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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regional distribution of the postsynaptic microtubule-associated protein 2 (MAP2) and the presynaptic marker protein synaptophysin was investigated by immunohistochemistry in brains of rats submitted to 30-min forebrain ischemia by four-vessel occlusion. The following brain temperature profiles during ischemia were compared: (1) constant brain temperature of 36 degrees C (normothermia; n = 5); (2) spontaneous temperature decline from 36 degrees to 31 degrees C (spontaneous hypothermia; n = 5) and (3) constant temperature of 30 degrees C (induced hypothermia; n = 5). Normothermia was produced by exposing the ischemic head to an external heat source, and induced hypothermia by cooling the head with liquid nitrogen vapours. Sham-operated animals were either kept at ambient temperature or exposed to the same heat source, as required for maintaining normothermia during ischemia. Seven days after sham operation or ischemia, brains were fixed by perfusion and processed for immunohistochemistry using monoclonal antibodies against MAP2 and synaptic vesicle-specific protein (synaptophysin). Normothermic ischemia resulted in complete loss of MAP2 immunostaining in the whole hippocampus, spontaneous hypothermic ischemia in complete loss of MAP2 in CA1 sector, and induced hypothermic ischemia only in variable loss of MAP2 in CA1 sector. Post-ischemic immunostaining of synaptophysin revealed a temperature-dependent increase in stratum lacunosum-moleculare of CA1 sector, the density of which correlated inversely with MAP2 staining. Comparison with morphological alterations showed a close relationship between loss of MAP2 staining and histological injury. The post-ischemic activation of synaptophysin may reflect regenerative processes associated with synaptic remodelling and, therefore, is an indirect marker of the severity of ischemic injury.
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PMID:Temperature effect on immunostaining of microtubule-associated protein 2 and synaptophysin after 30 minutes of forebrain ischemia in rat. 849 60

The utility of microtubule-associated protein 2 (MAP2) immunostaining as a marker of acute focal ischemic injury was investigated. Permanent middle cerebral artery occlusion (MCAO) elicited a rapid reduction in MAP2 immunostaining that was visible 1 h post-MCAO and that increased in intensity and area encompassed over time. The ischemic lesion borders were well defined by loss of MAP2 immunostaining, but alterations in staining within the lesion were more heterogeneous. Lesion volume increased significantly from 1 to 4 h post-MCAO (from 63.8 +/- 10.8 to 111.3 +/- 19.0 mm3, mean +/- SD). Thus, MAP2 immunostaining is a sensitive, quantifiable indicator of acute brain injury following focal ischemia.
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PMID:Acute focal ischemia-induced alterations in MAP2 immunostaining: description of temporal changes and utilization as a marker for volumetric assessment of acute brain injury. 853 May 50

Using a silver impregnation (argyrophil III) and immunohistochemistry, acute cytopathic features after cerebral ischemia were investigated. Additionally, functional recovery and interconnection between the host and graft was also explored after neural graft. Animals were embolized in unilateral middle cerebral artery for 1 h. Argyrophil III method demonstrated "collapsed" dark neurons in the striatum, cortex, reticular thalamus, amygdala, and hypothalamus on ischemic side. These neurons exhibited characteristic shrunken somata with corkscrew-like dendrites, suggesting changes in cytoskeletal protein. In the above mentioned areas, the loss of immunoreactivity for mu-calpain proenzyme and microtubule-associated protein 2 was also detected. Neural graft into the ischemic striatum was made 2 weeks after the ischemia paradign. The grafted striatal cells were prepared from E15 fetuses to make cell suspension marked by rhodamine-labeled latex microspheres. Methamphetamine-evoked rotations were detected after ischemia. These motor alterations were reduced gradually but significantly at 8 weeks after the graft. Interconnecton between the host and grafted cells was then studied in a brain slice preparation after loading fura-2 AM. About 10% of grafted cells tested from rats that showed motor amelioration exhibited [Ca2+]i increase to the electrical stimulation applied to the neighboring host tissue. Data indicate that, in the very early stage after ischemia, cytoskeletal damages, especially on microtubules, started and this would lead to later infarct. The graft survived in the ischemic striatum having connections with the host, and this might be partly involved in the amelioration of motor function.
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PMID:Early cytopathic features in rat ischemia model and reconstruction by neural graft. 863 48

Argyrophil III silver impregnation is a very sensitive method to detec t the early damage to neurons following brain ischemia. The argyrophil III staining and microtubule-associated protein 2 (MAP2) immunocytochemistry were performed on PC12D cells and MAP2C cDNA-transfected COS7 cells to detect the changes cytoskeletal proteins (microtubules/MAP2). After exposing these cells to simulated ischemic condition (oxygen and/or glucose free), the correlation between the appearance of the argyrophilia and the disappearance of MAP2 was investigated. The PC12D cells expressed very low MAP2 and became argyrophilic very easily depending on the degree of the ischmeia-like insult, whereas MAP2C cDNA-transfected COS7 cells expressed a higher level of MAP2C and were resistant to argyrophilia, although the diameter of their immunoreactive processes became thinner. Thus, when MAP2C is expressed at a higher level, cells became resistant to argyrophilia, suggesting a correlation between the argyrophilia and the damage on microtubules and MAPs.
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PMID:Microtubule-associated protein 2 expressing COS7 cells are resistant to argyrophilia under oxygen- and glucose-free condition. 863 51

