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Biomedical subjects

K Kogure

Publications and source records attributed to K Kogure.

At least 289 records · Page 16Linked to original sources
PubMed1991

Distribution of protein kinase C in the hippocampus of the gerbil and rat: autoradiographic analysis by [3H]phorbol 12,13-dibutyrate.

In-vitro quantitative receptor autoradiography with [3H]phorbol 12,13-dibutyrate (PDBu) was used to determine the affinity constant (Kd) and the maximum number of receptor sites (Bmax) for protein kinase C (PKC) in subregions of the gerbil hippocampus, and to compare the distribution of [3H]PDBu binding sites in the gerbil hippocampus with that in the rat hippocampus. The Kd and Bmax values in the subregions of the gerbil hippocampus were estimated at 2.6-3.8 nM and 2.38-2.54 pmol (mg tissue)-1, respectively. The distribution of hippocampus [3H]PDBu binding sites was uniform in the gerbil but not in the rat. The [3H]PDBu binding activities in the strata oriens of the CA1 and CA3 subfields and the molecular layer of the dentate gyrus in the rat hippocampus were significantly higher than in the gerbil hippocampus. However, binding activity in the stratum lacunosum-moleculare of the rat CA1 subfield was statistically lower. These data demonstrate a difference in the distribution of [3H]PDBu binding activity in the hippocampus between the gerbil and rat.

Animals↗
PubMed1991

Immunocytochemical analysis of the cellular infiltrate in brain lesions in subacute sclerosing panencephalitis.

We studied lymphocyte subsets and major histocompatibility complex (MHC) class II antigens in frozen brain tissues from three patients with subacute sclerosing panencephalitis (SSPE) using immunocytochemical techniques. Perivascular cuffs consisted predominantly of T cells and MHC class II-positive cells. In the parenchymal lesions, there were frequent B and CD4+ cells. MHC class II-positive cells were also diffusely distributed throughout the parenchyma. There were more CD4+ than CD8+ cells both in the parenchyma and in the perivascular cuffs. These findings suggest an overrepresentation of CD4+ cells in SSPE lesions and that CD4+ cells may be involved in the pathogenesis of SSPE.

Adult↗
PubMed1991

Interleukin-6 in cerebrospinal fluid of HTLV-I-associated myelopathy.

We demonstrated significant titers of interleukin-6 (IL-6) in the CSF from 6 of 11 patients with HTLV-I-associated myelopathy (HAM). The patients positive for IL-6 generally had more severe clinical symptoms and signs than those negative for IL-6. There was no correlation between the value of IL-6 and inflammatory findings in the HAM CSF.

Adult↗
PubMed1991

Effect of mergocriptine on postischemic brain damages.

The effects of mergocriptine (2-methyl-a-ergocryptine; CBM36-733; CAS 81968-16-3) on ischemia-induced brain damages were studied using both a global and a focal ischemia model. First, immediately after 5 min of forebrain ischemia induced by ligation of the bilateral carotid arteries of Mongolian gerbils, the animals were intraperitoneally injected with 3 mg/kg or 10 mg/kg CBM36-733. Seven days after ischemia, perfusion-fixed brains were processed by conventional histology. The number of neurons per mm in the CA 1 pyramidal cell layer was calculated and they were labelled neuronal density. In the control group, the neuronal density was 69.7 +/- 7.2 (mean +/- SEM/mm), in the vehicle group and 3 mg/kg of CBM36-733 treated group, they were 12.2 +/- 4.4 and 11.6 +/- 5.1, respectively. The neuronal density in the 10 mg/kg of CBM36-733 treated group was 42.2 +/- 8.4. These data indicate that 10 mg/kg of CBM36-733 protects on the CA 1 neurons against ischemia induced delayed neuronal death. Second, the effect of long-term administration of 3 mg/kg CBM36-733 on focal brain ischemia of the rats was studied by measuring regional cerebral blood flow and glucose metabolism by autoradiograms. After 90 min of middle cerebral artery occlusion, the rats were intraperitoneally injected with 3 mg/kg of CBM36-733 every day for 2 weeks. There were no significant differences in cerebral blood flow and glucose metabolism between the treated group and the vehicle group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Protein kinase C activity in the gerbil hippocampus after transient forebrain ischemia: morphological and autoradiographic analysis using [3H]phorbol 12,13-dibutyrate.

