons in the culture. When chicken embryonic brain cells were pretreated for 2 h with i mM betaine followed by exposure to 100 .mu.M glutamate for 42 h, lactate dehydrogenase levels within the cells remained at 62% of .mu.M untreated control values while glutamate-treated control fell to 0% lactate dehydrogenase. Betaine also exerted attenuating effects on N-methyl-D-asparte-, kainate-and quisqualate-induced neurotoxicity in a similar manner to that observed with glutamate. Similar neuroprotective effects of betaine with rat cortical cultures.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.1-8
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• 2016

Damage in the periphery or spinal cord induces maladaptive plastic changes along the somatosensory nervous system from the periphery to the cortex, often leading to chronic pain. Although the role of neural circuit remodeling and structural synaptic plasticity in the 'pain matrix' cortices in chronic pain has been thought as a secondary epiphenomenon to altered nociceptive signaling in the spinal cord, progress in whole brain imaging studies on human patients and animal models has suggested a possibility that plastic changes in cortical neural circuits may actively contribute to chronic pain symptoms. Furthermore, recent development in two-photon microscopy and fluorescence labeling techniques have enabled us to longitudinally trace the structural and functional changes in local circuits, single neurons and even individual synapses in the brain of living animals. These technical advances has started to reveal that cortical structural remodeling following tissue or nerve damage could rapidly occur within days, which are temporally correlated with functional plasticity of cortical circuits as well as the development and maintenance of chronic pain behavior, thereby modifying the previous concept that it takes much longer periods (e.g. months or years). In this review, we discuss the relation of neural circuit plasticity in the 'pain matrix' cortices, such as the anterior cingulate cortex, prefrontal cortex and primary somatosensory cortex, with chronic pain. We also introduce how to apply long-term in vivo two-photon imaging approaches for the study of pathophysiological mechanisms of chronic pain.

• YAKHAK HOEJI
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• v.46 no.3
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• pp.185-191
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• 2002

Alzheimer's disease (AD) involves neuronal degeneration with impaired cholinergic transmission, particularly in areas of the brain associated with learning and memory. Several cholinesterase inhibitors are widely prescribed to ameliorate the cognitive deficits in AD patients. In an attempt to examine if tacrine and donepezil, two well-known cholinesterase inhibitors, exhibit additional pharmacological actions in primary cultured rat cortical cells, we investigated the effects on neuronal injuries induced by glutamate or N-methyl-D-aspartate (NMDA), $\beta$-amyloid fragment ( $A_{{beta}25-35)}$), and various oxidative insults. Both tacrine and donepezil did not significantly inhibit the excitotoxic neuronal damage induced by glutamate. However, tacrine inhibited the toxicity induced by NMDA in a concentration-dependent fashion. In addition, tacrine significantly inhibited the $A_{{beta}25-35)}$-induced neuronal injury at the concentration of 50 $\mu$M. In contrast, donepezil did not reduce the NMDA- nor $A_{{beta}25-35)}$-induced neuronal injury. Tacrine and donepezil had no effects on oxidative neuronal injuries in cultures nor on lipid peroxidation in vitro. These results suggest that, in addition to its anticholinesterase activity, the neuroprotective effects by tacrine against the NMDA- and $A_{{beta}25-35)$-induced toxicity may be beneficial for the treatment of AD. In contrast, the potent and selective inhibition of central acetylcholinesterase appears to be the major action mechanism of donepezil.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.47-56
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• 1998

In the present study, we assayed a number of compounds isolated from Panax ginseng C. A. Meyer (Araliaceae) for an ability to protect rat cortical cell cultures from the deleterious effects of the neurotoxicant, glutamate. We found that ginsenosides Rbl and Rg3 significantly attenuated glutamate-induced neurotoxicity. Brief exposure of cultures to excess glutamate caused extensive neuronal death. Glutamate-induced neuronal cell damage was significantly reduced by pretreatment with Rbl and Rgl. Ginsenosides Rbl and Rg3 inhibited the overproduction of nitric oxide which routinely follows glutamate neurotoxicity and preserved the level of superoxide dismutase in glutamate-treated cells. Furthermore, in cultures treated with glutamate, these ginsenosides inhibited the formation of malondialdehyde, a compound produced during lipid peroxidation, and diminished the influx of calcium. These results show that ginsenosides Rbl and Rg1 exerted significant neuroprotective effects on cultured cortical cells. As such, these compounds may be efficacious in protecting neurons from oxidative damage produced by exposure to excess glutamate.

