Activation energy in the mammalian brain slice as determined by oxygen micro-electrode measurements.

Fujii, Takanori; Buerk, Donald G.; Whalen, William J.

doi:10.2170/jjphysiol.31.279

Cited by 12 publications

(14 citation statements)

References 5 publications

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“…Two processes affect the oxygen distribution in the tissue preparation: oxygen diffusion from the aCSF to the tissue, and tissue oxygen consumption. Usually the OC falls to zero at a depth of less than 250 m into the tissue (15,16). This diffusion depth is much smaller than the length and width of a typical tissue slice (several millimeters) used in tissue-preparation experiments.…”

Section: Mri Effects Of O 2 Dissolved In Water/tissuementioning

confidence: 99%

“…The tissue oxygen consumption is specified by the oxygen consumption rate (V O2 ). The OC distribution (C( x)) in the tissue and aCSF can be expressed as (15)(16)(17):…”

Section: Mri Effects Of O 2 Dissolved In Water/tissuementioning

confidence: 99%

“…1). D BT (ϭ1.54 ϫ 10 Ϫ5 cm 2 /s) is the diffusion coefficient of oxygen in tissue (15), C b is the OC in the uniform aCSF, 2 where D aCSF (ϭ2.48 ϫ 10 Ϫ5 cm 2 /s) is the diffusion coefficient of oxygen in aCSF (15)(16), d max ϭ ͌ 2D BT C 0 /V O2 is the maximum oxygen diffusion depth, and d DL (Ϸ0.20 mm) (15) (15) is the thickness of the aCSF diffusion layer between the uniform aCSF and the tissue.…”

Section: Mri Effects Of O 2 Dissolved In Water/tissuementioning

confidence: 99%

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Modeling oxygen effects in tissue‐preparation neuronal‐current MRI

Luo

Liu

Parris

et al. 2007

Magnetic Resonance in Med

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Tissue-preparation neuronal-current MRI (ncMRI) was recently developed to directly detect neuronal activity without hemodynamic contamination. However, as a paramagnetic substance, the oxygen molecules present in the tissue may also alter the ncMRI signal through relaxivity and susceptibility effects. To study the effects of oxygen on the ncMRI signal and estimate their impact on tissue-preparation experiments, oxygen-induced MRI signal changes were formulated as a function of oxygen concentration (OC) of gas, oxygen consumption rate, and imaging parameters. Under favorable conditions of these parameters, the maximum oxygen-induced signal magnitude and phase change were estimated to be 0.32% and 3.85°, respectively. Considering that the ncMRI signal changes obtained in previous tissue-preparation experiments (3-5% in magnitude, 0.8 -1.7°in phase) were tens or hundreds of times larger than the corresponding oxygen-induced signal changes (0.03% in magnitude, 0.03-0.07°in phase), it is concluded that the oxygen had negligible effects in the previous experiments. Magn Reson Med 58:407-412, 2007.

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Section: Mri Effects Of O 2 Dissolved In Water/tissuementioning

confidence: 99%

“…The tissue oxygen consumption is specified by the oxygen consumption rate (V O2 ). The OC distribution (C( x)) in the tissue and aCSF can be expressed as (15)(16)(17):…”

Section: Mri Effects Of O 2 Dissolved In Water/tissuementioning

confidence: 99%

Section: Mri Effects Of O 2 Dissolved In Water/tissuementioning

confidence: 99%

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Modeling oxygen effects in tissue‐preparation neuronal‐current MRI

Luo

Liu

Parris

et al. 2007

Magnetic Resonance in Med

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“…e have previously used our recessed oxygen microelectrode 12 to measure tissue Po 2 distributions in vivo in cat cortex 3 and have determined metabolic parameters in vitro from slices of cat cortex, 4 rat cortex, 36 and guinea pig olfactory cortex 7 by fitting curves of measured Po 2 gradients to mathematical models for oxygen consumption, including Michaelis-Menten kinetics. We have also determined local metabolic rates in vivo by measuring oxygen disappearance following total blood flow occlusion in extensive studies of the cat carotid body.…”

mentioning

confidence: 99%

Comparisons of oxygen metabolism and tissue PO2 in cortex and hippocampus of gerbil brain.