The influence of transient forebrain ischemia on the temporal alteration of protein kinase C (PKC) activity in the gerbil hippocampus was analyzed by quantitative autoradiography using [3H]phorbol 12,13-dibutyrate (PDBu). The [3H]PDBu binding activity in the stratum oriens of the CA1 subfield increased at 6 h after ischemia, but the binding activity in this subfield decreased at 7 days after ischemia. In contrast, the [3H]PDBu binding activity increased in the molecular layer of the dentate gyrus at 7 days after ischemia. Pre-treatment of pentobarbital prevented an increase in the [3H]PDBu binding activity in the stratum oriens of the CA1 subfield at 7 days after ischemia. These results indicate the possibilities that PKC may play a pivotal role in the post-ischemic neuronal damage in the hippocampal CA1 subfield.

Animals↗
PubMed1990

Effects of cycloheximide on delayed neuronal death in rat hippocampus.

The effect of cycloheximide, a protein synthesis inhibitor, on hippocampal selective neuronal death was morphologically studied in rats subjected to 10 min forebrain ischemia using a 4-vessel occlusion model. Neuronal damage in the hippocampal CA1 subfield 72 h after ischemic insult was dramatically decreased by the lasting inhibition of protein synthesis through consecutive administration of cycloheximide. Cycloheximide, which was administered once within the first 24 h of recirculation, showed protective action on ischemic cell necrosis and its most potent effect was observed when injected at 12 h of post-ischemia. After 36 h of recirculation, however, treatment with cycloheximide could no longer prevent cell death. The possibility is considered that hippocampal delayed neuronal death following transient ischemia is caused by abnormal protein(s).

Animals↗
PubMed1990

Postischemic alterations of spontaneous activities in rat hippocampal CA1 neurons.

Changes of spontaneous impulse discharges in rat hippocampal neurons during and after transient forebrain ischemia were investigated electrophysiologically. Spontaneous impulse frequencies of CA1 neurons before ischemia were varied from 0.4 to 20.0 impulses/s and its average was 5.8 +/- 1.2 (means +/- S.E., n = 36). These spontaneous discharges were completely suppressed during forebrain ischemia except for the transient hyperactivity observed just after the beginning of ischemia. Recovery of spontaneous discharges of CA1 neurons from suppression induced by 5 min ischemia started at 5 min, and neuronal activities were restored to pre-ischemic levels approximately 30 min after reperfusion. On the other hand, spontaneous impulse frequencies at all time points recorded after 20 min ischemia were less than 40% of the pre-ischemic levels. These continuous suppression of spontaneous activity after 20 min ischemia may suggest that neuronal function is impaired during and/or in the early stages of reperfusion, and functional disorders precede morphological degeneration.

Anesthesia↗
PubMed1990

Neuronal damage and calcium accumulation following repeated brief cerebral ischemia in the gerbil.

We investigated the distribution of neuronal damage following brief cerebral transient ischemia and repeated ischemia at 1-h intervals in the gerbil, using light microscopy and 45Ca autoradiography as a marker for detection of ischemic damage. The animals were allowed to survive for 7 days after ischemia induced by bilateral carotid artery occlusion. Following 2-min ischemia, neuronal damage determined by abnormal calcium accumulation was not observed in the forebrain regions. Following 3-min ischemia, however, abnormal calcium accumulation was recognized only in the hippocampal CA1 sector and part of the striatum. Two 2-min ischemic insults caused extensive abnormal calcium accumulation in the dorsolateral part of striatum, the hippocampal CA1 sector, the thalamus, the substantia nigra and the inferior colliculus. The ischemic insults were more severe than that of a single 3-min ischemia. However, three 1-min ischemic insults caused abnormal calcium accumulation only in the striatum. On the other hand, three 2-min ischemic insults caused severe abnormal calcium accumulation in the brain. The abnormal calcium accumulation was found in the dorsolateral part of striatum, the hippocampal CA1 sector, the thalamus, the medial geniculate body, the substantia nigra and the inferior colliculus. Gerbils subjected to three 3-min ischemic insults revealed most severe abnormal calcium accumulation. Marked calcium accumulation was seen not only in the above sites, but also spread in the neocortex, the septum and the hippocampal CA3 sector. Morphological study after transient or repeated ischemia indicated that the distribution and frequency of the neuronal damage was found in the sites corresponding to most of the regions of abnormal calcium accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Exo-focal postischemic neuronal death in the rat brain.

