• Title, Summary, Keyword: 도파민성 신경원

Search Result 7, Processing Time 0.037 seconds

A Study on Acupuncture-generated Blood-Oxygen-Level Dependant Signals in Substantia Nigra and Other Areas in Extrapyramidal Tract (대뇌흑질과 추체외로에서 자침에 의한 BOLD 신호)

  • Choe, Il-Hwan;Park, Hi-Joon;Yoon, Hyo-Woon;Shin, Hyung-Chul;Lee, Sang-Hoon;Lee, Yun-Ho;Lim, Sabina
    • Journal of Acupuncture Research
    • /
    • v.25 no.1
    • /
    • pp.211-219
    • /
    • 2008
  • 목적 : 전통적으로 태충($LR_3$)과 양릉천($GB_{34}$)은 운동기능과 관련된 질환에 사용되어 왔다. 우리는 두뇌에 신경독을 주입하여 파킨슨병 쥐모델을 제작하였고, 쥐는 운동기능이 손상되고 도파민성 신경세포가 선택적으로 소멸하였다. 병증 모델 쥐에게 태충과 양릉천에 자침한 결과 운동기능이 개선되고 신경세포보호효과가 나타남을 관찰한 바 있다. 이에 실제로 태충과 양릉천에 자침하여 운동기능과 관련된 추체외로 영역에서 신경의 활성화가 나타나는지를 fMRI를 통하여 관찰하였다. 방법 : 자침은 수기침을 선택하였으며, 혈위는 (1) 태충, (2) 양릉천, (3) 태충+양릉천의 세군데를 설정하였고, 자침에 대한 대조자극으로 피부자극을 채택하였다. fMRI 스캐너는 3T를 사용하였고 뇌신경 활성화의 신호는 BOLD(blood-oxygen-level dependant)를 관찰하였다. 두뇌에서 관찰부위는 중뇌를 중심으로 추체외로로 한정하였다. 결과 : 태충에 자침하였을 때 두뇌의 substantia nigra, subthalamic nucleus, red nucleus, pons 등이 활성화 되었다. 양릉천에 자침하였을 때 substantia nigra, subthalamic nucleus, caudate nucleus, thalamus가 활성화 되었다. 태충과 양릉천에 동시에 자침하였을 때는 substantia nigra, subthalamic nucleus, red nucleus, globus pallidus가 활성화되었다. 대조자극에 의해서는 위의 영역들이 활성화되지 않았다. 결론 : 태충, 양릉천, 태충+양릉천 자극은 대뇌에서 추체외로 영역을 활성화시키며 특히 substantia nigra의 활성화는 파킨슨병과 같은 질환의 조절가능성을 시사한다.

  • PDF

Effects of Treadmill Exercise on Alpha-synuclein Mutation and Activated Neurotrophins in Nigrostriatal Region of MPTP-induced Parkinson Models (MPTP 파킨슨 모델의 트레드밀 운동이 알파시누크린 변성과 흑질선조체내 신경성장인자 활성화에 미치는 영향)

  • Park, Jae-Sung;Kim, Jeong-Hwan;Yoon, Sung-Jin
    • Journal of Korean Medicine Rehabilitation
    • /
    • v.19 no.2
    • /
    • pp.73-88
    • /
    • 2009
  • Objectives : Neuronal changes that result from treadmill exercise for patients with Parkinson's disease(PD) have not been well documented, although some clinical and laboratory reports suggest that regular exercise may produce a neuroprotective effect and restore dopaminergic and motor functions. However, it is not clear if the improvements are due to neuronal alterations within the affected nigrostriatal region or result from a more general effect of exercise on affect areas and motivation. In this study, we demonstrate that motorized treadmill exercise improves the neuronal outcomes in rodent models of PD. Methods : We used a chronic mouse model of parkinsonism, which was induced by injecting male C57BL/6 mice with 10 doses(Every 12 hour) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (30 mg/kg) and probenecid (20 mg/kg) over 5 days. These mice were able to sustain an exercise training program on a motorized rodent treadmill at a speed of 18 m/min, $0^{\circ}$ of inclination, 40 min/day, 5 days/week for 4 weeks. At the end of exercise training, we extracted the brain and compared their neuronal and neurochemical changes with the control(saline and sedentary) mice groups. Synphilin protein is the substance that manifestly reacts with ${\alpha}$-synuclein. In this study, we used Synphilin as a manifest sign of recovery from neurodegeneration. We analyze the brain stems of the substantia nigra and striatum region using the western blotting technique. Results : There were no expression of synphilin in the saline-induced groups. The addition of MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) greatly accelerated synphilin expression which meant an aggregation of ${\alpha}$-synuclein. But, the MPTP-induced treadmill exercise group showed significantly lower expression than the MPTP-induced sedentary group. This means treadmill exercise has a definite effect on the decrease of ${\alpha}$-synuclein aggregation. Conclusions : In this study, our results suggest that treadmill exercise promoted the removal of the aggregation of ${\alpha}$-synuclein, resulting in protection against disease development and blocks the apoptotic process in the chronic parkinsonian mice brain with severe neurodegeneration.

