Astrocytes Couple Synaptic Activity to Glucose Utilization in the Brain

Physiology ◽  
1999 ◽  
Vol 14 (5) ◽  
pp. 177-182 ◽  
Author(s):  
Pierre J. Magistretti ◽  
Luc Pellerin
Keyword(s):  
Positron Emission Tomography ◽  
Glucose Metabolism ◽  
Glucose Utilization ◽  
Glutamate Uptake ◽  
Synaptic Cleft ◽  
Synaptic Activity ◽  
Emission Tomography ◽  
Functional Characteristics ◽  
Positron Emission ◽  
The Brain

Astrocytes have functional characteristics that make them particularly well suited to couple glutamate uptake from the synaptic cleft to Na+-K+-ATPase activation and glucose utilization. The changes in glucose metabolism associated with these processes may provide signals detected by positron emission tomography.

FDG and Amyloid Positron Emission Tomography

CNS Spectrums ◽  
2008 ◽  
Vol 13 (S16) ◽  
pp. 21-24 ◽  
Author(s):  
Mark A. Mintun
Keyword(s):  
Positron Emission Tomography ◽  
Glucose Metabolism ◽  
Pet Imaging ◽  
Glutamate Release ◽  
Synaptic Activity ◽  
Emission Tomography ◽  
Neural Firing ◽  
Positron Emission ◽  
Excitatory Activity ◽  
The Brain

For over 20 years, researchers have used the tracer [18F]fluorodeoxyglucose (FDG) in positron emission tomography (PET) imaging. FDG PET imaging has been utilized to study the characteristic metabolic changes in Alzheimer’s disease (AD), and as more molecular imaging tracers become available for human research, PET will likely assume many new roles for investigating more specific abnormalities, such as amyloid deposition, in the future.FDG is a glucose analog that images glucose metabolism and also illustrates neural firing. Different synapse activity, particularly excitatory activity from glutamate release, appears to change FDG uptake. AD will affect both brain infrastructure by decreasing the amount of cell bodies and synapses as well as decreasing synaptic activity, which are both changes that decrease the amount of FDG. AD is not a perfectly uniform process, and this is reflected by distinct progressive patterns of decreased FDG and decreased metabolism across different regions of the brain.FDG enters the brain via blood flow, and then into brain tissue by both diffusion and facilitated transport. Once it enters the glia and neurons, FDG can be phosphorylated, a step that is essentially irreversible, but then cannot be processed further by the cells, effectively trapping the FDG in situ. The amount of trapping that occurs in the brain over the first 10–20 minutes is very high and constitutes over 80% of the uptake. Thus, after the first 10–20 minutes uptake phase, a pattern of FDG emerges that mirrors the distribution of glucose metabolism in all subcortical and cortical structures.

scholarly journals The Effect of Diazepam Sedation on Cerebral Glucose Metabolism in Alzheimer's Disease as Measured Using Positron Emission Tomography

1987 ◽  
Vol 7 (4) ◽  
pp. 415-420 ◽  
Author(s):  
Norman L. Foster ◽  
Abraham F. L. VanDerSpek ◽  
Michael S. Aldrich ◽  
Stanley Berent ◽  
Richard H. Hichwa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Glucose Metabolism ◽  
Metabolic Activity ◽  
Glucose Utilization ◽  
Activity Level ◽  
Emission Tomography ◽  
Positron Emission ◽  
Intravenous Diazepam

The effect of sedation induced by intravenous diazepam on cerebral glucose metabolic activity was examined with [18F]2-fluoro-2-deoxy-D-glucose (FDG) and positron emission tomography (PET) in five patients with probable Alzheimer's disease. Each subject was studied on 2 separate days: on one occasion at rest with eyes patched and ears open, and on the second when sedated with intravenous diazepam titrated to maintain stage II sleep by clinical and EEG criteria. Similar patterns of glucose uptake were observed in both the presence and the absence of sedation, but overall glucose utilization was depressed an average of 20% and was closely correlated with the amount of diazepam administered prior to the injection of FDG. The predominant temporoparietal hypometabolism and relative sparing of frontal metabolism observed in this disease are therefore not explained by differences in anxiety or activity level in this patient group. Utilization of diazepam sedation for PET study appears to be safe and may permit the study of patients otherwise unable to cooperate with FDG-PET procedures.

scholarly journals Combined Study of Cerebral Glucose Metabolism and [11C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

1996 ◽  
Vol 16 (3) ◽  
pp. 399-408 ◽  
Author(s):  
E. Salmon ◽  
M. C. Gregoire ◽  
G. Delfiore ◽  
C. Lemaire ◽  
C. Degueldre ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Glucose Metabolism ◽  
Clinical Symptoms ◽  
Synaptic Activity ◽  
Emission Tomography ◽  
Tissue Loss ◽  
Positron Emission

