• 제목/요약/키워드: Cortical neurons

검색결과 141건 처리시간 0.028초

해조류 기반 엘리시터 처리에 의한 꽃송이버섯의 GABA 함량 증가 및 흥분성 신경세포의 수상돌기 발달 억제 (Enhanced GABA content from sodium alginate-induced Sparassis latifolia influences dendrite development in primary cortical neurons)

  • 최문희;기성환;이성은;이금화;신현재
    • 한국버섯학회지
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    • 제17권4호
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    • pp.275-283
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    • 2019
  • Sparassis latifolia is a fungus abundant in β-glucan and amino acids and is highly valued as a medicinal mushroom. Among amino acids, γ-aminobutyric acid (GABA) is a free amino acid and has biological effects, such as increase/decrease of hypertension, improvement of cerebral blood flow, and prevention of dementia. In this study, biological elicitors were used to increase bioactive substances as a biofortification method. Sodium alginate extracted from seaweed (Sargassum horneri, Sargassum fulvellum, Sargassum fusiforme) were used as the elicitor. The levels of β-glucan and GABA in the mycelium and fruiting body grown by adding the elicitor to the medium were investigated. Addition of sodium alginate positively affected GABA production and negatively affected the β-glucan production in these fungi. Sodium alginates extracted from S. fulvellum induced the highest increase in GABA in the mycelium and fruiting bodies. Moreover, we investigated the effects of the extracts from mycelium and fruiting bodies on dendrite development in primary cortical neurons. We found that the extract from the fruiting bodies of sodium alginate treated fungi with increased levels of GABA inhibited the dendrite outgrowth of excitatory neurons, but not inhibitory neurons.

Curcuma longae Radix, Phellinus linteus 및 Scutellariae Radix 혼합추출물의 $A{\beta}$ (25-35) 유도 배양신경세포독성 및 마우스기억손상 억제효과 (Ethanol Extract of Three Plants of Curcuma longae Radix, Phellinus linteus, and Scutellariae Radix Inhibits Amyloid $\beta$ Protein (25-35)-Induced Neurotoxicity in Cultured Neurons and Memory Impairment in Mice)

  • 김주연;정하연;반주연;유재국;배기환;성연희
    • 한국약용작물학회지
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    • 제17권6호
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    • pp.388-396
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    • 2009
  • The present study investigated an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix for possible neuroprotective effects on neurotoxicity induced by amyloid $\beta$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to $10\;{\mu}M$ $A{\beta}$ (25-35) for 36 h induced neuronal apoptotic death. At $1-50\;{\mu}g/m{\ell}$, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $A{\beta}$ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol $A{\beta}$ (25-35) was inhibited by chronic treatment with HS0608 (25, 50 and 100 mg/kg, p.o. for 7 days) as measured by a passive avoidance test. From these results, we suggest that the antidementia effect of HS0608 is due to its neuroprotective effect against $A{\beta}$ (25-35)-induced neurotoxicity and that HS0608 may have a therapeutic role in preventing the progression of Alzheimer's disease.

Amyloid β protein (25-35)-유도 배양신경 세포독성 및 마우스기억손상에 대한 목과의 억제효과 (Inhibitory Effect of Chaenomeles sinensis Fruit on Amyloid β Protein (25-35)-Induced Neurotoxicity in Cultured Neurons and Memory Impairment in Mice)

  • 정명환;송경식;성연희
    • 한국약용작물학회지
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    • 제20권1호
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    • pp.8-15
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    • 2012
  • The present study investigated an ethanol extract of Chaenomeles sinensis fruit (CSF) for possible neuroprotective effects on neurotoxicity induced by amyloid ${\beta}$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons and also for antidementia activity in mice. Exposure of cultured cortical neurons to $10{\mu}M\;A{\beta}$ (25-35) for 36 h induced neuronal apoptotic death. At $0.1-10{\mu}g/m{\ell}$, CSF inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $A{\beta}$ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of mice with 15 nmol $A{\beta}$ (25-35) was inhibited by chronic treatment with CSF (10, 25 and 50 mg/kg, p.o. for 7 days) as measured by a passive avoidance test. CSF (50 mg/kg) inhibited the increase of cholinesterase activity in $A{\beta}$ (25-35)-injected mice brain. From these results, we suggest that the antidementia effect of CSF is due to its neuroprotective effect against $A{\beta}$ (25-35)-induced neurotoxicity and that CSF may have a therapeutic role for preventing the progression of Alzheimer's disease.

