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  • 1
    Electronic Resource
    Electronic Resource
    Saturable Retention of Vasopressin by Hippocampus Vessels In Vivo, Associated with Inhibition of Blood-Brain Transfer of Large Neutral Amino Acids (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 49 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Vasopressin receptors have been reported in the endothelium of brain capillaries. The function of these receptors is not known. To test the prediction that vasopressin receptors in brain capillary endothelium affect amino acid transport across the blood-brain barrier and to assess the role of vasopressin transport across the cerebral vascular endothelium, we measured (a) the endothelial permeability to the large neutral amino acid leucine in the absence and presence of arginine vasopressin (AVP) and (b) the permeability of the blood-brain barrier to AVP relative to mannitol. In brain regions protected by the blood-brain barrier, after circulation for 20 s, coinjection of leucine and AVP intravenously led to a decrease of leucine transport unrelated to changes of blood flow. The decrease was most pronounced in hippocampus (42%) and least pronounced in olfactory bulb and colliculi (17 and 19%, respectively). In the latter regions, the endothelial permeability to AVP did not significantly exceed that of mannitol. In hippocampus and in regions with no blood-brain barrier (pituitary and pineal glands), AVP retention in excess of mannitol retention was blocked by unlabeled AVP. The findings do not contradict the hypothesis of a role for AVP in the regulation of large neutral amino acid transfer into brain tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb01016.x
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  • 2
    Electronic Resource
    Electronic Resource
    Regional Cerebral Glucose Phosphorylation and Blood Flow After Insertion of a Microdialysis Fiber Through the Dorsal Hippocampus in the Rat (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 49 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Local cerebral glucose metabolism (LCMRglc) and local cerebral blood flow (LCBF) were studied following implantation of a microdialysis fiber in rat dorsal hippocampus. Recovery time after implantation varied from 0 to 24 h. All rats showed pronounced disturbances in LCMRglc and LCBF during the first 2 h of implantation. The changes consisted of (a) a general decrease in blood flow and glucose phosphorylation and (b) small areas (spots) around the fiber with increased glucose phosphorylation and decreased blood flow. Animals allowed to recover for 24 h demonstrated a near normalization of LCMRglu and LCBF, and the focal disturbances (spots) of glucose phosphorylation and blood flow disappeared. The slight reduction in blood flow and glucose metabolism at this time must be accepted, because extension of the recovery period beyond 24 h may give interpretation problems due to the developing gliosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb00954.x
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  • 3
    Electronic Resource
    Electronic Resource
    Early loss of somatostatin neurons in dentate hilus after cerebral ischemia in the rat precedes CA-1 pyramidal cell loss (1987)
    Springer
    Acta neuropathologica 73 (1987), S. 110-114 
    Details
    ISSN: 1432-0533
    Keywords: Ischemia ; CA-1 delayed neuron death ; Postischemic hyperactivity ; Somatostatin ; Cholecystokinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Somatostatin (SS)- and cholecystokinin (CCK)-immunopositive cell somata in the rat hippocampus were quantitated at day 1, 2, 3 and 4 after cerebral ischemia. A significant (P〈0.01) 60%–80% loss of hilar and CA-3c SS neurons took place. No CCK neurons were lost. Damage to SS neurons was significant on the second postischemic day and preceded the delayed loss of CA-1 neurons. We speculate that loss of SS neurons, which presumably innervate the inhibitory GABAergic (γ-aminobutyric acid) interneurons, may induce hyperactivity stimulating the Ca-1 neurons to death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00693775
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  • 4
    Electronic Resource
    Electronic Resource
    Temporal profile of interneuron and pyramidal cell protein synthesis in rat hippocampus following cerebral ischemia (1990)
    Springer
    Acta neuropathologica 81 (1990), S. 14-19 
    Details
    ISSN: 1432-0533