Protective Effects of Quercetin-3-O-glucuronide against 1-methyl-4-phenylpyridinium-induced Neurotoxicity (1-methyl-4-phenylpyridinium으로 유도된 신경 손상에 대한 quercetin-3-O-glucuronide의 보호 효과)

  • Pariyar, Ramesh;Bastola, Tonking;Seo, Jungwon
    • Journal of Life Science
    • /
    • v.29 no.2
    • /
    • pp.191-197
    • /
    • 2019
  • Parkinson's disease (PD) is a progressive neurodegenerative disease that mainly affects motor system with clinical features such as bradykinesia, rigidity, tremor and abnormal posture. PD is characterized by the death of dopaminergic neurons in the substantia nigra pars compacta, which is associated with accumulation of oxidative stress and dysregulation of intracellular signaling pathway. Quercetin-3-O-glucuronide (Q3GA), a major metabolite of quercetin, has been reported to have neuroprotective effects. In this study, we examined the neuroprotective effect of Q3GA against 1-methyl-4-phenyl pyridinium ($MPP^+$)-induced neurotoxicity of PD and the underlying molecular mechanisms in SH-SY5Y cells. MTT and LDH assay showed that Q3GA significantly decreased $MPP^+$-induced cell death, which is accompanied by a reduction in poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore, it attenuated $MPP^+$-induced intracellular reactive oxygen species (ROS) with the reduction of Bax/ Bcl-2 ratio. Moreover, Q3GA significantly increased the phosphorylation of Akt and cAMP response element binding protein (CREB), but it has no effects on the phosphorylation of extracellular signal-regulated kinase (ERK). Taken together, these results demonstrate that Q3GA significantly attenuates $MPP^+$-induced neurotoxicity through ROS reduction and Akt/CREB signaling pathway in SH-SY5Y cells. Our findings suggest that Q3GA might be one of the potential candidates for the prevention and/or treatment of PD.

A clinical report of a patient with Tourett's disorder (뚜렛 장애(Tourett's disorder) 환자(患者) 1례(例)에 대한 증례보고(症例報告))

  • Sung, Woo-Yong;Lee, Seung-Hyun;Son, Ji-Hyung;Han, Seung-Hea;Jung, Hyo-Chang
    • Journal of Oriental Neuropsychiatry
    • /
    • v.14 no.2
    • /
    • pp.213-218
    • /
    • 2003
  • This is a case report of a patient with Tourett's disorder treated by Ukgan-san. We evaluated the patient Tourett's disorder by behavior and sound. His tic behaviors like eye blinking, shoulder shrugging, head jerking, facial frimace have been shown frequently, and His phonic tic symptoms like coughing, throat clearing, sniffing have been presented frequently, too. We diagnosed his condition as Wind-syndrome Caused by Hyperactivity of Liver-yang by patient's redish face, taut pulse, Left umbilical throb. So we treated the patient with Ukgan-san. and the score of Yale Global Tic Severity Scale(YGTSS) was 30 at the start of treatment. and the score of YGTSS was 3 at the end. We found that Ukgan-san was effective for the patient with Tourett's disorder.