Spatial Information Processing between Hippocampus and Prefrontal cortex: a Hypothesis Based on Anatomy and Physiology

  • Jung, Min-Whan
    • Animal cells and systems
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    • 제2권1호
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    • pp.65-69
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    • 1998
  • The hippocampus and prefrontal cortex are regarded as the highest-order association cortices. The hippocampus has been proposed to store "cognitive maps" of external environments, and the prefrontal cortex is known to be involved in the planning of behavior, among other functions. Considering the prominent functional roles played by these structures, it is not surprising to find direct monosynaptic projections from the hippocampus to the prefrontal cortex. Rhythmic stimulation of this projection patterned after the hippocampal EEG theta rhythm induced stable long-term potentiation of field potentials in the prefrontal cortex. Comparison of behavioral correlates of hippocampal and prefrontal cortical neurons during an a-arm radial maze, working memory task shows a striking contrast. Hippocampal neurons exhibit clear place-specific firing patterns, whereas prefrontal cortical neurons do not show spatial selectivity, but are correlated to different stages of the behavioral task. These data lead to the hypothesis that the role of hippocampal projection to the prefrontal cortex is not to impose spatial representations upon prefrontal activity, but to provide a mechanism for learning the spatial context in which particular behaviors are appropriate.propriate.

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경두개 전침과 발효황금 병행 투여가 흰쥐의 허혈성 뇌세포 손상에 미치는 효과 (Combination of Transcranial Electro-Acupuncture and Fermented Scutellaria baicalensis Ameliorates Motor Recovery and Cortical Neural Excitability Following Focal Stroke in Rats)

  • 김민선;구호;최명애;문세진;양승범;김재효
    • Korean Journal of Acupuncture
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    • 제35권4호
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    • pp.187-202
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    • 2018
  • Objectives : Non-invasive transcranial electrical stimulation is one of therapeutic interventions to change in neural excitability of the cortex. Transcranial electro-acupuncture (TEA) can modulate brain functions through changes in cortical excitability as a model of non-invasive transcranial electrical stimulation. Some composites of fermented Scutellaria baicalenis (FSB) can activate intercellular signaling pathways for activation of brain-derived neurotrophic factor that is critical for formation of neural plasticity in stroke patients. This study was aimed at evaluation of combinatory treatment of TEA and FSB on behavior recovery and cortical neural excitability in rodent focal stroke model. Methods : Focal ischemic stroke was induced by photothrombotic injury to the motor cortex of adult rats. Application of TEA with 20 Hz and $200{\mu}A$ in combination with daily oral treatment of FBS was given to stroke animals for 3 weeks. Motor recovery was evaluated by rotating bean test and ladder working test. Electrical activity of cortical pyramidal neurons of stroke model was evaluated by using multi-channel extracellular recording technique and thallium autometallography. Results : Compared with control stroke group who did not receive any treatment, Combination of TEA and FSB treatment resulted in more rapid recovery of forelimb movement following focal stroke. This combination treatment also elicited increase in spontaneous firing rate of putative pyramidal neurons. Furthermore expression of metabolic marker for neural excitability was upregulated in peri-infract area under thallium autometallography. Conclusions : These results suggest that combination treatment of TEA and FSB can be a possible remedy for motor recovery in focal stroke.