    Keywords: Hippocampus ; Cerebral ischemia ; Protein synthesis ; Autoradiography ; Interneurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cellular protein synthesis was investigated in the rat hippocampus 2–100 h following 20 min of cerebral ischemia induced by four-vessel occlusion. [3H]-Phenylalanine was retrogradely infused through the external carotid artery for 30 min. This method limited the distribution of the tracer to one hemisphere and required 1/50th of the tracer amount used for intravenous tracer infusion. Cellular [3H]phenylalanine incorporation was examined in hematoxyline and eosin-stained sections coated with nuclear emulsion. A score for relative protein synthesis was estimated from counts of silver grains across neuron somata with undamaged morphology. Shortly after ischemia a generalized complete arrest of protein synthesis was observed. In CA1 pyramidal cells, this was followed by a transient incomplete regeneration (9–20 h) and later (46–100 h) persistent cessation of protein synthesis. By contrast protein synthesis in interneurons, CA3c pyramidal cells and granule cells recovered to preischemic levels 9–100 h after ischemia, as did the CA3ab pyramidal cells 46–100 h postischemia. Moreover, eosinophilic cell changes were seen in hilar and CA3c neurons at all postischemic stages and in CA1 pyramidal cells 46–72 h after ischemia. [3H]Phenylalanine incorporation was absent in neurons demonstrating eosinophilic cell changes. From the rapid recovery of protein synthesis in hippocampal interneurons, we conclude that changes in interneuronal protein synthesis per se are not involved in the pathophysiology of the delayed ischemic CA1 pyramidal cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00662632
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  • 5
    Electronic Resource
    Electronic Resource
    Myelin changes in the rats CNS following intraventricular injection of serum (1986)
    Springer
    Cellular and molecular life sciences 42 (1986), S. 37-39 
    Details
    ISSN: 1420-9071
    Keywords: Serum ; intrathecal injection ; CNS ; dissociated myelin ; demyelination ; multiple sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Normal human or rat serum administered by intraventricular injection induced demonstrable changes in the rat CNS myelin as seen from an increased recovery of dissociated myelin (DM), i.e. a myelin-related low density membrane fragments, from the tissue homogenates. The yield of DM reached a maximum on the third postinjection day and returned to the control level by day 5. In spite of the increased recovery of DM, no physico-chemical alternations in myelin isolates and no histological abnormalities in the tissue could be detected. The production of DM seems to be a sensitive index of serum-induced alteration of the myelin sheath.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01975883
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  • 6
    Electronic Resource
    Electronic Resource
    Focal ischemia of the rat brain, with special reference to the influence of plasma glucose concentration (1987)
    Springer
    Acta neuropathologica 73 (1987), S. 131-137 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Hyperglycemia ; Hypoglycemia ; Experimental diabetes ; Selective neuronal injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Focal cerebral ischemia was induced by occlusion of the right middle cerebral artery in hypoglycemic, normoglycemic, as well as in acute and chronic diabetic rats. The brain damage was studied after 4 days. The volume of infarction was decreased in hypoglycemia (29±19 mm3 (mean±SD) versus 58±35 mm3,P〈0.0046), unaltered in acute diabetes (61±45 mm3), and increased in chronic diabetes (91±22 mm3,P〈0.0463). The cortex adjacent to the infarct showed selective neuronal injury affecting the cortical layers 2 and 3. The damage was enhanced by hypoglycemia and prevented in most of the diabetic animals. The findings indicate that different mechanisms cause infarction and selective neuronal injury outside infarcts, but that both are influenced by the plasma glucose concentration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00693778
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  • 7
    Electronic Resource
    Electronic Resource
    Removal of the entorhinal cortex protects hippocampal CA-1 neurons from ischemic damage (1987)
    Springer
    Acta neuropathologica 73 (1987), S. 189-194 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Hippocampus ; Entorhinal cortex ; CA-1 pyramidal cell protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The excitatory (glutamatergic) innervation seems to determine a nerve cells vulnerability to complete, transient ischemia. Interruption of the excitatory afferents to the hippocampus by removal of the entorhinal cortex prior to ischemia allows examination of this hypothesis. Groups of adult male Wistar rats were subjected to 20 min of ischemia (fourvessel occlusion) 4 days following a sham procedure, unilateral or bilateral entorhinotomy. CA-1 pyramidal cell survival following ischemia was assessed by light microscopic examination (cell counts) 4 days after ischemia. Compared to control animals unilateral entorhinotomy protected 50% of the CA-1 pyramidal neurons ipsilateral to the lesion, whereas bilateral entorhinotomy resulted in 84% protection. The pathophysiology of ischemic brain damage is discussed, and it is suggested that the protection of CA-1 pyramidal neurons after entorhinotomy is due to interruption of the input to the dentate granule cells, which forms a link in the trisynaptic pathway from the entorhinal cortex to the CA-1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00693788