We describe delayed neuronal damage in ipsilateral areas remote from the ischemic area of rat brain after transient focal ischemia induced by embolization of the right middle cerebral artery (MCA). After 15, 30, 60 and 90 min of MCA occlusion, recirculation was achieved by removal of the embolus. Chronological changes in the distribution of the neuronal damage were determined by using the 45Ca autoradiographic technique and the histological method, and the mechanism involved was investigated by measuring local cerebral glucose metabolism. Depending on the duration of ischemia, 45Ca accumulation extended to the lateral segment of the caudate putamen and to the cerebral cortex, both supplied by the occluded MCA. Moreover, 3 days after ischemic insult, 45Ca had accumulated in the ipsilateral substantia nigra and ventral posterior nucleus of the thalamus. Histological examination revealed that the neurons in both areas suffered damage and were selectively reduced in number. Cerebral glucose utilization decreased in the thalamus, but increased approximately 30% (P less than 0.01) in the substantia nigra compared with the value in the corresponding contralateral area. Both areas lie outside the ischemic area, but have transsynaptic connections with the ischemic focus. Based on the present study, we suggest that the mechanisms of delayed neuronal death in these two remote areas may not be identical, but that this phenomenon may be caused by a transsynaptic process associated with the ischemic focus.

Animals↗
PubMed1990

The regional difference of neuronal susceptibility in the dentate gyrus to hypoxia.

The effects of hypoxia on neuronal activity in dentate gyrus granule cells were studied in submerged guinea pig hippocampal slices. In all regions of the dentate gyrus granule, the amplitude of the population spike recorded from the dentate granule cell layers, in response to electrical stimulation of the perforant path, decreased during hypoxia and recovered during reoxygenation. However, the ventral dentate gyrus granule cells (upper blade) were more susceptible to hypoxia than the dorsal ones (lower blade), indicating regional differences of neuronal susceptibility to hypoxia in the dentate gyrus.

Action Potentials↗
PubMed1990

Ca2+/calmodulin-dependent protein kinase II immunoreactivity in the rat hippocampus after forebrain ischemia.

The influence of transient forebrain ischemia on the temporal alteration of Ca2+/calmodulin-dependent kinase II (CaM kinase II) in the rat hippocampus was analysed by the immunohistochemical method using antigen-affinity purified polyclonal antibodies against CaM kinase II of rat brain. Six to twenty-four hours after ischemia, CA1 and CA3 pyramidal cells, and dentate granule cells lost CaM kinase II immunoreactivity in neuronal perikarya, although immunoreactivity in the dendritic fields was preserved. The recovery of immunoreactivity of the CA3 pyramidal cells and dentate granule cells was noted 3 days after recirculation. Seven days after ischemia, immunoreactivity in the CA1 subfield was greatly reduced. These results suggest that CaM kinase II molecules in the CA1 subfield are preferentially located on the CA1 pyramidal cells and that CaM kinase II plays a critical role in the reconstruction of neuronal cytoskeleton and neuronal networks damaged by ischemic insult.

Animals↗
PubMed1990

Role of the excitotoxic mechanism in the development of neuronal damage following repeated brief cerebral ischemia in the gerbil: protective effects of MK-801 and pentobarbital.

Pretreatment with MK-801 (an NMDA antagonist) or pentobarbital (a GABAA receptor-effector) ameliorated histopathological neuronal damage to the hippocampal CA1 subfield and to the thalamus following three 2-min forebrain ischemia at 1-h intervals in the gerbil. Flunarizine, a calcium antagonist, failed to prevent the neuronal damage. The results suggest that the excitotoxic mechanism plays a role in the neuronal damage following repeated ischemia.