머루전초, 독활전초, 감초 혼합추출물의 Amyloid β Protein (25-35) 유발 신경 독성에 대한 억제효과 (Inhibitory Effect of an Ethanol Extract Mixture of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix on Amyloid β Protein (25-35)-Induced Neurotoxicity)

  • 장지연;성연희
    • 한국약용작물학회지
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    • 제22권2호
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    • pp.105-112
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    • 2014
  • The present study investigated an ethanol extract (SSB) of a mixture of three medicinal plants of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix for possible neuroprotective effects on neurotoxicity induced by Amyloid ${\beta}$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to $15{\mu}M$ $A{\beta}$ (25-35) for 36 h induced neuronal apoptotic death. At $1-30{\mu}g/m{\ell}$, SSB inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $A{\beta}$ (25-35) in cultured cortical neurons. Memory impairment and increase of acetylcholinesterase activity induced by intracerebroventricular injection of mice with 16 nmol $A{\beta}$ (25-35) was inhibited by chronic treatment with SSB (25, 50 and 100 mg/kg, p.o., for 8 days). From these results, it is suggested that antidementia effect of SSB is due to its neuroprotective effect against $A{\beta}$ (25-35)-induced neurotoxicity and that SSB may have a therapeutic role in preventing the progression of Alzheimer's disease.

이침자극(耳鍼刺戟)이 절식(絶食) Stress로 인(因)한 흰쥐 대뇌피질(大腦皮質)의 NADPH-diaphorase 신경세포(神經細胞)에 미치는 영향(影響) (Effects of Auricular Acupuncture on NADPH-diaphorase Neurons in Brain Cortex of Fasted Rats)

  • 이정현;김이화;이은용
    • Journal of Acupuncture Research
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    • 제18권2호
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    • pp.79-90
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    • 2001
  • Objective : The aim of the present study is to investigate whether stimulating a specific auricular point(胃點) is effect on suppression of appetite. Methods : This study evaluated the changes of Reduced-Nicotinamide-Adenine-inucieotide-Phosphate-diaphorase(NADPH-d)-positive neurons using a histoehemical method. Staining intensities of NADPH-d-positive neurons were assessed in a quantitative fashion using a microdensitometrical method based on optical density by means of an image analyzer. Results : The results show as follows ; 1. In the RSG/RSA, FRI/FR2, HL, PAR1 area, The optical density of NADPH-d-positive neurons of fasted group was significantly decreased in comparison to fed group. 2. In most cortical area, It was not significant statistically, But the optical density of NADPH-d-positive neurons of fed with auricular acupuncture group was decreased in comparison to fed group. 3. In most cortical area, It was not significant statistically, But fasted with auricular acupuncture group increased the optical density of NADPH-d-positive neurons comparison to fasted group. Conclusions : We conclude that stimulating the specific auricular points is able to effect on NO(Nitric Oxide)-expression in the brain cortex of sprague dawley rats, The results suggest that auricular acupuncture may be useful for controlling obesity.

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일차 배양한 흰쥐 대뇌피질세포의 흥분성 및 산화적 신경세포손상에 대한 소전재조환의 억제효과 (Inhibitory Effects of Xiaoshuan Zaizao Wan on Excitotoxic and Oxidative Neuronal Damage Induced in Primary Cultured Rat Cortical Cells)

  • 조정숙
    • 약학회지
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    • 제47권6호
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    • pp.369-375
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    • 2003
  • Xiaoshuan Zaizao Wan (XZW) has been used in China to improve hemiplegia, deviation of eye and mouth, and dysphasia due to cerebral thrombosis. To characterize pharmacological actions of XZW, we evaluated its effects on neuronal cell damage induced in primary cultured rat cortical cells by various oxidative insults, glutamate or N-methyl-D-aspartate (NMDA), and $\beta$-amyloid fragment ($A_{\beta(25-35)}$). XZW was found to inhibit the oxidative neuronal damage induced by $H_2O_2$, xanthine/xanthine oxidase, or $Fe^{2+}$/ascorbic acid. It also attenuated the excitotoxic damage induced by glutamate or NMDA. The NMDA-induced neurotoxicity was more effectively inhibited than the glutamate-induced toxicity. In addition, we found that XZW protected neurons against the $A_{\beta(25-35)}$-induced toxicity. Moreover; XZW exhibited dramatic inhibition of lipid peroxidation in rat brain homogenates and mild 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity. Taken together; these results demonstrate that XZW exerts neuroprotective effects against oxidative, excitotoxic, or $A_{\beta(25-35)}$-induced neuronal damage. These findings may provide pharmacological basis for its clinical usage treating the sequelae caused by cerebral thrombosis. Furthermore, XZW may exert beneficial effects on Alzheimer's disease and other oxidative stress-related neurodegenerative disorders.