There is a characteristic decrease in glucose metabolism in associative frontal and temporo-parietal cortices of patients suffering from Alzheimer's disease (AD). The decrease in metabolism might result from local neuronal loss or from a decrease of synaptic activity. We measured in vivo [11C]methionine accumulation into proteins with positron emission tomography (PET) to assess cortical tissue loss in AD. Both global regional activity and compartmental analysis were used to express [11C]methionine accumulation into brain tissue. Glucose metabolism was measured with [18F]fluorodeoxyglucose and autoradiographic method. Combined studies were performed in 10 patients with probable AD, compared to age-matched healthy volunteers. There was a significant 45% decrease of temporo-parietal glucose metabolism in patients with AD, and frontal metabolism was lowered in most patients. Temporo-parietal metabolism correlated to dementia severity. [11C]methionine incorporation into temporo-parietal and frontal cortices was not significantly decreased in AD. There was no correlation with clinical symptoms. Data suggest that regional tissue loss, assessed by the decrease of [11C]methionine accumulation, is not sufficient to explain cortical glucose hypometabolism, which reflects, rather, reduced synaptic connectivity.

scholarly journals Cerebral Glucose Metabolism in Parkinson’s Disease

1984 ◽  
Vol 11 (S1) ◽  
pp. 169-173 ◽  
Author(s):  
W.R.W. Martin ◽  
J.H. Beckman ◽  
D.B. Calne ◽  
M.J. Adam ◽  
R. Harrop ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Glucose Metabolism ◽  
Glucose Utilization ◽  
Emission Tomography ◽  
Metabolic Rates ◽  
Local Cerebral Glucose Utilization ◽  
Positron Emission

ABSTRACTLocal cerebral glucose utilization was measured in patients with predominantly unilateral Parkinson’s disease using 18F-2-fluoro-deoxyglucose and positron emission tomography. Preliminary results indicate the presence of asymmetric metabolic rates in the inferior basal ganglia. The structure comprising the largest portion of basal ganglia at this level is globus pallidus. These findings are consistent with metabolic studies on animals with unilateral nigrostriatal lesions in which pallidal hypermetabolism on the lesioned side has been demonstrated. Increased pallidal activity is likely secondary to a loss of inhibitory dopaminergic input to the striatum from substantia nigra.

Sherpa brain glucose metabolism and defense adaptations against chronic hypoxia

1996 ◽  
Vol 81 (3) ◽  
pp. 1355-1361 ◽  
Author(s):  
P. W. Hochachka ◽  
C. M. Clark ◽  
C. Monge ◽  
C. Stanley ◽  
W. D. Brown ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Glucose Metabolism ◽  
Emission Tomography ◽  
The Tibetan Plateau ◽  
Metabolic Rates ◽  
Atp Production ◽  
Healthy Humans ◽  
Positron Emission ◽  
Metabolic States ◽  
The Brain

The brain of hypoxia-tolerant vertebrates is known to survive extreme oxygen limitation at least in part because of very low rats of ATP utilization and ATP production. To asses whether similar adaptations are involved in healthy humans during hypoxia adaptation over generational time, we initially used positron-emission tomography measurements of glucose metabolic rates in the brain of Quechuas, whose ancestors have been indigenous to the Andes at altitudes between approximately 3,300 and 4,500 m for several hundred years. Workers in this field generally believe that the lineage of Sherpas has been indigenous to the Himalayas for even longer and that Sherpas and other peoples indigenous to the Tibetan plateau are perhaps the most exquisitely hypoxia adapted of all humans. For this reason, in this study we extended our database to include Sherpas. With the use of the same protocol as before, two metabolic states were analyzed: 1) the presumed normal (hypoxia-adapted) state, monitored as soon as possible after subjects left the Himalayas and 2) the deacclimated state, monitored after 3 wk at low altitudes. Positron-emission tomography measurements of 2-[18F]deoxy-2-fluoro-D-glucose metabolic rates, quantified in 26 regions of the brain, indicated that the Sherpas' brain metabolism differed significantly from that of Quechuas but was essentially identical to that of lowlanders. Region-by-region patterns were similar in all three groups, indicating that the regional organization of glucose metabolism in the brain is a conservative, relatively constant characteristic.

