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  • 1
    ISSN: 1432-0533
    Keywords: Key words: Striatum – Substantia nigra – Apomorphine – Rotational behavior – Transient cerebral ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Behavioral and histological studies were performed on a reversible ischemia model in rats. At 60 days after unilateral transient middle cerebral artery occlusion for 30 min, the operated rats exhibited the ipsiversive rotational behavior elicited by systemic administration of dopamine receptor agonist apomorphine in a dose-dependent manner. Histologically, the ipsilateral striatum of the rats showed a subdivisional ischemic injury, while the nigral dopaminergic neurons appeared intact. The striatal lesions having a cell type-specific injury were located in the dorsolateral portion of the rostral striatum and in the lateral portion of the caudal part of the nucleus. Thus, the transient cerebral ischemia could successfully produce selective damage of a striatal subdivision, which causes an abnormality in motor controls in response to dopamine receptor stimulation. The present data may provide a part of functional and anatomical basis for understanding the movement disorders associated with basal ganglia dysfunction (e.g., parkinsonism), which may occur in patients with cerebrovascular disorders.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Transient cerebral ischemia ; Striatonigral system ; Calcineurin ; Parvalbumin ; Choline acetyltransferase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A topographical and cellular immunohistochemical analysis was performed on the striatonigral system of rats with unilateral, reversible middle cerebral artery (MCA) occlusion. Antibodies to calcineurin (CaN), parvalbumin (PV), choline acetyltransferase (ChAT) and glial fibrillary acidic protein (GFAP) were used in this study. Sixty days after the operation, the ipsilateral striatum showed a characteristic cell type-specific injury in the dorsolateral part of the nucleus (i.e., non-limbic striatum): a marked reduction in the number of medium-sized spinous neurons expressing CaN immunoreactivity and a selective sparing of PV-and ChAT-positive interneurons. There was also a marked depletion of striatonigral afferents visualized by CaN immunostaining in the lateral portion of the substantia nigra pars reticulata, which is considered to be implicated with motor function. In addition, it was noted that such striatonigral involvement was accompanied by marked gliosis showing strong GFAP immunolabeling. The present data suggest that rats with reversible MCA occlusion can be a useful animal model for studying cell type-specific ischemic injury and subdivisional involvement of the striatonigral pathway as a part of the cortico-subcortical loop subserving motor function.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: MK-801 ; Rotational behavior ; Basal ganglia circuits ; Transient cerebral ischemia ; 6-Hydroxydopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study shows that systemic administration of the selective, non-competitive N-methyl-d-aspartate antagonist MK-801 [(+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)-cyclohepten-5,10-imine] dose-dependently induces ipsiversive rotational behavior in the rats with a unilateral striatal lesion produced by transient middle cerebral artery occlusion or in those with a unilateral nigrostriatal lesion produced by 6-hydroxydopamaine. In relation to a functional model of the basal ganglia-thalamocortical ‘motor’ circuit, the present data suggest that the striatum may be one of the most important sites where MK-801 acts in the basal ganglia, with its being responsible for the circling behavior of the animal models.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Key words Cerebral aneurysm ; Immunohistochemistry ; Smooth muscle cell ; Phenotypic modulation ; Myosin heavy chain isoforms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We used immunohistochemical methods to analyze the phenotypes of smooth muscle cells (SMCs) in human cerebral arteries and aneurysmal walls. Thirty-two aneurysmal walls were studied; 31 aneurysmal walls were resected at operation and 1 aneurysm was obtained at autopsy. Seven control arteries were obtained at autopsy. Semiserial sections were subjected to immunohistochemical staining with antibodies to α-smooth muscle actin (α-SMA), desmin and smooth muscle myosin heavy chain isoforms: SM1, SM2 and SMemb. In control cerebral arteries, SMCs in the media were strongly immunostained for α-SMA, desmin, SM1 and SM2; immunoreactivity for SMemb was faint or weakly positive. SMCs in both non-ruptured and ruptured aneurysmal walls showed no staining for desmin; the expression of α-SMA was well preserved. Compared with control cerebral arteries, in 4 of 11 non-ruptured aneurysmal walls, the staining intensity of SMCs for SMemb was clearly increased. In ruptured aneurysmal walls, the expression of SM2 was lower than in control cerebral arteries and non-ruptured aneurysmal walls. Our study suggests that the phenotype of SMCs in aneurysmal walls is different from the contractile type in the media of normal cerebral arteries, at least partially changing to the synthetic type in some non-ruptured aneurysms. SMCs in ruptured aneurysmal walls may have lost both phenotypes before rupture. Phenotypic modulation of SMCs in the aneurysmal walls appears to be related to a remodeling of the aneurysmal wall and to a rupture mechanism.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0533
    Keywords: Glutamic acid decarboxylase ; Transient cerebral ischemia ; Rat brain Immunohistochemistry ; Cortical ischemic lesion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the expression of glutamic acid decarboxylase (molecular weight 67,000; GAD67) immunohistochemically in the rat cerebral cortex following transient middle cereral artery occlusion (MCAO) capable of producing slowly progressive neuronal damage. An increase in GAD67 immunoreactivity was observed in the cerebral cortex ipsilateral to the ischemic insult, most prominent in lamina IV, 3 to 14 days after MCAO. At this stage, light microscopy showed GAD67-positive puncta to be larger and more strongly immunoreactive in the ipsilateral cortex than those in the contralateral side. The elevated expression of GAD67 in the insulted cortex may reflect part of the adaptive functional changes in GABA transmission with slowly progressive cortical ischemic damage.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0533
