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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Striatal microdialysis was performed in rats subjected to 20 min of transient forebrain ischemia produced by occlusion of the carotid arteries during hemorrhagic hypotension. Extracellular changes of dopamine, serotonin, and their metabolites were monitored before, during, and after the ischemic insult at 10-min intervals by on-line HPLC analysis. During ischemia, extracellular dopamine increased dramatically (156 times baseline), as did 3-methoxytyramine (3-MT), whereas 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) decreased (15–25% of baseline). Upon reperfusion, dopamine was cleared from the extracellular fluid within 40 min and reached a stable level (70% of baseline). DOPAC and HVA increased (250–330%) transiently and reached their maximum 1 h following reperfusion, whereas 3-MT decreased to undetectable levels within 20 min. Although baseline levels of serotonin were not detectable, serotonin and 5-hydroxyindoleacetic acid showed a qualitatively similar temporal pattern to dopamine and its acid metabolites. Killing rats by cervical dislocation produced changes in extracellular dopamine, serotonin, and their metabolites that were almost identical to those seen during ischemia. Pargyline pretreatment 2 h before ischemia had marginal effects on the postischemic clearing of dopamine. The pargyline pretreatment, however, did increase the survival rate of rats subjected to ischemia, and this protective effect might be due to the pargyline-induced blockade of the postischemic monoamine oxidase-mediated increase in dopamine metabolism and the concurrent production of the potentially neurotoxic molecule, hydrogen peroxide.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Hippocampus CA1 region ; Ischemia ; Transplantation ; In vitro slice ; Intracellular recordings
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Severe forebrain ischemia was used to damage selectively the CA1 region of the rat hippocampal formation. One week later the CA1 region was repopulated with suspensions of 18 day old fetal hippocampal tissue. Intracellular recordings were made from single units within the transplants by using the “in vitro” slice preparation, two to nine months following transplantation. Based on firing characteristics during depolarizing current injection, pyramidal-like and interneuron-like cells were identified within the transplants. Synaptic potentials could be evoked in the pyramidal-like neurons by stratum radiatum and stratum oriens stimulation demonstrating that normal afferent contacts had been made. Local inhibitory circuits were not obvious within the transplanted regions as demonstrated by prolonged EPSP's and the absence of early or late after-hyperpolarization. This was supported by the lack of conductance fluctuation in the active membrane when compared with the resting cell. Antidromic spikes could be evoked by applying shocks to the stratum oriens, towards the fimbria and subiculum, suggesting that the transplanted neurons were projecting basal neurites, quite long distances, along the normal efferent pathways. Thus, the transplanted neurons have the capacity to reconstruct damaged circuitries and develop intrinsic properties similar to their normal counterparts.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1106
    Keywords: Cerebral ischemia ; Calbindin-D28K ; Parvalbumin ; retrograde axonal tracing ; CNS repair ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cerebral ischemia can be caused by many diverse conditions such as cardiac arrest and severe hypotension and is often the cause of secondary brain damage following head injury or infantile birth trauma. The inadequate cerebral blood flow can result in permanent loss of essential brain circuitries and neurological deficits. The CA1 region of the hippocampal formation is the region of the brain that is most often lesioned following transient forebrain ischemia and is associated with impairments of learning and memory. Furthermore, the loss of such a large target area can lead to detrimental post-trauma synaptic reorganization. Since methods are not currently available for the prevention of neuronal loss following cerebral ischemia, a number of anatomical methodologies were utilized to investigate whether transplanted neurons had the potential to afford some measure of repair. The hippocampal CA1 region of the rat brain was lesioned by transient forebrain ischemia and subsequently repopulated with suspensions of fetal hippocampal tissue. The ability of the transplanted neurons to remain viable when placed into a degenerating environment was confirmed by the histological demonstration of 3H-thymidine labelled neurons in the lesioned region. Histological and immunohistochemical techniques showed that the transplanted neurons developed cytological features that were indistinguishable from their normal CA1 counterparts, often showed a remarkable degree of organization, and expressed some of the same neuron specific proteins; specifically calbindin-D28K and parvalbumin. Acetylcholinesterase histochemistry and retrograde axonal transport of Fluorogold demonstrated that some afferent and efferent fibre projections to and from the septal nucleus could be reinstated. The data have shown that the transplanted neurons can demonstrate many of the anatomical properties that are characteristic of the adult cells they have replaced and therefore have great potential for the reconstruction of severe focal lesions due to ischemia.
    Type of Medium: Electronic Resource
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