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  • 1
    Electronic Resource
    Electronic Resource
    A role forγ-aminobutyric acid (GABA) in the evolution of delayed neuronal death following ischemia (1988)
    Springer
    Metabolic brain disease 3 (1988), S. 287-292 
    Details
    ISSN: 1573-7365
    Keywords: γ-aminobutyric acid (GABA) ; hippocampus ; delayed neuronal death ; selective vulnerability ; ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A series of putative neuroprotective agents was tested to determine their efficacy in preventing the loss of the CA 1 neurons of the hippocampus at 4 days following 5 min of bilateral ischemia in the gerbil. Agents associated with the GABAergic system were determined to be the most effective, but only when given prior to the ischemic episode, suggesting that there was aγ-aminobutyric acid (GABA)-related event during ischemia which triggers the delayed neuronal death of these cells. In this report, the unidirectional release of GABA and glutamate from gerbil hippocampal slices was determined under conditions mimicking anoxia and/or ischemia. Pentobarbital, the most effective of the GABAergic agents, had little or no effect on the time-dependent release of glutamate. In contrast, pentobarbital reduced in release of GABA in both anoxia and ischemia, but only after 25 to 30 min of incubation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999539
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Lactate compartmentation in hippocampal slices: Evidence for a transporter (1990)
    Springer
    Metabolic brain disease 5 (1990), S. 143-154 
    Details
    ISSN: 1573-7365
    Keywords: lactate efflux ; hippocampal slice ; tissue acid-base balance ; in vitro model of ischemia ; lactate transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lactic acid accumulation has been implicated in the evolution of brain damage after ischemia. Since compartmentation of lactate may play a role in acid-base balance, lactate release from gerbil hippocampal slices was examined during a number of metabolic stresses including elevated [K+]e, ischemia, anoxia, and aglycemia. Slices were preincubated for 1 hr in artificial cerebrospinal fluid (ACSF) equilibrated with 95% O2/5% CO2 (pH 7.4 at 37°C) and then transferred to tubes containing 300μl of test medium. The rate of lactate release in control slices was 9.64 nmol/min/mg protein and increased 2.6- and 3.2-fold in the presence of 60 mM potassium and anoxia, whereas the rate of lactate release was decreased by 50 and 25% during ischemia and aglycemia. Lactate release was temperature dependent and was only minimally influenced by removing Ca2+ or by adding 5 mM d-lactate to the ACSF. In contrast, pyruvate inhibited lactate release with an apparent Ki of 2.4 mM. The results suggest that lactate can be released from cells via a saturable and stereospecific lactate transporter with an apparentK m of 10.7 mM andV max of 43.7 nmol/mg protein/min. Such a relatively high-capacity transporter system can rapidly equilibrate brain lactate but is probably not involved in regulating intracellular acid-base balance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999841
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Cerebral ischemia: Changes in monoamines are independent of energy metabolism (1989)
    Springer
    Neurochemical research 14 (1989), S. 1-7 
    Details
    ISSN: 1573-6903
    Keywords: Cerebral ischemia ; energy metabolism ; monoamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship of neurotransmitters and neuroeffectors to the energy state of the brain was examined in the gerbil model of ischemia after 5 and 15 min of bilateral common carotid artery occlusion only or with 1 hr of reperfusion. The gerbil brains were fixed by microwave irradiation and a total of 15 metabolites were measured from a single piece of tissue from either the hippocampus or the striatum. The rapid alterations in energy-related compounds and cyclic nucleotides appeared to be directly related both to the loss of oxygen and glucose during ischemia and the resupply of these nutrients during reflow. Significant reduction in the level of monoamines occurred prinicipally during reflow, at a time when the energy-related metabolites were restored. It is proposed that the changes in monoamines were triggered by other ischemic-induced events unrelated to energy depletion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00969750
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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