Nair¹,

Buerk²,

Halsey³

1987

Stroke

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Recessed oxygen microelectrodes (tip diameter < 2 (j.m) were positioned stereotactically into either the cerebral cortex or the hippocampus of sodium pentobarbital anesthetized gerbils (n = 21). The mean tissue P02 levels (± SEM) were not significantly different between cortex (35.4 ± 1.7 torr) and hippocampus (33.6 ± 1.4 torr) although differences in the tissue P02 distributions were seen. The disappearance rate for oxygen ( -dPo^dt) was measured after brief (< 15 seconds) bilateral carotid artery (total brain blood flow) occlusion. The mean (±SEM) disappearance rate was significantly higher (p<0.05) in the cortex (Z3.8 ± 1.5 torr/sec, 160 locations in 21 gerbils) than In the hippocampus (17.0 ± 0.7 torr/sec, 119 locations in 16 gerbils). The maximum oxygen consumption rates (Vc^max) for Michaelis-Menten kinetics were calculated from the disappearance rates, correcting for gerbil oxyhemoglobin. The mean Vo^max was 8.28 ± 0.51 and 6.13 ± 0.25 ml O 2 /100 g/rain for the cortex and hippocampus, respectively. The apparent Michaelis-Menten kinetic constants (K_) for the 2 regions were not significantly different (overall mean 3.3 ± 0.4 torr The present study was undertaken to quantify oxygen metabolism at highly localized sites by the oxygen disappearance technique, correcting for the influence of oxyhemoglobin. Measurements were made in 2 regions of the gerbil brain, the cortex and the hippocampus, which are of interest due to marked differences in susceptibility to ischemic damage (selective vulnerability), even within a region. The gerbil model of ischemia was chosen because blood flow to the brain can be stopped completely with bilateral carotid artery occlusion since the circle of Willis has no connections to the basilar artery for a source of collateral blood flow. Materials and MethodsMongolian gerbils, aged 3-4 months, weighing 50-90 g, were maintained on standard laboratory food and water ad libitum. They were anesthetized with 30-40 mg/kg i.p. sodium pentobarbital, tracheotomized, and allowed to breathe spontaneously. Both common carotid arteries were exposed through ventral midline cervical incisions and isolated from the accompanying nerves and vein. Surgical sutures were placed around the arteries for causing occlusions. In by guest on May 9, 2018 http://stroke.ahajournals.org/ Downloaded from

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“…It can also be explained by the hypoxic conditions to which the neuronal tissues were exposed during hyperthermia [15,16], as, since the increased oxygen consumption and rate of energy use are dependent on the temperature increase, the partial pressure of oxygen in the tissue falls dramatically during hyperthermia [1,21,22].…”

Section: Discussionmentioning

confidence: 99%

Effects of temperature on adenosine A1 receptor activation in guinea pig hippocampus in vitro

Fujii

Katô

Kuroda

2002

Pflugers Arch - Eur J Physiol

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The effects of temperature on adenosine A1 receptor activation were studied both by electrophysiological analysis of synaptically evoked responses in CA1 neurons in guinea pig hippocampal slices, and by measuring the binding of adenosine analogues to adenosine A1 receptors in crude synaptosomes from guinea pig hippocampal neurons. Increasing the temperature of the perfusing medium from 30 degrees C to 45 degrees C attenuated the amplitude of the synaptically and the non-synaptically evoked CA1 population spikes. Bath application of 1 microM 8-cyclopentyltheophylline, an adenosine A1 receptor antagonist, did not affect non-synaptically evoked CA1 population spikes, but significantly increased the amplitude of synaptically evoked population spikes in the upper range of hyperthermia (37-43 degrees C). In contrast, application of 5 microM L- N(6)-phenylisopropyladenosine, an adenosine A1 receptor agonist, did not affect non-synaptically evoked CA1 population spikes, but significantly decreased the amplitude of synaptically evoked population spikes in the upper range of hyperthermia. Binding assays using crude hippocampal synaptosomes showed that the affinity of adenosine A1 receptors for a radio-labeled adenosine analogue increased in response to a temperature increase. These results suggest that increased activation of adenosine A1 receptors in response to a temperature increase depresses excitatory synaptic responses in hippocampal CA1 neurons.

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Activation energy in the mammalian brain slice as determined by oxygen micro-electrode measurements.

Cited by 12 publications

References 5 publications

Modeling oxygen effects in tissue‐preparation neuronal‐current MRI

Modeling oxygen effects in tissue‐preparation neuronal‐current MRI

Comparisons of oxygen metabolism and tissue PO2 in cortex and hippocampus of gerbil brain.

Effects of temperature on adenosine A1 receptor activation in guinea pig hippocampus in vitro

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