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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immunoreactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.
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PMID:An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia. 172 31

Differential vulnerability of the major components of microtubules was examined in ischemic gerbil brains by a light microscopic, immunohistochemical method using monoclonal antibodies for microtubule-associated protein (MAP) 1A and MAP2, polyclonal antibody for MAP1 and 2 as well as monoclonal antibody for alpha-tubulin. Progressive cerebral ischemia during unilateral carotid occlusion for 5, 15 and 120 min and reperfusion for 3, 12 and 48 h following bilateral carotid occlusion for 10 min were studied. Ischemic lesions in the subiculum-CA1 region were visualized by all antibodies after ischemia for 5 min but the antibody for alpha-tubulin was less sensitive. The antibody for alpha-tubulin was also less sensitive than antibodies for MAPs for detection of early postischemic lesions. Differential sensitivity was also observed in the cerebral cortex and other brain regions. Microtubules in myelinated axons were more stable than those in dendrites. The observed loss of immunohistochemical reactivities for MAPs and alpha-tubulin may have been caused by activation of calcium-dependent proteolytic enzymes such as calpains. The discrepancy between MAPs and alpha-tubulin could be due to differences in affinities or topographic distributions of these proteins within microtubules.
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PMID:Differential vulnerability of microtubule components in cerebral ischemia. 225 7

Degradation of neurofilament (NF) triplet proteins (Mw 200,000 (NF200), Mw 150,000 (NF150), Mw 68,000 (NF68], high molecular weight microtubule-associated proteins (MAP1 and MAP2) and other cytoskeletal proteins in rat brain during ischemia was investigated by sodium dodecyl sulfate (SDS)-gel electrophoresis and immunoblot methods using anti-NF200 monoclonal antibody. Selective degradation of NF200 and NF150 was observed during the initial 10 to 15 minutes of ischemia: and the degradation of MAP1 and MAP2 during the initial 15 to 30 minutes of ischemia. These degradations suggest that the activation of a protease occurs at the very early stage of cerebral ischemia, which are the earliest irreversible neuronal changes ever to be reported. Effect of ischemia on polymerization of microtubule proteins was also investigated by turbidity assay. A rapid decrease of the ability of polymerizing microtubules was observed during the initial 5 minutes of ischemia. This loss of polymerization ability was apparently independent of the degradation of MAP1 and MAP2.
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PMID:[Degradation of cytoskeletal proteins in cerebral ischemia]. 280 16

Sequential changes of [3H]glycine binding in the gerbil were investigated in selectively vulnerable areas 1 h to 7 days after 10 min of cerebral ischemia. A significant reduction in [3H]glycine binding was found in the hippocampus and thalamus from as early as 1 h after ischemia. In contrast, the striatum and frontal cortex showed a significant decline in [3H]glycine binding from 5 h after recirculation. Thereafter, a severe reduction in [3H]glycine binding was observed in all regions 7 days after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity was unaffected in the hippocampus, frontal cortex and thalamus up to 48 h after ischemia. Thereafter, a severe loss of MAP2-immunoreactive neurons was found in these regions, especially in the hippocampal CA1 sector. However, the striatum showed a severe loss of MAP2 immunoreactivity from 24 h after ischemia. These results demonstrate that transient cerebral ischemia causes severe reduction in [3H]glycine binding throughout the brain, and this reduction precedes the neuronal damage in selectively vulnerable areas. These findings suggest that a neurotransmitter, glycine, may play a key role in the pathogenesis of post-ischemic neurodegeneration in selectively vulnerable areas.
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PMID:Post-ischemic changes of [3H]glycine binding in the gerbil brain after cerebral ischemia. 767 5

Immunohistochemical changes of striatal interneurons in the gerbil were investigated 1 h-7 days after 10 min cerebral ischemia. Marked reduction of parvalbumin-immunoreactive interneurons was seen in the striatum from 24 h after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity markedly decreased in striatal neurons 5 h after ischemia but was unaffected in interneurons. Thereafter, a severe loss of MAP2 immunoreactivity in the interneurons was found 48 h and 7 days after ischemia. The results demonstrate that transient cerebral ischemia can cause a loss of parvalbumin and MAP2 immunoreactivity in interneurons in the dorsolateral striatum in a delayed fashion as compared with a rapid loss of striatal neurons.
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PMID:Delayed damage of striatal interneurons after cerebral ischemia in the gerbil. 797 Feb 28

