کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9426720 | 1295932 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Interaction between tissue oxygen tension and NADH imaging during synaptic stimulation and hypoxia in rat hippocampal slices
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کلمات کلیدی
HSDaCSFfEPSPPO2P50fMRI - تصویرسازی تشدید مغناطیسی کارکردیfunctional magnetic resonance imaging - تصویرسازی تشدید مغناطیسی کارکردیOxygen tension - تنش اکسیژنSynaptic physiology - فیزیولوژی سیناپتیسartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیMetabolism - متابولیسم Mitochondria - میتوکندریاNADH - نادانHypoxia - هیپوکسیfield excitatory post-synaptic potential - پتانسیل پس از سیناپسی مزمن تحریک پذیر
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Oxygen and NADH are essential components in the production of ATP in the CNS. This study examined the dynamic interaction between tissue oxygen tension (pO2) and NADH imaging changes within hippocampal tissue slices, during metabolic stresses including hypoxia and synaptic activation. The initiation of abrupt hypoxia (from 95% O2 to 95% N2) caused a rapid decrease in pO2, onset of hypoxic spreading depression (hsd; at 6.7±1.3 mm Hg; n=15), and a monophasic increase in NADH. Provided that reoxygenation was prompt, synaptic responses, pO2 and NADH levels returned to baseline following hsd. Longer hypoxia caused irreversible neuronal dysfunction, an increase in pO2 beyond baseline (due to decreased tissue demand), and hyperoxidation of NADH (10±2% decrease below baseline; n=7). Synaptic activation in ambient 95% O2 caused a decrease or 'initial dip' in pO2 and a biphasic NADH response (oxidation followed by reduction). The oxidizing phase of the NADH response was mitochondrial as it was synchronous with the 'initial' dip in pO2. Following slow graded reductions in ambient oxygen levels to 8%, four of seven slices developed hsd following synaptic stimulation. The hypoxic threshold for graded oxygen reductions occurred at 7.9±5.8 mm Hg O2 (n=7). Our hypoxic threshold range (6.7-7.9 mm Hg O2 from abrupt and graded oxygen reduction, respectively) correlates well with reported in vivo values of <12 mm Hg O2. The major findings of this study include: 1) determination of the critical physiological threshold of pO2 (based upon hsd), which is a marker of imminent neuronal death if oxygen is not rapidly restored; 2) NADH hyperoxidation and an increase in pO2 beyond baseline levels following longer periods of hypoxia; and 3) the occurrence of a pO2 'dip' during synaptic stimulation, which correlates with the early oxidizing phase of the biphasic NADH response.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 132, Issue 3, 2005, Pages 645-657
Journal: Neuroscience - Volume 132, Issue 3, 2005, Pages 645-657
نویسندگان
K.A. Foster, C.J. Beaver, D.A. Turner,