  • PDF

Metabolic Topography of Parkinsonism

  • Kim, Jae-Seung
    • Nuclear Medicine and Molecular Imaging
    • /
    • v.41 no.2
    • /
    • pp.141-151
    • /
    • 2007
  • Parkinson's disease is one of the most frequent neurodegenerative diseases, which mainly affects the elderly. Parkinson's disease is often difficult to differentiate from atypical parkinson diorder such as progressive supranuclear palsy, multiple system atrophy, dementia with Lewy body, and corticobasal ganglionic degeneration, based on the clinical findings because of the similarity of phenotypes and lack of diagnostic markers. The accurate diagnosis of Parkinson's disease and atypical Parkinson disorders is not only important for deciding on treatment regimens and providing prognosis, but also it is critical for studies designed to investigate etiology and pathogenesis of parkinsonism and to develop new therapeutic strategies. Although degeneration of the nigrostriatal dopamine system results in marked loss of striatal dopamine content in most of the diseases causing parkinsonism, pathologic studies revealed different topographies of the neuronal cell loss in Parkisonism. Since the regional cerebral glucose metabolism is a marker of integrated local synaptic activity and as such is sensitive to both direct neuronal/synaptic damage and secondary functional disruption at synapses distant from the primary site of pathology, an assessment of the regional cerebral glucose metabolism with F-18 FDG PET is useful in the differential diagnosis of parkinsonism and evaluating the pathophysiology of parkisonism.

Neural Circuits Mediating Stress (스트레스의 신경생물학적 이해)

  • Yu, Bum-Hee;Woo, Jong-Min
    • Korean Journal of Psychosomatic Medicine
    • /
    • v.9 no.1
    • /
    • pp.81-92
    • /
    • 2001
  • Stress has been linked to the pathophysiology and pathogenesis of various psychiatric illnesses. Over the past few years, our understanding of the brain and neuroendocrine systems that are linked to stress responses has increased enormously. This article reviews a series of animal and human studies to understand what are the central pathways by which stress is perceived, processed, and transduced into a neuroendocrine response. We focus on the limbic-hypothalamic-pituitary-adrenal(LHPA) axis and several neurotransmitter systems such as norepinephrine, CRF, serotonin, acetylcholine, and dopamine. LHPA stress circuit is a complex system with multiple control mechanisms which are altered in pathological states. CRF and related peptides in the central nervous system appear to enhance behavioral responses to stressors. Norepinephrine systems are also activated by stressors and cause the release of catecholamines from the autonomic nervous system. CRF-norepinephrine interaction makes a feed-forward system which may be important for an organism to mobilize not only the pituitary system but also the central nervous system, in response to environmental challenges. The interactions among several neurotransmitters and endocrine systems appear to play key roles in mediating various behavioral and psychological stress responses involving abnormal responses to stressors such as anxiety and affective disorders.

  • PDF

Brain Regions Associated With Anhedonia in Healthy Adults : a PET Correlation Study (정상 성인에서 양전자방출단층촬영을 통해 관찰한 무쾌감증 관련 뇌 영역)

  • Jung, Young-Chul;Seok, Jeong-Ho;Chun, Ji-Won;Park, Hae-Jeong;Lee, Jong-Doo;Kim, Jae-Jin
    • The Korean Journal of Nuclear Medicine
    • /
    • v.39 no.6
    • /
    • pp.438-444
    • /
    • 2005
  • Purpose: Anhedonia has been proposed to be the result of a basic neurophysiologic dysfunction and a vulnerability marker that precede and contribute to the liability of developing schizophrenia. We hypothesized that anhedonia, as a construct reflecting the decreased capacity to experience pleasure, should be associated with decreased positive hedonic affect trait. This study examined the relationship between anhedonia and positive hedonic affect trait and searched for the brain legions which correlate with anhedonia in normal subjects. Materials and Methods: Using $^{18}F$-FDG PET scan, we investigated the brain activity of twenty one subjects during resting state. Questionnaires were administrated after the scan in order to assess the self-rated individual differences in physical/social anhedonia and positive/negative affect traits. Results: Negative correlation between physical anhedonia score and positive affect trait score was significant (Pearson coefficient =-0.440, p<0.05). The subjects physical and social anhedonia scores showed positive correlation with metabolic rates in the cerebellum and negative correlation with metabolic rates in the inferior temporal gyrus and middie frontal gyrus. In addition, the positive affect trait score positively correlated with various areas, most prominent with the inferior temporal gyrus. Conclusion: These results suggest that neural substrates, such as the inferior temporal gyrus and prefrontal-cerebellar circuit, which dysfunction has been proposed to be involved with the cognitive deficits of schizophrenia, may also play a significant role in the liability of affective deficits like anhedonia.