Nitric Oxide Modulation of GABAergic Synaptic Transmission in Mechanically Isolated Rat Auditory Cortical Neurons

  • Lee, Jong-Ju
    • The Korean Journal of Physiology and Pharmacology
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    • 제13권6호
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    • pp.461-467
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    • 2009
  • The auditory cortex (A1) encodes the acquired significance of sound for the perception and interpretation of sound. Nitric oxide (NO) is a gas molecule with free radical properties that functions as a transmitter molecule and can alter neural activity without direct synaptic connections. We used whole-cell recordings under voltage clamp to investigate the effect of NO on spontaneous GABAergic synaptic transmission in mechanically isolated rat auditory cortical neurons preserving functional presynaptic nerve terminals. GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) in the A1 were completely blocked by bicuculline. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), reduced the GABAergic sIPSC frequency without affecting the mean current amplitude. The SNAP-induced inhibition of sIPSC frequency was mimicked by 8-bromoguanosine cyclic 3',5'-monophosphate, a membrane permeable cyclic-GMP analogue, and blocked by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger. Blockade of presynaptic $K^+$ channels by 4-aminopyridine, a $K^+$ channel blocker, increased the frequencies of GABAergic sIPSCs, but did not affect the inhibitory effects of SNAP. However, blocking of presynaptic $Ca^{2+}$ channels by $Cd^{2+}$, a general voltage-dependent $Ca^{2+}$ channel blocker, decreased the frequencies of GABAergic sIPSCs, and blocked SNAP-induced reduction of sIPSC frequency. These findings suggest that NO inhibits spontaneous GABA release by activation of cGMP-dependent signaling and inhibition of presynaptic $Ca^{2+}$ channels in the presynaptic nerve terminals of A1 neurons.

Cytoprotective Effects of Dihydrolipoic Acid and Lipoic Acid on the Oxidative Stress in Cultured Rat Cortical Neurons

  • Kim, Won-Ki
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권4호
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    • pp.427-433
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    • 1998
  • In brain hypoxic-ischemia, an excess release of glutamate and a marked production of reactive oxygen species (ROS) occur in neuronal and non-neuronal cells. The present study investigated the effect of the biological antioxidants dihydrolipoic acid (DHLA) and lipoic acid (LA) on N-methyl-D-aspartate (NMDA)- and ROS-induced neurotoxicity in cultured rat cortical neurons. DHLA enhanced NMDA-evoked rises in intracellular calcium concentration ($[Ca^{2+}]_i$). In contrast, LA did not alter the NMDA-evoked calcium responses but decreased after a brief treatment of dithiothreitol (DTT), which possesses a strong reducing potential. Despite the modulation of NMDA receptor-mediated rises in $[Ca^{2+}]_i$, neither DHLA nor LA altered the NMDA receptor-mediated neurotoxicity, as assessed by measuring the amount of lactate dehydrogenase released from dead or injured cells. DHLA, but not LA, prevented the neurotoxicity induced by xanthine/xanthine oxidase-generated superoxide radicals. Both DHLA and LA decreased the glutathione depletion-induced neurotoxicity. The present data may indicate that biological antioxidants DHLA and LA protect neurons from ischemic injuries via scavenging oxygen free radicals rather than modulating the redox modulatory site(s) of NMDA receptor.

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