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      In vivo imaging of spontaneous ultraweak photon emission from a rat’s brain correlated with cerebral energy metabolism and oxidative stress

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          Abstract

          Living cells spontaneously emit ultraweak light during the process of metabolic reactions associated with the physiological state. The first demonstration of two-dimensional in vivo imaging of ultraweak photon emission from a rat's brain, using a highly sensitive photon counting apparatus, is reported in this paper. It was found that the emission intensity correlates with the electroencephalographic activity that was measured on the cortical surface and this intensity is associated with the cerebral blood flow and hyperoxia. To clarify the mechanism of photon emission, intensity changes from whole brain slices were examined under various conditions. The removal of glucose from the incubation medium suppressed the photon emission, and adding 50 mM potassium ions led to temporal enhancement of emission and subsequent depression. Rotenone (20 microM), an inhibitor of the mitochondrial electron transport chain, increased photon emission, indicating electron leakage from the respiratory chain. These results suggest that the photon emission from the brain slices originates from the energy metabolism of the inner mitochondrial respiratory chain through the production of reactive oxygen. Imaging of ultraweak photon emission from a brain constitutes a novel method, with the potential to extract pathophysiological information associated with neural metabolism and oxidative dysfunction of the neural cells.

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          Most cited references30

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          Oxidative stress, glutamate, and neurodegenerative disorders

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            Reversal of long-term potentiation (depotentiation) induced by tetanus stimulation of the input to CA1 neurons of guinea pig hippocampal slices.

            The reduction of the long-term potentiated response induced by tetanus (depotentiation (DP) of LTP) was investigated by the delivery of a train of low-frequency afferent stimuli (depotentiating stimulation: DPS) after the tetanus (100 Hz, 100 pulses) in CA1 neurons of the guinea pig's hippocampal slice. The parameters of DPS (frequencies of 1, 2, 5 and 10 Hz; number of pulses of 200 and 1000; and the time-lag after tetanus of 20 and 100 min) were altered systematically and their effects on LTP were evaluated through the analysis of the slope of field EPSP (S-EPSP) and amplitude and peak latency of population spike (A- and L-PS). DPS of 1 Hz, 1000 pulses, given 20 min after tetanus, reduced the potentiated component of S-EPSP, A-PS and L-PS by 68.5%, 80.1% and 56.1%, respectively (mean, n = 6), whereas it reduced the control response by 4.3%, 7.1%, and 1.9%, respectively (n = 6). Significantly less effectiveness was observed for DPS at higher frequencies (2-10 Hz), with smaller numbers of pulses, featuring a longer time-lag after tetanus and under APV administration. When DPS was applied before tetanus, significantly less robust LTP was observed. However, these effects were blocked by the administration of APV during DPS.
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              Organ chemiluminescence: noninvasive assay for oxidative radical reactions.

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                Author and article information

                Journal
                Neuroscience Research
                Neuroscience Research
                Elsevier BV
                01680102
                July 1999
                July 1999
                : 34
                : 2
                : 103-113
                Article
                10.1016/S0168-0102(99)00040-1
                10498336
                060002fa-d083-4d93-bc9d-7b365f2d775e
                © 1999

                https://www.elsevier.com/tdm/userlicense/1.0/

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