Imaging the Effects of Propofol on Human Cerebral Glucose Metabolism Using Positron Emission Tomography

2008 ◽  
Vol 36 (6) ◽  
pp. 1305-1310 ◽  
Author(s):  
X Sun ◽  
H Zhang ◽  
C Gao ◽  
G Zhang ◽  
L Xu ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Glucose Metabolism ◽  
Emission Tomography ◽  
Control Group ◽  
Target Region ◽  
Cortical Areas ◽  
Positron Emission ◽  
Pet Scanning ◽  
Subcortical Regions ◽  
The Brain

The effects of propofol on glucose metabolism in different cerebral regions were observed, using positron emission tomography (PET) technology, to determine a possible cerebral target region. Seven healthy volunteers were injected with 18F-fluorodeoxyglucose developing agent for PET scanning whilst awake (control group T1), during sedation (induced by 1.5 μg/ml propofol administered by target controlled injection [TCI], group T2) and when unconsciousness (induced by 2.5 μg/ml propofol administered by TCI, group T3). Whole brain glucose metabolism was reduced during propofol anaesthesia; this was initially observed in the cortical areas at the lower dose of propofol (group T2) but extended to the subcortical regions, especially the thalamus and hippocampus, at the higher dose (group T3). This suggests that these regions of the brain might be important targets that are susceptible to propofol.

scholarly journals Brain Activity Associated with Chronic Cancer Pain

2010 ◽  
Vol 5;13 (5;9) ◽  
pp. E342-E342
Author(s):  
Asokumar Buvanendran
Keyword(s):  
Positron Emission Tomography ◽  
Chronic Pain ◽  
Prefrontal Cortex ◽  
Glucose Metabolism ◽  
Severe Pain ◽  
Brain Activity ◽  
Emission Tomography ◽  
Positron Emission ◽  
Affective Pain ◽  
The Brain

Background: The number of neuroimaging studies that examine chronic pain are relatively small, and it is clear that different chronic pain conditions activate diverse regions of the brain. Objective: Cancer patients presenting for diagnostic positron emission tomography (PET) imaging were asked to rate their spontaneous baseline pain score. Twenty patients with either no pain (NRS = 0) or with moderate to severe pain (NRS ≥ 4) were invited to participate in this study to determine the difference in brain activity in cancer patients with moderate to severe chronic pain versus no pain. Study Design: Prospective, non-randomized, observational report. Setting: Academic medical center. Methods: Patients had a 2-D PET scan with the radionuclide 18F-fluoro-2-deoxyglucose (FDG) at a dose of approximately 20 mCi. Each individual raw PET scan was coregistered and normalized to standard stereotactic space. Differences in regional glucose metabolism were then statistically compared between patients with moderate-to-severe pain and patients with no pain. Results: The NRS pain score in the patients with moderate to severe pain (n = 11) was 4.5 [4.0- 6.0] (median[interquartile range]) versus 0.0 [0.0-0.0] (p < 0.001) in the group with no pain (n = 9). Compared to patients with no pain, patients with moderate to severe pain had increased glucose metabolism bilaterally in the prefrontal cortex, BA 9-11. Unilateral activation was found in the right parietal precuneus cortex, BA 7. There were no areas of the brain in which there was decreased activity due to moderate to severe pain. Conclusions: Our results showing a preferential activation of the prefrontal cortex are consistent with results from studies showing that affective pain perception and negative emotions play an important part in the chronic pain experience. Limitations: This was not a randomized clinical trial. Patient medication was not controlled. Key words: chronic pain, cancer pain, positron emission tomography, brain imaging, prefrontal cortex, affective pain, negative emotions

scholarly journals Human Cerebral Glucose Metabolism Determined by Positron Emission Tomography: A Revisit

1987 ◽  
Vol 7 (4) ◽  
pp. 427-432 ◽  
Author(s):  
Rodney A. Brooks ◽  
Jun Hatazawa ◽  
Giovanni Di Chiro ◽  
Stephen M. Larson ◽  
Donn S. Fishbein
Keyword(s):  
Positron Emission Tomography ◽  
White Matter ◽  
Glucose Utilization ◽  
Direct Determination ◽  
Macaque Monkey ◽  
Jugular Bulb ◽  
Emission Tomography ◽  
Utilization Rate ◽  
Positron Emission ◽  
The Brain

The cerebral glucose utilization rate was studied for 27 normal volunteers with 18F-deoxyglucose positron emission tomography (PET). The scanner has a spatial resolution of 6–7 mm and contains corrections for scatter, attenuation, and random coincidences. The lumped constant (tracer-to-glucose dynamic uptake ratio) was determined by comparing the average global uptake of tracer in representative slices with average glucose utilization rates measured by the Kety-Schmidt method as reported in the literature. The resulting value of 0.50 is in excellent agreement with a recent direct determination done by arterial and jugular bulb blood sampling. Gray and white matter values of glucose utilization in various areas of the brain were determined by placing small regions of interest over various cortical, basal, and white matter structures. These values are within 20% of published autoradiographic data on the macaque monkey. The average ratio of gray to white glucose utilization was 2.9, compared with a range of 3–5 for the monkey study and 1.6–2.2 reported in previous PET studies. The effect of instrumental errors on the results is analyzed and discussed.

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