Progression of ischemic damage was investigated immunohistochemically in neural dendrites using microtubule-associated protein 2 (MAP2) as a dendritic marker in the rat's brainstem. Neuronal soma and dendrites were clearly stained by this protein but some structures such as axonal bundles, glia and endothelial cells were not visualized. When the anterior inferior cerebellar artery (AICA) was occluded unilaterally for 30 min, a wide ischemic lesion was detected in the occluded side of the brainstem and was observed as a loss of reaction to MAP2. After ischemia for 2 h, loss of reaction in the perikarya and dendrites was seen to expand to the ipsilateral (occluded side) cochlear nucleus. When the basilar artery was blocked, ischemic damage in the vestibular nucleus was more intense than that in the cochlear nucleus. In all specimens studied, differences in anatomical blood supply demonstrated selective tissue vulnerability for ischemic damage.
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PMID:Brainstem ischemic damage following occlusion of the blood vessels in the rat's posterior cerebral circulation. 865 61

Calpain, a neutral protease activated by calcium, may promote microtubular proteolysis in ischemic brain. We tested this hypothesis in an animal model of focal cerebral ischemia without reperfusion. The earliest sign of tissue injury was observed after no more than 15 min of ischemia, with coiling of apical dendrites immunolabeled to show microtubule-associated protein 2 (MAP2). After 6 h of ischemia, MAP2 immunoreactivity was markedly diminished in the infarct zone. Quantitative Western analysis demonstrated that MAP2 was almost unmeasurable after 24 h of ischemia. An increase in calpain activity, shown by an antibody recognizing calpain-cleaved spectrin fragments, paralleled the loss of MAP2 immunostaining. Double-labeled immunofluorescent studies showed that intraneuronal calpain activity preceded evidence of MAP2 proteolysis. Perikaryal immunolabeling of tau protein became increasingly prominent between 1 and 6 h in neurons located within the transition zone between ischemic and unaffected tissue. Western blot experiments confirmed that dephosphorylation of tau protein occurred during 24 h of ischemia, but was not associated with significant loss of tau antigen. We conclude that focal cerebral ischemia is associated with early microtubular proteolysis caused by calpain.
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PMID:Microtubular proteolysis in focal cerebral ischemia. 889 91

The effects of prostaglandin E1 (PGE1) on transient forebrain ischemia were studied in the gerbil. The animals were randomly divided into six groups of 6 each according to the method of administration as follows: group 1, no administration; group 2, subcutaneous administration with 5 ml.kg-1 of physiological saline, 30 min prior to ischemia; group 3, the same method with 3 mg.kg-1 of PGE1; group 4, 3 mg.kg-1 of PGE1, during 24 hours (12 hours prior to ischemia, and 12 hours following ischemia); group 5, 3 mg.kg-1 of PGE1, during 96 hours (12 hours prior to ischemia and 84 hours following ischemia); and group 6, sham operation. They were anesthetized with isoflurane and transient forebrain ischemia was induced by occluding bilateral common carotid arteries for 5 min. The extracranial electroencephalogram (EEG) was recorded from the electrodes placed at the vertex. During the experimental procedures, temperatures at tympanic membrane and rectum were maintained at 37.0 +/- 0.2 degrees C by means of a heating mat and control of the air temperature in all groups. After 6 days of survival, they were sacrificed, and the brain tissues were fixed for the immunohistochemical and histopathological analyses. The hippocampal CA 1 regions were stained for monoclonal anti microtubule-associated protein 2 (MAP 2), and hematoxylin and eosin. In the 4th group, EEG recovery was recognized earlier than the other groups. Immunoreactivities for MAP 2 and the number of surviving pyramidal cells after ischemia in the CA 1 regions were also well maintained. These results suggest the PGE1, has protective effects against degradation of cytoskeletal proteins and delayed neuronal death in the gerbil, and it might be due to direct protective action of cell membrane in addition to its microcirculatory improvement.
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PMID:[Effects of prostaglandin E1 on transient forebrain ischemia, especially in hippocampal CA 1 regions of the gerbil]. 893 17