    Keywords: Synaptophysin (protein p38) ; Striatum ; Immunoperoxidase ; Immunofluorescence ; Choline acetyltransferase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An immunoperoxidase technique was used to locate synaptophysin (protein p38), a major integral membrane glycoprotein of synaptic vesicles, in the rat brain. In addition to a diffuse distribution of nerve terminal stainings for synaptophysin appearing as numerous small puncta, the large-sized cells with spindled or polygonal shapes revealed perikaryal staining for synaptophysin in the striatum. The double labeling with immunofluorescence technique disclosed that the cell bodies, immunoreactive for synaptophysin, appeared to be those of the striatal giant cholinergic neurons. In addition, in rats that underwent the transient middle cerebral artery occlusion, the striatal ischemic lesions with cell type-specific injury revealed a survival of synaptophysin-positive large cells, presumably identical with the cholinergic neurons. The present study suggests that the metabolism and/or axonal transportation of synaptophysin of the giant cholinergic cells may be different from those of other neuronal populations in the striatum. Also, synaptophysin can act as a neurochemical marker for identification of the giant cholinergic neurons in the striatum of rats.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The exposure of cultured rat hippocampal neurons to 500 µM glutamate for 20 min induced a 55% decrease in the total Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) activity. The Ca2+-independent activity and autophosphorylation of CaM kinase II decreased to the same extent as the changes observed in total CaM kinase II activity, and these decreases in activities were prevented by pretreatment with MK-801, an N-methyl-d-aspartate (NMDA)-type receptor antagonist, and the removal of extracellular calcium but not by antagonists against other types of glutamate receptors and protease inhibitors. Similarly, the decrease in the CaM kinase II activity was induced by a Ca2+ ionophore, ionomycin. Immunoblot analysis with the anti-CaM kinase II antibody revealed a significant decrease in the amount of the enzyme in the soluble fraction, in contrast with the inverse increase in the insoluble fraction; thus, the translocation was probably induced during treatment of the cells with glutamate. These results suggest that glutamate released during brain ischemia induces a loss of CaM kinase II activity in hippocampal neurons, by stimulation of the NMDA receptor, and that inactivation of the enzyme may possibly be involved in the cascade of the glutamate neurotoxicity following brain ischemia.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have investigated regional and temporal alterations in Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) and calcineurin (Ca2+/calmodulin-dependent protein phosphatase) after transient forebrain ischemia. Immunoreactivity and enzyme activity of CaM kinase II decreased in regions CA1 and CA3, and in the dentate gyrus, of the hippocampus early (6–12 h) after ischemia, but the decrease in immunoreactivity gradually recovered over time, except in the CA1 region. Furthermore, the increase in Ca2+/calmodulin-independent activity was detected up to 3 days after ischemia in all regions tested, suggesting that the concentration of intracellular Ca2+ increased. In contrast to CaM kinase II, as immunohistochemistry and regional immunoblot analysis revealed, calcineurin was preserved in the CA1 region until 1.5 days and then lost with the increase in morphological degeneration of neurons. Immunoblot analysis confirmed the findings of the immunohistochemistry. These results suggest that there is a difference between CaM kinase II and calcineurin in regional and temporal loss after ischemia and that imbalance of Ca2+/calmodulin-dependent protein phosphorylation-dephosphorylation may occur.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0533
    Keywords: Key words Calretinin ; Striatum ; Transient cerebral ; ischemia ; Parvalbumin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study concerns the vulnerability of striatal interneurons immunopositive for the Ca2+-binding protein calretinin to ischemic neuronal injury. An immunohistochemical study was carried out on the striata of rats which had undergone transient middle cerebral artery occlusion. Two weeks after the ischemia, there was a marked reduction in the number of calretinin-positive neurons in the ipsilateral ischemic lesion, although the striatal interneurons positive for parvalbumin, which are a neuronal population distinct from the calretinin-immunoreactive cells in the striatum, were spared in the insulted areas. The present data indicate that the striatal calretinin-positive neurons are less resistant to transient ischemia, suggesting that there may exist vulnerability differences among the striatal interneurons in ischemia-induced neuronal injury.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0533
    Keywords: Calretinin ; Striatum ; Transient cerebral ischemia ; Parvalbumin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study concerns the vulnerability of striatal interneurons immunopositive for the Ca2+-binding protein calretinin to ischemic neuronal injury. An immunohistochemical study was carried out on the striata of rats which had undergone transient middle cerebral artery occlusion. Two weeks after the ischemia, there was a marked reduction in the number of calretinin-positive neurons in the ipsilateral ischemic lesion, although the striatal interneurons positive for parvalbumin, which are a neuronal population distinct from the calretinin-immunoreactive cells in the striatum, were spared in the insulted areas. The present data indicate that the striatal calretinin-positive neurons are less resistant to transient ischemia, suggesting that there may exist vulnerability differences among the striatal interneurons in ischemia-induced neuronal injury.
    Type of Medium: Electronic Resource
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