Changes in drebrin, MAP2 (postsynaptic marker) and synaptophysin (presynaptic marker) in rat brains were examined after 20 min of transient cerebral ischemia. Immunoreactivity for drebrin and MAP2 in hippocampus CA1 area decreased 7 days after ischemia. The immunoreactivity for debrin in stratum lucidum of hippocampus CA3 area increased 7 days after ischemia. Sodium dodecyl sulfate gel electrophoresis and immunoblot procedures using an antibody to drebrin, MAP2 and synaptophysin were carried out. The levels of drebrin and MAP2 in hippocampus decreased significantly 4 hours and 7 days after recirculation. In contrast, the level of synaptophysin was unchanged. The levels of each protein in cerebral cortex showed no significant changes. The changes after ischemia seemed to occur at the same time both in the dendritic spines and in their shafts, and the increase of the immunoreactivity for drebrin in CA3 might suggest the change of cytoskeletal protein synthesis in survived neurons.
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PMID:[The changes of central nervous synapses after transient cerebral ischemia]. 858 59

Modifications of microtubule-associated proteins (MAP) have been reported in both acute and chronic degenerative conditions, such as cerebral ischaemia and Alzheimer's disease, and may be associated with cytoskeletal breakdown. Glutamate excitotoxicity has been implicated in the pathogenesis of both of these conditions and has been shown in some in vitro studies to induce changes in tau similar to those occurring in Alzheimer's disease. This study examines the effects of high extracellular glutamate concentrations on the distribution of tau and MAP2 in vivo in order to determine whether glutamate induces similar changes in tau to those previously reported in vitro in the intact, adult central nervous system. Monosodium glutamate was perfused into the rat parietal cortex for 90 min using in vivo microdialysis and at 4 h after the start of perfusion the distribution of tau and MAP2 was determined by immunohistochemistry. At the core of the glutamate-induced lesion tau immunostaining, as detected with the Tau 1 antibody, was decreased in axons and increased within perikarya compared to controls. Increased immunostaining was not apparent with polyclonal antibodies raised against full-length tau or towards the N or C termini of the protein. In contrast, increased tau immunoreactivity was detected, with all the antibodies used in this study, within oligodendrocytes following either glutamate or sodium chloride perfusion. MAP2 immunoreactivity was increased within perikarya at the core of the glutamate-induced lesion, while dendritic immunoreactivity was reduced. These results suggest that glutamate excitotoxicity in vivo may not be involved in neurofibrillary tangle formation but may be important in the progression of cytoskeletal pathology following cerebral ischaemia.
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PMID:Intracortical perfusion of glutamate in vivo induces alterations of tau and microtubule-associated protein 2 immunoreactivity in the rat. 884 65

Breakdown or disruption of the cytoskeleton has been implicated in the neurodegenerative processes of a variety of diseases, including Alzheimer disease (AD) and stroke. Studies of such diseases in the human involve the use of postmortem brain tissue. Postmortem delay may vary considerably from a few hours to a few days, and within this period, a degree of cytoskeletal breakdown may occur. It is therefore crucial to examine alterations occurring in the cytoskeleton as a result of postmortem delay and subtract these from those caused by the disease. In this study, the distribution of tau, MAP2, and MAP5 immunohistochemistry was examined following postmortem intervals of 0-72 h in the rat cerebral cortex, corpus callosum, caudate nucleus, and hippocampus. Each microtubule-associated protein (MAP) underwent unique changes that were dependent both on postmortem interval and the brain region examined. Following long postmortem delays, some of the changes in these proteins were similar to those seen in rodent models of cerebral ischemia. These results demonstrate that MAPs are not stable during postmortem delay in the rat. Therefore, caution must be exercised when interpreting changes in MAPs in human postmortem tissue, especially in cases where ischemic injury may be involved. Examination of control tissue carefully matched for postmortem delay is therefore essential to allow meaningful interpretation of cytoskeletal abnormalities in human neurodegenerative disease.
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PMID:The effect of postmortem delay on the distribution of microtubule-associated proteins tau, MAP2, and MAP5 in the rat. 916 90

