Fair enough, just dumped some material
http://grande.nal.us....&therow=228518
QUOTE
The stimulation of D1 and D2 dopamine (DA) receptors by selective agonists produced large increases in brain glucose concentrations. D2 receptor stimulation also produced large increases in blood glucose.
Dopamine agonist treatment ameliorates hyperglycemia, hyperlipidemia, and the elevated basal insulin release
Serotonin mediates rapid changes of striatal glucose and lactate metabolism after systemic 3,4-methylenedioxymethamphetamine (MDMA, “Ecstasy”) administration in awake rats
http://www.sciencedi...bfaa53cbdf97794
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A single dose of MDMA (2–10–20 mg/kg i.v.) evoked a transient increase of interstitial glucose concentrations in striatum (139–223%) with rapid onset and of less than 2 h duration, a concomitant but more prolonged lactate increase (>187%) at the highest MDMA dose and no significant depletions of striatal serotonin. Blood glucose and lactate levels were also transiently elevated (163 and 135%) at the highest MDMA doses. The blood glucose rises were significantly related to brain glucose and brain lactate changes. The metabolic perturbations in striatum and the hyperthermic response (+1.1 °C) following systemic MDMA treatment were entirely blocked in p-chlorophenylalanine pre-treated rats, indicating that these effects are mediated by endogenous serotonin
Regional brain glucose metabolism: Correlations to biochemical measures and anxiety in patients with schizophrenia
http://www.sciencedi...d5b71a231922bcd
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In all subjects, positive correlations were found between the level of anxiety and the regional glucose metabolism.
http://www.ncbi.nlm..../pubmed/8489322
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Global or absolute measures of metabolism did not statistically differ between groups, although hyperactive girls had a 17.6% lower absolute brain metabolism than normal girls. As compared with the values for the controls, normalized glucose metabolism was significantly reduced in six of 60 specific regions of the brain, including an area of the left anterior frontal lobe (P < .05). Lower metabolism in that specific region of the left anterior frontal lobe was significantly inversely correlated with measures of symptom severity (P < .001-.009, r = -.56 to -.67).
http://www.ncbi.nlm....pubmed/11513813
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Quote:
At least some forms of ADHD may be viewed as cortical, energy-deficit syndromes secondary to catecholamine-mediated hypofunctionality of astrocyte glucose and glycogen metabolism, which provides activity-dependent energy to cortical neurons. Several tests of this hypothesis are proposed.
Relationship between personality trait and regional cerebral glucose metabolism assessed with positron emission tomography
http://www.ncbi.nlm....pubmed/12270587
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There have been no studies systematically investigating relationships between biogenetic temperament dimensions and patterns of brain glucose metabolism. Nineteen healthy subjects were evaluated regarding the biogenetic temperament using Cloninger's Temperament and Character Inventory (TCI). In addition, [18F] fluorodeoxyglucose (FDG) positron emission tomography (PET) was used to measure regional brain glucose metabolism. Voxel-based correlation analysis was used to test correlations between regional brain glucose metabolism and scores on the TCI. We identified that each temperament dimension, such as Novelty Seeking, Harm Avoidance, and Reward Dependence, was significantly correlated with specific brain regions. The majority of correlations were observed in the areas of paralimbic regions and temporal lobes. The current study provides evidence linking each biogenetic temperament dimension with specific brain areas and provides a promising base for future personality research.
here is evidence that patients with major depression have reduced blood flow and metabolism in the prefrontal cortex, particularly when they exhibit psychomotor retardation. Abnormalities are also found in the anterior cingulate gyrus and the basal ganglia
Mood disorders may be associated with global and regional changes in cerebral blood flow and metabolism. The accumulated functional neuroimaging findings in mood disorders were reviewed in order to examine a proposed neuroanatomic model of pathophysiology. Global cerebral blood flow and glucose metabolism appear normal, but may be decreased in late-life depression. Regional cerebral blood flow and glucose metabolism deficits are present, and may be indicators of brain regions participating in neuroanatomic circuits involved in mood disorders. Decreased pre-frontal cortex blood flow and metabolism in depressed unipolar and bipolar patients are the most consistently replicated findings, and correlate with severity of illness. Basal ganglia abnormalities have been found in depressed unipolar and bipolar patients, involving decreased blood flow and metabolism. Temporal lobe abnormalities are present in bipolar disorder patients, and perhaps unipolar depression. There is conflicting evidence of abnormalities in other limbic regions. Cognitive impairment may correlate with decreased metabolism in frontal and cerebellar areas. The relationship between functional neuroimaging findings and clinical course, and therefore state and trait characteristics, has not been systematically investigated. Antidepressant medications, but not ECT, seem to reverse some of the identified functional brain changes in the depressed state. The structural, neurotransmitter and neuropathological correlates of these functional abnormalities are yet to be determined. Functional abnormalities in frontal, subcortical and limbic structures appear to be part of the pathoph
Glycolysis regulates the induction of lactate utilization for synaptic potentials after hypoxia in the granule cell of guinea pig hippocampus.
http://www.ncbi.nlm....pubmed/15567484
QUOTE
Lactate is considered an alternative substrate that is capable of replacing glucose in maintaining synaptic function in adult neurons. But, we found recently that lactate could be utilized for maintenance of synaptic potentials only after the activation of NMDA and voltage-dependent-calcium channel during glucose deprivation. To clarify more on the relationship between glycolysis and induction of lactate utilization, we tested lower concentration of glucose with hypoxia to induce a relative shortage of anaerobic energy production. Population spikes are not maintained with lactate following hypoxia in 10 mM glucose medium, but are maintained at their original levels with lactate after exposure to hypoxia in lower concentration (5 mM) of glucose. Hypothermia during low glucose-hypoxia, bath application of the NMDA channel blocker and the voltage-sensitive calcium channel blocker, as well as the omission of extracellular calcium prevented the induction of the lactate-supported population spikes. ATP levels in the tissue slices are relatively preserved in the conditions that block the induction of lactate-supported population spikes. From these observations, we propose that the energy source for maintenance of synaptic function in adult neuron changes from adult form (glucose alone) to immature one (glucose and/or lactate) after short of glucose supply.