Increased intracellular calcium and cytoskeletal damage play a crucial role in neuronal death following injury such as cerebral ischemia. The effect of brain temperature on early intracellular calcium increase and neuronal cytoskeletal damage following cerebral ischemia has not been rigorously investigated. In the current communication we evaluated calmodulin (CaM) and microtubule-associated protein 2 (MAP2) in the same brain section using a double labeling immunohistochemical technique, and obtained evidence that the brain temperature has a significant effect on the early calcium increase and cytoskeletal damage as well as the delayed neuronal death occurring in CA1 sector of the gerbil hippocampus after transient forebrain ischemia. In the normothermia (36.7 degrees C) group, CaM and MAP2 immunoreactivity were markedly decreased within 48 h after ischemia and thereafter dramatic neuronal death (grade 3) was seen in the CA1 sector at 7 days. Mild hypothermia (33.3 degrees C) significantly protected against all these changes, whereas cytoskeletal damage and delayed neuronal death were aggravated by mild hyperthermia (39.7 degrees C). We conclude that mild hypothermia protects the brain against transient forebrain ischemia by reducing early cytoskeletal damage and subsequent neuronal death.
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PMID:Effects of brain temperature on calmodulin and microtubule-associated protein 2 immunoreactivity in the gerbil hippocampus following transient forebrain ischemia. 906 42

In order to achieve a better understanding of the pathophysiology of ischemic white matter lesions, oligodendrocytic degeneration and subsequent proliferation were examined in the mouse model of middle cerebral artery occlusion. In situ hybridization histochemistry for proteolipid protein messenger RNA was employed as a sensitive and specific marker of oligodendrocytes, and immunohistochemistry for myelin basic protein was used as a compact myelin marker. Immunohistochemistry for microtubule-associated protein 2 and albumin was employed to monitor neuronal degeneration and the breakdown of the blood brain barrier, respectively. In the ischemic core of the caudoputamen, the immunoreactivity for microtubule-associated protein 2 disappeared and massive albumin extravasation occurred several hours after vessel occlusion, while proteolipid protein messenger RNA signals remained relatively strong at this time. The messenger RNA signals began to attenuate 12 h after ischemia and were hardly detectable 24 h after ischemia in the whole ischemic lesion. In situ end-labeling of fragmented DNA showed some cells with proteolipid protein messenger RNAs to have DNA fragmentation at this period. In contrast to proteolipid protein messenger RNA signals, the immunoreactivity for myelin basic protein was detected as long as five days after ischemia. An apparent increase in the cells possessing strong proteolipid protein messenger RNA signals was found five days after ischemia, mainly in the corpus callosum and the cortex bordering the infarcted areas. A double simultaneous procedure with in situ hybridization for proteolipid protein messenger RNA and immunohistochemistry for glial fibrillary acid protein or lectin histochemistry for macrophages/microglia showed proliferating oligodendrocytes to be co-localized with reactive astrocytes and macrophages/microglia. These findings show that oligodendrocytic damage occurred following ischemic neuronal damage and the breakdown of the blood brain barrier, but preceded the breakdown of myelin proteins in the ischemic lesion, that an apoptosis-like process was involved in ischemic oligodendrocytic death, and that surviving oligodendrocytes responded and proliferated in the outer border of the infarcted area.
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PMID:Ischemic damage and subsequent proliferation of oligodendrocytes in focal cerebral ischemia. 907 Jul 57

We examined the immunohistochemical regional distribution of calcineurin (Ca2+/calmodulin-dependent protein phosphatase) in the adult rat hippocampus, following various regional destruction. In the normal adult rat hippocampus, the calcineurin immunoreactivity showed a characteristic pattern. This protein phosphatase was detected in all layers of the CA1 subfield, including the cytoplasm of the pyramidal cells, whereas it was strongly evident in the stratum lucidum and moderately so in the cytoplasm of pyramidal cells in the CA3 subfield. Seven days after transient forebrain ischemia, which induced destruction of CA1 pyramidal cells, the calcineurin immunoreactivity decreased in all layers of the CA1 subfield, while the immunoreactivity for synapsin I, a marker of the presynaptic site, was preserved. Seven days after the intraventricular injection of kainate, which induced destruction of CA3 pyramidal cells, the calcineurin immunoreactivity in the stratum lucidum was preserved, although the immunostaining pattern of the stratum lucidum changed when CA3 pyramidal cells were destroyed. Seven days after mechanical destruction of the dentate gyrus and CA4 subfield, which induced destruction of mossy fibers, the calcineurin immunoreactivity in the stratum lucidum was lost, except in the far site of the stratum lucidum. In the CA1 subfield, calcineurin was mainly located in postsynaptic sites, while it was mainly located in the presynaptic sites in the mossy fibers of the CA3 subfield. The immunohistochemistry of adjacent sections with antibodies of microtubule-associated protein 2 and synapsin I, which are markers of postsynaptic and presynaptic sites respectively, supports these results. Thus, calcineurin has a different synaptical distribution in the rat hippocampus.
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PMID:Calcineurin in the adult rat hippocampus: different distribution in CA1 and CA3 subfields. 915 50


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