• Title/Summary/Keyword: Developmental Cerebral cortex

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THE SINGLE PHOTON EMISSION COMPUTED TOMOGRAPHY FINDINGS IN DEVELOPMENTAL LANGUAGE DISORDERS (발달성언어장애아(發達性言語障碍兒)의 단일광자방출전산화단층촬영(單一光子防出電算化斷層撮影) 소견(所見)에 관한 연구)

  • Park, Jin-Seng;Cho, Soo-Churl;Lee, Myung-Chul
    • Journal of the Korean Academy of Child and Adolescent Psychiatry
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    • v.3 no.1
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    • pp.46-55
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    • 1992
  • The pathophysiology of developmental language disorder is a highly controversial matter. In order to investigate the neural mechanisms involved in developmental language disorders, the authors studied three dimensional regional cerebral blood flow(rCBF) using Tc-99mH-MPAO in 42 children with developmental language disorders. The results are summarized as follows : 1) 61.9% (26/42) of this series revealed decreased perfusion in SPECT. 2) Regions of hypoperfusion were seen in cerebral cortex(47.6%, 20/42), thalamus(33.3%, 14/42), basal ganglia(11.9%, 5/42) and cerebellum(7.1%, 3/42). This study suggests that developmental language disorder could be due to specific functional impairment of the local brain regions which could not detected by conventional investigations such as brain CT or EEG.

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Effects of Melatonin on Improvement of Neurological Function in Focal Cerebral Ischemic Rats

  • Lee, Seung-Hoon;Shin, Jin-Hee;Lee, Min-Kyung;Lee, Sang-Kil;Lee, Sang-Rae;Chang, Kyu-Tae;Hong, Yong-Geun
    • Reproductive and Developmental Biology
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    • v.35 no.2
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    • pp.167-174
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    • 2011
  • Acute ischemic stroke results from sudden decrease or loss of blood supply to an area of the brain, resulting in a coinciding loss of neurological function. The antioxidant action of melatonin is an important mechanism among its known effects to protective activity during ischemic/reperfusion injury. The focus of this research, therapeutic efficacy of melatonin on recovery of neurological function following long term treatment in ischemic brain injured rats. Male Sprague-Dawley rats (n=40; 8 weeks old) were divided into the control group, and MCAo groups (Vehicle, MT7 : MCAo+ melatonin injection at 7:00, MT19 : MCAo+melatonin injection at 19:00, and MT7,19 : MCAo+melatonin injection at 7:00 and 19:00). Rat body weight and neurological function were measured every week for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of zoletil (40 mg/kg) and xylazine (10 mg/kg) and sacrificed for further analysis. Tissues were then collected for RNA isolation from brain tissue. Also, brain tissues were analyzed by histological procedures. We elucidated that melatonin was not toxic in vital organs. MT7,19 was the most rapidly got back to mild symptom on test of neurological parameter. Also, exogenous melatonin induces both the down-regulation of detrimental genes, such as NOSs and the up-regulation of beneficial gene, including BDNF during long term administration after focal cerebral ischemia. Melatonin treatment reduced the loss of primary motor cortex. Therefore, we suggest that melatonin could be act as prophylactic as well as therapeutic agent for neurorehabilitative intervention.

Evidence for the Drp1-dependent Mitochondrial Fission in the Axon of the Rat Cerebral Cortex Neurons (흰쥐 대뇌 피질 신경세포의 축삭에서 Drp1 의존적 미토콘드리아의 분열)

  • Cho, Bong-Ki;Lee, Seung-Bok;Sun, Woong;Kim, Young-Hwa
    • Applied Microscopy
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    • v.41 no.4
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    • pp.249-255
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    • 2011
  • Neurons utilize a large quantity of energy for their survival and function, and thereby require active mitochondrial function. Mitochondrial morphology shows dynamic changes, depending on the cellular condition, and mitochondrial dynamics are required for neuronal development and function. In this study, we found that the length of mitochondria in the distal axon is significantly shorter than that of mitochondria in dendrites or proximal axons of cerebral cortical neurons, and the reason for this difference is the local fission within the axon. We also found that suppression of Drp1, a key regulator of mitochondrial fission, resulted in significant elongation of mitochondria in axons. Collectively, these results suggest that local mitochondrial fission within the axon contributes to region-dependent mitochondrial length differences in the axons of cortical neurons.