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  • 1
    ISSN: 1432-1076
    Keywords: Key words [18F]-Fluorodeoxyglucose-positron emission tomography  ;  Periventricular leukomalacia  ;   Hypsarrhythmia  ;  Preterm infant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two preterm infants with extensive periventricular leukomalacia (PVL) were examined by [18F]-fluorodeoxyglucose-positron emission tomography (FDG-PET) at the corrected ages of 18 and 34 days. They showed similar clinical courses including oculoclonic seizure, hypsarrhythmia and severe mental retardation, in addition to spastic quadriplegia. FDG-PET study of these two infants with severe PVL disclosed poorly developed metabolic activity in the primary sensorimotor cortex, while the MRI images displayed only periventricular white matter lesions. Conclusion Positron emission tomography may dis‐close cortical involvement in infants with severe periventricular leukomalacia.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1463
    Keywords: Keywords: Brain slice, [18F]FDG, hypoxia, glucose metabolism, positron.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Fresh rat brain slices were incubated with 2-deoxy-2-[18F]-fluoro-D-glucose ([18F]FDG) in oxygenated Krebs-Ringer solution at 36°C, and serial two-dimensional time-resolved images of [18F]FDG uptake were obtained from these specimens on imaging plates. The fractional rate constant (= k3*) of [18F]FDG proportional to the cerebral glucose metabolic rate (CMRglc) was evaluated by applying the Gjedde-Patlak graphical method to the image data. With hypoxia loading (oxygen deprivation) or glucose metabolism inhibitors acting on oxidative phosphorylation, the k3* value increased dramatically suggesting enhanced glycolysis. After relieving hypoxia ≤10-min, the k3* value returned to the pre-loading level. In contrast, with ≥20-min hypoxia only partial or no recovery was observed, indicating that irreversible neuronal damage had been induced. However, after loading with tetrodotoxin (TTX), the k3* value also decreased but returned to the pre-loading level even after 70-min TTX-loading, reflecting a transient inhibition of neuronal activity. This technique provides a new means of quantifying dynamic changes in the regional CMRglc in living brain slices in response to various interventions such as hypoxia and neurotoxic chemical-loading as well as determining the viability and prognosis of brain tissues.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1463
    Keywords: Keywords: Brain slice ; positron emitting tracer ; triazolam ; muscarinic acetylcholine receptor ; amnesia.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The effect of triazolam, a potent benzodiazepine (BZ) agonist, on muscarinic acetylcholinergic receptor (mAChR) binding was investigated in living brain slices by use of a novel positron-based imaging technique. Fresh rat brain slices were incubated with [11C]N-methyl-4-piperidylbenzilate ([11C]NMPB), a mAChR antagonist, in oxygenated Krebs-Ringer solution at 37°C. During incubation, time-resolved imaging of [11C]NMPB binding in the slices was constructed on the storage phosphor screens. Addition of triazolam (1 μM) plus muscimol (30 μM), a GABAA receptor agonist, to the incubation mixture decreased the specific binding of [11C]NMPB. Ro15-1788, a BZ receptor antagonist, prevented this effect, indicating that the effect was exerted through the GABAA/BZ receptor complex. These results demonstrated that stimulation of the GABAA/BZ receptor lowers the affinity of the mAChR for its ligand, which may underlie the BZ-induced amnesia, a serious clinical side effect of BZ. No such effect in the P2-fraction instead implies that the integrity of the neuronal cells and/or their environment is prerequisite for the modulation of mAChR by GABAA/BZ stimulation.
    Type of Medium: Electronic Resource
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