• 제목/요약/키워드: Cortical neurons

검색결과 140건 처리시간 0.031초

Developmental Anomalies of Central Nervous System in Human

  • Chi, Je G.
    • Toxicological Research
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    • 제17권
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    • pp.11-16
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    • 2001
  • The development of the central nervous system is a continuous process during the embryonic and fetal periods. For a better understanding of congenital anomalies of central nervous system, three major events of normal development, i.e., neurulation (3 to 4 weeks), brain vesicle formation (4 to 7 weeks) and mantle formation (over 8 weeks) should be kept in mind. The first category of anomalies is neural tube defect. Neural tube defects encompass all the anomalies arise in completion of neurulation. The second category of central nervous system anomalies is disorders of brain vesicle formation. This is anomaly that applies for "the face predicts the brain". Holoprosencephaly covers a spectrum of anomalies of intracranial and midfacial development which result from incomplete development and septation of midline structures within the forebrain or prosencephalon. The last category of central nervous system malformation is disorders involving the process of mantle formation. In the human, neurons are generated in two bursts, the first from 8 to 10 weeks and next from 12 to 14 weeks. By 16 weeks, most of the neurons have been generated and have started their migration into the cortex. Mechanism of migration disorders are multifactorial. Abnormal migration into the cortex, abnormal neurons, faulty neural growth within the cortex, unstable pial-glial border, degeneration of neurons, neural death by exogenous factors are some of the proposed mechanism. Agyria-pachygyria are characterized by a four-layerd cortex. Polymicrogyria is gyri that are too numerous and too small, and is morphologically heterogeneous. Cortical dysplasia is characterized by the presence Q[ abnormal neurons and glia arranged abnormally in focal areas of the cerebral cortex. Neuroglial malformative lesions associated with medically intractable epilepsy are hamartia or hamartoma, focal cortical dysplasia and microdysgenesis.ysgenesis.

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과산화수소수로 유도된 배양신경세포손상에 대한 참죽나무잎 추출물의 보호효과 (Extract of Cedrela sinensis Leaves Protects Neuronal Cell Damage Induced by Hydrogen Peroxide in Cultured Rat Neurons)

  • 이순복;김주연;조순옥;반주연;주현수;배기환;성연희
    • 한국약용작물학회지
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    • 제15권6호
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    • pp.444-450
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    • 2007
  • Dried leaves from Cedrela sinensis A. Juss. (CS), have been observed to possess various pharmacological activity and contain various antioxidant constituents. The protective effect of ethanol extract of CS on hydrogen peroxide $(H_2O_2)-induced$ neurotoxicity was examined using primary cultured rat cortical neurons in the present study. Exposure of cultured neurons to 100 ${\mu}M\;H_2O_2$ caused a significant neuronal death as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. The addition of CS, over a concentration range of 10 to $50{\mu}g/m{\ell}$, concentration-dependently prevented the $H_2O_2-induced$ neuronal apoptotic death. CS $(50{\mu}g/m{\ell})$ significantly inhibited $H_2O_2-induced$ elevation of the cytosolic $Ca^{2+}$ concentration $([Ca^{2+}]_c)$, which was measured by a fluorescent dye, Fluo-4 AM. CS (30 and $50{\mu}g/m{\ell})$ inhibited glutamate release and generation of reactive oxygen species (ROS) induced by $100{\mu}M\;H_2O_2$. These results suggest that CS may mitigate the $H_2O_2-induced$ neurotoxiciy by interfering with the increase of $[Ca^{2+}]_c$, and then inhibiting glutamate release and generation of ROS in cultured neurons.

배양한 흰쥐 대뇌신경세포에서 신경미세섬유 3(NF-M)의 발생학적 표현 (Developmental Expression of Neurofilament 3 (NF-M) in the Cultured Rat Cortical Neurons)

  • 정재섭;조선정;진익렬;정승현;문일수
    • 생명과학회지
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    • 제15권4호
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    • pp.600-606
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    • 2005
  • 신경미세섬유(neurofilament, NF) 단백질은 신경세포의 주된 중간세사로서, NF-L (61 kDa), NF-M (90 kDa) 및 NF-H (115 kDa) 단백질의 공동중합체로 구성된다. 신경세사섬유는 신경세포의 성장, 구성, 형태 및 가소성에 중요한 역할을 하지만 발생학적 표현에 대하여는 아직 잘 알려지지 않았다. 본 연구에서는 NF-M에 특이한 항체를 제조하여 배양한 대뇌신경세포에서 NF-M의 표현을 조사하였다. 배양 12 및 24시간 세포에서 NF-M은 축삭과 그 성장추 그리고 축삭에 가까운 세포체에 강하게 표현하였다. 배양 4 및 14일 신경세포를 NF-M과 PSD95 항체로 이중염색한 결과 NF-M은 축삭과 가지돌기에 공히 강하게 표현되었으며, PSD95와 같이 위치할 경우에는 점박이로 나타났다. .면역염색에서도 NF-M이 PSD 분획에서 검출되었는데, 따라서 이 점박이는 가지돌기가시임을 시사한다. 본 연구의 결과는 NF-M이 신경세포의 초기 형태발달과정에서 축삭으로 강하게 몰려가며, 성숙한 신경세포에서는 가지돌기 및 가지돌기가시에도 위치하여 특정기능을 수행함을 시사한다.