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  • 8
    Electronic Resource
    Electronic Resource
    Cellular reactions to implantation of a microdialysis tube in the rat hippocampus (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 234-238 
    Details
    ISSN: 1432-0533
    Keywords: Microdialysis ; Hippocampus ; Tissue reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microdialysis tubes, used for measurements of extracellular neurotransmitter concentrations, were implanted in rat dorsal hippocampus to study the adjacent tissue reaction. The brain was examined 1–60 days after the implantation. Within the first 2 days, normal neuropil and only occasional hemorrhage surrounded the microdialysis tube. Three days following the implantation astrocytes close to the dialysis tube, hypertrophied. Hypertrophic astrocyte processes invaded the spongy fiber wall. There was no increase in the number of astrocytes. Fourteen days after the fiber insertion layers of reticulin-positive fibers separated astrocytes and the remaining neuropil from the fiber wall. Late tissue changes (1 and 2 months) consisted of collagen deposits and occasional granuloma formation. These results can be used to predict the optimal time for commencing microdialysis after the fiber implantation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688186
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  • 9
    Electronic Resource
    Electronic Resource
    Kainic acid neurotoxicity: in vivo test of two new non-N-methyl-d-aspartate receptor antagonists (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 255-260 
    Details
    ISSN: 1432-0533
    Keywords: Kainic acid ; non-N-methyl-d-aspartate antagonists ; α-Amino-3-carboxy-methoxy-5-methyl-4-isoxazolepropionic acid (AMOA) ; α-Amino-2-(3-hydroxy-5-methyl-4-isoxazolyl)methyl-5-methyl-3-oxo-4-isoxazoline-4-propionic acid (AMNH) ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible neuroprotective effects of two new non-N-methyl-d-aspartate receptor antagonists were determined by quantitative light microscopy after intracerebral administration of kainic acid (KA) in two rat brain regions. KA alone or KA in combination with the antagonists α-amino-3-carboxy-methoxy-5-methyl-4-isoxazolepropionic acid (AMOA) and α-amino-2-(3-hydroxy-5-methyl-4-isoxazolyl)methyl-5-methyl-3-oxo-4-isoxazoline-4-propionic acid (AMNH) were stereotaxically injected into the striatum or into the CA3 region of hippocampus. Seven days later neuropathological examination including cell counts was performed on paraffin sections from the two brain regions. In the striatum, AMOA almost completely attenuated KA-induced cell damage, whereas AMNH showed no protective effect. In the hippocampal CA3 region none of the test compounds possessed neuroprotective properties against KA. These results seem to be consistent with a difference in the mechanisms responsible for the neurotoxic action of KA in the hippocampus compared to the striatum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00305866
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  • 10
    Electronic Resource
    Electronic Resource
    Capillary size and density in the cerebral cortex of rats with a porto-caval anastomosis (1977)
    Springer
    Acta neuropathologica 40 (1977), S. 117-122 
    Details
    ISSN: 1432-0533
    Keywords: Brain cortex ; Brain capillaries ; Alkaline phosphatase ; Porto-caval anastomosis ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Morphometric investigation by automatic image analysis of alkaline phosphatase positive brain capillaries was performed in control rats and in rats with a 30 days old porto-caval anastomosis. Rats with a porto-caval anastomosis showed an increased capillary diameter Di and as a consequence of this a decreased capillary surface-to-volume ratio Si/Vi. The free capillary distance was increased and the capillary length per unit brain volume LVi was decreased in the shunted rats compared to the controls. There was no difference in the percentage of the projected capillary area $$A_{A_i }$$ % between the two groups. It is suggested that the dilatation of the capillaries in rats with a porto-caval anastomosis is caused by the altered haemodynamic properties with a low mean blood pressure although the cardiac output is increased and that the alteration in free capillary distance and length per unit brain volume LVi is caused by dispersion by cortical edema induced by the porto-caval anastomosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688699
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