• Archives of Pharmacal Research
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• v.29 no.8
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• pp.699-706
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• 2006

The present study evaluated antioxidant and neuroprotective activities of hesperidin, a flavanone mainly isolated from citrus fruits, and its aglycone hesperetin using cell-free bioassay system and primary cultured rat cortical cells. Both hesperidin and hesperetin exhibited similar patterns of 1,1-diphenyl-2-picrylhydrazyl radical scavenging activities. While hesperidin was inactive, hesperetin was found to be a potent antioxidant, inhibiting lipid peroxidation initiated in rat brain homogenates by $Fe^{2+}$ and L-ascorbic acid. In consistence with these findings, hesperetin protected primary cultured cortical cells against the oxidative neuronal damage induced by $H_2O_2$ or xanthine and xanthine oxidase. In addition, it was shown to attenuate the excitotoxic neuronal damage induced by excess glutamate in the cortical cultures. When the excitotoxicity was induced by the glutamate receptor subtype-selective ligands, only the N-methyl-D-aspartic acid-induced toxicity was selectively and markedly inhibited by hesperetin. Furthermore, hesperetin protected cultured cells against the $A_{{\beta}(25-35)}-induced$ neuronal damage. Hesperidin, however, exerted minimal or no protective effects on the neuronal damage tested in this study. Taken together, these results demonstrate potent antioxidant and neuroprotective effects of hesperetin, implying its potential role in protecting neurons against various types of insults associated with many neurodegenerative diseases.

• Animal cells and systems
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• v.9 no.3
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• pp.145-152
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• 2005

A retrograde tracer, WGA-apo-HRP-gold, was injected into midline thalamic nuclei and subsequently orexin-A immunostaining was performed on the tuberal region of the hypothalamus in order to investigate orexinergic projections to the midline thalamus. Injection site was targeted within one specific region, i.e., paraventricular, centromedian, rhomboid, reuniens, or intermediodorsal nucleus, but it proved to be either one or a combination of these thalamic nuclei. The distribution of WG/orexin-double-labeled neurons exhibited a general pattern in that the majority of labeled cells were observed within the ventral portion of the lateral hypothalamus as well as the perifornical nucleus (PeF). A small number of double-labeled cells were also observed at the dorsomedial nucleus, the area dorsal to the PeF, dorsal portion of the lateral hypothalamus, and the posterior hypothalamus. These orexin-immunoreactive neurons might have wake-related influences over a variety of functions related with midline thalamic nuclei, which include autonomic control, associative cortical functions, and limbic regulation.

• BMB Reports
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• v.57 no.8
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• pp.363-368
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• 2024

Parkinson's disease (PD), characterized by dopaminergic neuron degeneration in the substantia nigra, is caused by various genetic and environmental factors. Current treatment methods are medication and surgery; however, a primary therapy has not yet been proposed. In this study, we aimed to develop a new treatment for PD that induces direct reprogramming of dopaminergic neurons (iDAN). Achaete-scute family bHLH transcription factor 1 (ASCL1) is a primary factor that initiates and regulates central nervous system development and induces neurogenesis. In addition, it interacts with BRN2 and MYT1L, which are crucial transcription factors for the direct conversion of fibroblasts into neurons. Overexpression of ASCL1 along with the transcription factors NURR1 and LMX1A can directly reprogram iDANs. Using a retrovirus, GFP-tagged ASCL1 was overexpressed in astrocytes. One week of culture in iDAN convertsion medium reprogrammed the astrocytes into iDANs. After 7 days of differentiation, TH+/TUJ1+ cells emerged. After 2 weeks, the number of mature TH+/TUJ1+ dopaminergic neurons increased. Only ventral midbrain (VM) astrocytes exhibited these results, not cortical astrocytes. Thus, VM astrocytes can undergo direct iDAN reprogramming with ASCL1 alone, in the absence of transcription factors that stimulate dopaminergic neurons development.

• 한국약용작물학회:학술대회논문집
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• 2007.05a
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• pp.292-293
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• 2007

• Journal of Microbiology and Biotechnology
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• v.12 no.4
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• pp.691-691
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• 2002

In the course of our screening for neuroprotective agents, a new compound (1) was isolated together with a known compound, caruilignan C (2), from the fruiting body of Daldinia concentrica. Their structures were determined on the basis of various spectral studies. Both compounds exhibited neuroprotective effect against iron-induced neurodegeneration in a primary culture of mouse cortical neurons.