확률적 신경망 모델에서 느린 금지뉴런의 역할 (The Role of Slow Inhibitory Neurons in a Stochastic Neural Network Model with IF Neurons)

  • C.J. Park;In Sun Shin;Kwang Suk Park
    • 대한의용생체공학회:의공학회지
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    • 제23권4호
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    • pp.329-332
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    • 2002
  • 일반적으로 금지뉴런의 효과는 신경망을 안정시킨다고 알려져 있다. 본 연구에서는 확률적 평균 필드 이론에 근거한 신경망 모델에서 느린 금지뉴런의 역할을 살펴보았다. 흥분뉴런과 빠른 금지뉴런으로 구성된 신경망에 느린 금지뉴런을 더하면, 느린 금지 뉴런이 없는 모델에서보다 매우 낮은 역치에서 안정적인 동시적 활동이 유도된다는 것을 발견하였다. 이 역치는 대뇌 피질 신경의 생리학적 역치와 일치하며. 느린 금지 뉴런만이 신경망에 낮은 발화율과 낮은 역치를 유지시키는 네거티브 피드백을 줄 수 있다.

Methanol Extract of Paeonia Japonica Root Protects Cultured Rat Cortical Neurons Against Oxidative Damage Induced by Hydrogen Peroxide

  • Park, Min-Su;Ban, Ju-Yeon;Lee, Ju-Hyun;Song, Kyung-Sik;Seong, Yeon-Hee
    • 한국약용작물학회지
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    • 제14권2호
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    • pp.70-76
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    • 2006
  • Paeoniae radix has been widely used for its anti-allergic, anti-inflammatory and analgesic effects, and demonstrated to have anticonvulsant, memory enhancing and anxiolytic activities. The present study was performed to examine the protective effect of methanol extract of Paeoniae radix (PR) from Paeoniae Japonica Miyabe et Takeda (Paeoniaceae) on hydrogen peroxide $(H_2O_2)-induced$ neurotoxicity using cultured rat cerebral cortical neuron. $H_2O_2$ produced a concentration-dependent reduction of neuronal viability, PR, over a concentration range of 10 to $100\;{\mu}g/ml$ showed concentration-dependent decrease of the $H_2O_2$$(100\;{\mu}M)-induced$ neuronal cell death, as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-di-phenyl-tetrazolium bromide assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. PR $(100\;{\mu}g/ml$ inhibited $100\;{\mu}M$ $H_2O_2-induced$ elevation of the cytosolic $Ca^{2+}$ concentration $([Ca^{2+}]_c)$, which was measured by a fluorescent dye, flue-4 AM. PR $(50\;{\mu}g/ml$ inhibited glutamate release into medium induced by $100\;{\mu}M$ $H_2O_2$, which was measured by HPLC, and generation of reactive oxygen species (ROS). These results suggest that PR may mitigate the $H_2O_2-induced$ neurotoxiciy by interfering with the increase of $[Ca^{2+}]_c$, and then inhibiting glutamate release and generation of ROS in cultured neurons.

Dehydroevodiamine·HCl enhances cognitive function in memory-impaired rat models

  • Shin, Ki Young;Kim, Ka Young;Suh, Yoo-Hun
    • The Korean Journal of Physiology and Pharmacology
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    • 제21권1호
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    • pp.55-64
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    • 2017
  • Progressive memory impairment such as that associated with depression, stroke, and Alzheimer's disease (AD) can interfere with daily life. In particular, AD, which is a progressive neurodegenerative disorder, prominently features a memory and learning impairment that is related to changes in acetylcholine and abnormal ${\beta}$-amyloid ($A{\beta}$) deposition in the brain. In the present study, we investigated the effects of dehydroevodiamine HCl (DHED) on cognitive improvement and the related mechanism in memory-impaired rat models, namely, a scopolamine-induced amnesia model and a $A{\beta}_{1-42}$-infused model. The cognitive effects of DHED were measured using a water maze test and a passive avoidance test in the memory-impaired rat models. The results demonstrate that DHED (10 mg/kg, p.o.) and Donepezil (1 mg/kg, p.o.) ameliorated the spatial memory impairment in the scopolamine-induced amnestic rats. Moreover, DHED significantly improved learning and memory in the $A{\beta}_{1-42}$-infused rat model. Furthermore, the mechanism of these behavioral effects of DHED was investigated using a cell viability assay, reactive oxygen species (ROS) measurement, and intracellular calcium measurement in primary cortical neurons. DHED reduced neurotoxicity and the production of $A{\beta}$-induced ROS in primary cortical neurons. In addition, similar to the effect of MK801, DHED decreased intracellular calcium levels in primary cortical neurons. Our results suggest that DHED has strong protective effects against cognitive impairments through its antioxidant activity and inhibition of neurotoxicity and intracellular calcium. Thus, DHED may be an important therapeutic agent for memory-impaired symptoms.