alpha-Phenyl-N-tert-butyl Nitrone (PBN) is a free radical scavenger which recently has proved to be neuroprotective in experimental studies on focal cerebral ischemia and infarction. We therefore studied the effect of this drug in a model of moderate compression injury to rat spinal cord at the midthoracic level. The compound was given intraperitoneally 0.5 h before (100 mg/kg b.w) and at 1.5 h (50 mg/kg b.w) and 3.5 h (50 mg/kg b.w) after compression. Treated animals and controls (vehicle alone) were allowed to survive for 1 or 9 days following trauma. The functional outcome was tested by the inclined plane method and the motor performance score. By using MAP2 immunostaining the number of nerve cell bodies in the ventral horn and the ratio of MAP2 immunostained area to area of whole section of the cord were assessed to detect loss of neurons and loss of dendrites in the compressed segment. beta APP and PGP9.5 immunostaining was used to demonstrate axonal lesions. Treated and control rats showed at day 1 when tested with the inclined plane method a marked reduction of the capacity angle. This abnormality recovered gradually over the following days and was normalized at day 9. The motor performance score showed a marked reduction at day 1 which almost normalized at day 9. There was no difference regarding the functional outcome between rats given PBN and controls in none one of these functional tests. The spinal cord of normal rats presented immunoreactivity to MAP2 in nerve cell bodies and dendrites but not in axons and other structures. Following compression there was at day 1 and 9 a marked loss of MAP2 immunoreactivity in dendrites and nerve cell bodies. We could not detect any difference between the PBN and the control rats regarding the degree of cell loss or degree of reduction of dendrite staining. No difference between the two groups was seen with the axonal immunostainings (beta APP and PGP9.5). In conclusion, our study did not reveal any neuroprotective effect of PBN on the functional outcome and morphology (immunostaining to MAP2, beta APP and PGP9.5) in this model of moderate compression trauma to rat spinal cord.
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PMID:Effects of alpha-phenyl-N-tert-butyl nitrone (PBN) on compression injury of rat spinal cord. 935 Apr 23

Dopamine D1 and D2 receptors and uptake sites were studied in the gerbil hippocampus, parietal cortex and thalamus 1 h to 7 days after 10 min of cerebral ischemia using the occlusion of bilateral common carotid arteries. [3H]SCH23390 ([N-methyl-3H]R[+]-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-be nzazepine) and [3H]mazindol were used as markers of dopamine D1 receptors and uptake sites, respectively. [3H]Nemonapride was used to label dopamine D2 receptors. No obvious alteration in [3H]SCH23390 and [3H]mazindol binding was found in the hippocampus up to 48 h after ischemia. These bindings showed a significant reduction in the hippocampus after 7 days of recirculation. In contrast, [3H]nemonapride binding was unaffected in the hippocampus during the recirculation periods. The parietal cortex and thalamus also exhibited no significant changes in [3H]SCH23390, [3H]nemonapride and [3H]mazindol binding after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity was unchanged in all regions up to 48 h after ischemia. Thereafter, a marked loss of MAP2-immunoreactive neurons was observed in the hippocampal CA1 and CA3 neurons 7 days after recirculation. These findings were consistent with histological observations with cresyl violet staining. Our results demonstrate that dopamine D1 receptors and dopamine uptake sites in the hippocampus are susceptible to cerebral ischemia, whereas dopamine D2 receptors in this region are particularly resistant. Furthermore, these findings suggest that dopamine transmission may not be major factor in producing ischemic hippocampal damage.
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PMID:Effect of cerebral ischemia on dopamine receptors and uptake sites in the gerbil hippocampus. 944 59


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