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- 발행기관 : Published on behalf of the European Neuroscience A (검색결과 4 건)
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Ham, Byung-Joo,Chey, Jeanyung,Yoon, Sujung J.,Sung, Younghoon,Jeong, Do-Un,Ju Kim, Seog,Sim, Minyoung E.,Choi, Namhee,Choi, Ihn-Geun,Renshaw, Perry F.,Lyoo, In Kyoon Published on behalf of the European Neuroscience A 2007 The European journal of neuroscience Vol.25 No.1
<P>Abstract</P><P>The purpose of this study was to investigate the concentration of <I>N</I>-acetyl-aspartate (NAA) in the brain and its relationship with clinical characteristics in patients with post-traumatic stress disorder (PTSD). Proton magnetic resonance spectroscopy was performed in order to measure NAA concentrations in the anterior cingulate cortex (ACC) and bilateral hippocampus in 26 subjects with fire-related PTSD, who were survivors of a subway fire in South Korea, and 25 age- and sex-matched healthy comparison subjects. There were decreased NAA levels in the ACC (<I>t</I> = −3.88, d.f. = 49, <I>P</I> < 0.001) and bilateral hippocampus (right, <I>t</I> = −3.88, d.f. = 49, <I>P</I> < 0.001; left, <I>t</I> = −3.62, d.f. = 49, <I>P</I> < 0.001) in the PTSD group relative to the healthy comparison group. Also, NAA levels of the ACC (<I>r = –</I>0.43, <I>n</I> = 26, <I>P</I> = 0.027) and bilateral hippocampus (right, <I>r = –</I>0.48, <I>n</I> = 26, <I>P</I> = 0.013; left, <I>r</I> = −0.40, <I>n</I> = 26, <I>P</I> = 0.04) were negatively correlated with re-experience symptom scores in subjects with PTSD. In conclusion, our findings suggest that subjects with PTSD had decreased neuronal viabilities in the ACC and bilateral hippocampus, and that these deficits may play an important role in the pathophysiology of PTSD, especially regarding the re-experiencing of traumatic events.</P>
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Transient receptor potential A1 mediates acetaldehyde-evoked pain sensation
Bang, Sangsu,Kim, Kyung Yoon,Yoo, Sungjae,Kim, Yoon Gyoon,Hwang, Sun Wook Published on behalf of the European Neuroscience A 2007 The European journal of neuroscience Vol.26 No.9
<P>Abstract</P><P>Six transient receptor potential (TRP) ion channels expressed in the sensory afferents play an important role as body thermosensors and also as peripheral pain detectors. It is known that a number of natural compounds specifically activate those sensory neuronal TRP channels, and a well-known example is cinnamaldehyde for TRPA1. Here we show that human and mouse TRPA1 are activated by acetaldehyde, an intermediate substance of ethanol metabolism, in the HEK293T cell heterologous expression system and in cultured mouse trigeminal neurons. Acetaldehyde failed to activate other temperature-sensitive TRP channels expressed in sensory neurons. TRPA1 antagonists camphor and gadolinium, and a general TRP blocker ruthenium red inhibited TRPA1 activation by acetaldehyde. Camphor, gadolinium and ruthenium red also suppressed the acute nociceptive behaviors induced by the intradermal administration of acetaldehyde into the mouse footpads. Intradermal co-application of prostaglandin E2 and acetaldehyde greatly potentiated the acetaldehyde-induced nociceptive responses, and this effect was reversed by treatment with the TRPA1 antagonist camphor. These results suggest that acetaldehyde causes nociception via TRPA1 activation. Our data may also help elucidate the mechanisms underlying acetaldehyde-related pathological symptoms such as hangover pain.</P>
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Impairment of microtubule-dependent trafficking by overexpression of alpha-synuclein.
Lee, He-Jin,Khoshaghideh, Farnaz,Lee, Stephen,Lee, Seung-Jae Published on behalf of the European Neuroscience A 2006 The European journal of neuroscience Vol.24 No.11
<P>Abnormal accumulation of alpha-synuclein (alpha-syn) has been linked to several neurological disorders, including Parkinson's disease (PD). However, the underlying mechanism by which alpha-syn accumulation affects neuronal function and survival remains unknown. Here, we provide data suggesting a possible effect of aggregated alpha-syn on the microtubule (MT) network. Consistent with the MT dysfunction, we also observed other degenerative changes, such as neuritic degeneration, trafficking defects, and Golgi fragmentation, which are common pathological features shared by many human neurodegenerative diseases. Neuritic degeneration and Golgi fragmentation were confirmed in primary cultures of dorsal root ganglia (DRG) neurons overexpressing alpha-syn. This effect of alpha-syn seems to have some selectivity to the MT system, as actin microfilaments and MT-independent trafficking remain unaffected. Within the degenerating neurites, we found numerous spherical co-aggregates of alpha-syn and tubulins, from which actin was excluded. These studies suggest that the MT system is a potential target of alpha-syn, and impairment of this system might have impacts on neuronal structure and function.</P>
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Bax-dependent and -independent death of motoneurons after facial nerve injury in adult mice
Park, Ok-hee,Lee, Kea Joo,Rhyu, Im Joo,Geum, Dongho,Kim, Hyun,Buss, Robert,Oppenheim, Ronald W.,Sun, Woong Published on behalf of the European Neuroscience A 2007 The European journal of neuroscience Vol.26 No.6
<P>Abstract</P><P>Nerve injury-induced neuronal death may occur after accidental trauma or nerve inflammation. Although the response to facial root avulsion has been examined in rodent models, there are conflicting results as to whether motoneuron (MN) death is mediated by apoptosis or necrosis. We examined the response of MNs and proximal nerves after facial nerve avulsion in adult mice. Following facial nerve avulsion in 4–5-week-old mice, we observed a progressive reduction of MNs such that by 4 weeks less than 10% of avulsed MNs remained compared with the control side. The profile of MN degeneration was distinct from axotomy-induced responses. For example, the onset of MN death was more rapid, and the extent of MN loss was greater compared with axotomy. Furthermore, the degeneration of oligodendrocytes and the activation of microglia were increased in the proximal nerve after avulsion. Ultrastructural observations suggested that root avulsion mainly induces non-apoptotic neuronal death, although a small subset of neurons appeared to die via apoptosis. To evaluate the contribution of apoptotic death, we evaluated MN responses in Bax-knockout (KO) mice in which neurons are rescued from apoptotic death. Surprisingly, although the majority of Bax-KO mice exhibited only a moderate MN loss after avulsion, a subset of Bax-KO mice (25%) exhibited extensive MN death and injury-induced changes in the nerve that were indistinguishable from events in wild-type littermates. These results suggest that both Bax-dependent and -independent forms of cell death are evoked by root avulsion, and that programmed cell death may be involved in triggering a robust necrotic response.</P>
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