Animals↗
PubMed1990

Protective effect of alpha-tocopherol on ischemic neuronal damage in the gerbil hippocampus.

The effect of alpha-tocopherol (vitamin E) on ischemic neuronal damage was studied in the gerbil. The animals were subjected to 5 min of cerebral ischemia by bilateral common carotid artery occlusion. Immediately after ischemia, alpha-tocopherol at a dose of 50 or 100 mg/kg was administered intravenously. Morphological changes in the CA1 sector of the hippocampus were evaluated after 7 days of survival. alpha-Tocopherol prevented ischemia-induced neuronal death. The average density of CA1 pyramidal neurons (cells/mm, mean +/- S.E.M.) was 252 +/- 8 (n = 8) in the sham-operated group, 50 +/- 20 (n = 8) in the ischemia group, and 140 +/- 35 (n = 8) and 182 +/- 36 (n = 8) in the groups treated with alpha-tocopherol at the doses of 50 and 100 mg/kg, respectively. The results suggest that free radical scavenging action of alpha-tocopherol played an important role in preventing the neuronal death.

Animals↗
PubMed1990

Nimodipine attenuates both ischaemia-induced brain oedema and mortality in a rat novel transient middle cerebral artery occlusion model.

A novel transient middle cerebral artery (MCA) occlusion model in rats was used to evaluate the effects of nimodipine on 45Ca accumulation, brain oedema and mortality. Nimodipine (1 microgram/kg/min, IV, 30 min) administered immediately after 3 hr of transient unilateral MCA occlusion significantly attenuated the post-ischaemic increase of tissue water content, partly 45Ca accumulation in the parietotemporal and frontal cortices ipsilateral to the left MCA occlusion 3 hr after reperfusion. Nimodipine decreased the mortality rate at 6 and 9 hr time points after recirculation, although the survival rate at the 24 hr point after recirculation was not different from the control group. These results suggest that nimodipine has beneficial effects in the early phase of reperfusion period.

Animals↗
PubMed1990

Experimental analysis of gastric mucosal blood flow after transient forebrain ischemia.

Gastric mucosal blood flow (GMBF) was measured by a laser doppler flow meter continually during and after transient forebrain ischemia in rats. The value of GMBF obtained after at 15 min of ischemia did not change significantly compared to that of the preischemic period. However, a 26% decrease of GMBF was detected after 30 min of ischemia. When circulation of the brain was restored, the GMBF increased slightly after 15 min. After 30, 45, and 60 min of restored cerebral circulation, the GMBF decreased significantly and the values were 63%, 58% and 51% of the control, respectively.

Animals↗
PubMed1990

Neuronal damage following non-lethal but repeated cerebral ischemia in the gerbil.

Brief, non-lethal transient forebrain ischemia in the gerbil can injure selectively vulnerable neurons when such ischemia is induced repeatedly. The influence of the number and interval of the ischemic insults on neuronal damage, as well as the time course of damage, following repeated 2-min forebrain ischemia were examined. A single 2-min ischemic insult caused no morphological neuronal damage. A moderate number of hippocampal CA1 neurons were destroyed following two ischemic insults with a 1-h interval, and destruction of almost all CA1 neurons resulted from three or five insults at 1-h intervals. Three and five insults also resulted in moderate to severe damage to the striatum and thalamus, depending on the number of episodes. Although three ischemic insults at 1-h intervals caused severe neuronal damage, this number of insults at 5-min and 4-h intervals caused destruction of relatively few neurons, and no neurons were destroyed at 12-h intervals. Following three ischemic insults at 1-h intervals, damage to the striatum, neocortex, hippocampal CA4 subfield and thalamus was observed at 6-24 h of survival, whereas damage to the hippocampal CA1 subfield appeared at 2-4 days. The results indicate that even a brief non-lethal ischemic insult can produce severe neuronal damage in selectively vulnerable regions when it is induced repeatedly at a certain interval. The severity of neuronal damage was dependent on the number and interval of ischemic episodes.

Animals↗