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Biomedical subjects

K Kogure

Publications and source records attributed to K Kogure.

At least 343 records · Page 19Linked to original sources
PubMed1989

Proto-oncogene c-fos is transiently induced in the rat cerebral cortex after forebrain ischemia.

The amounts of mRNAs for proto-oncogene c-fos and structural protein beta-actin were measured in the rat cerebral cortex after transient forebrain ischemia. A transient and specific induction of c-fos mRNA was noticed in the cerebral cortex 30-90 min after ischemia followed by decline to control value. In contrast, the level of mRNA for beta-actin was not altered throughout the recirculation period examined. These results suggest specific role of c-fos gene after brain damage.

Animals↗
PubMed1989

Protein kinase C activity in the rat hippocampus after forebrain ischemia: autoradiographic analysis by [3H]phorbol 12,13-dibutyrate.

The influence of transient forebrain ischemia on the temporal alteration of protein kinase C (PKC) activity in the rat hippocampus was analyzed by quantitative autoradiography using [3H]phorbol 12,13-dibutyrate [( 3H]PDBu). As reported previously, the grain density was highest in the strata oriens and radiatum in the CA1 subfield. After transient forebrain ischemia (20 min), the [3H]PDBu binding in the CA1 subfield gradually increased during early recirculation, and became maximum 6-12 h after ischemia, when no microscopic damage of the CA1 pyramidal cells was obvious. Thereafter, grain density decreased and binding activity in the CA1 was lost by approximately 40% 7 days after ischemia, when CA1 pyramidal cells had become necrotic. This indicated a close association of phorbol ester binding sites with CA1 pyramidal cells. By contrast, [3H]PDBu binding sites were unchanged in the stratum radiatum in the CA3 throughout the recirculation, although the number of binding sites in the stratum oriens of the CA3 was decreased during early recirculation period. Seven days after recirculation, in the molecular layer of the dentate gyrus, where granule cells remained intact, [3H]PDBu binding activity increased by 33%, with a higher grain density in the inner region (supragranular layer). These results suggest that enhancement of PKC activity and/or translocation of the enzyme play an important role in the postischemic modulation of synaptic efficacy in the hippocampal formation and neuronal death of CA1 pyramidal cells.

Animals↗
PubMed1989

Neuronal damage following repeated brief ischemia in the gerbil.

The effect of repetition of brief ischemia, which causes no morphological brain damage when given as a single insult, was studied. Two-minute forebrain ischemia was induced in gerbils singly and 3 or 5 times at 60-min intervals. Although 2-min ischemia induced no neuronal damage, 3 or 5 repeated ischemic insults caused neuronal damage in the selectively vulnerable regions, the severity being dependent on the number of episodes.

Animals↗
PubMed1989

Prevention of delayed neuronal death in gerbil hippocampus by a novel vinca alkaloid derivative (vinconate).

We investigated the effect of vinconate, a novel vinca alkaloid derivative, on delayed neuronal death using Mongolian gerbils. The animals were allowed to survive for 7 d after 3 or 5 min of forebrain ischemia induced by bilateral occlusion of the common carotid arteries. Morphological changes and calcium (45Ca) accumulation were evaluated in the CA1 sector of the hippocampus after ischemia. Vinconate (50, 100, and 300 mg/kg) showed protective effects against neuronal death in a dose-dependent manner when administered intraperitoneally (ip) 10 min before 5 min of ischemia. However, the administration of vinconate (100 and 300 mg/kg, ip) immediately after 5 min of ischemia showed no therapeutic effect, whereas a marked therapeutic effect of vinconate (50 and 100 mg/kg, ip) was observed when administered immediately after 3 min of ischemia. An anesthetic dose of pentobarbital (40 mg/kg, ip) also produced significant protection against neuronal death. Furthermore, a 45Ca autoradiographic study indicated that a marked calcium accumulation was found in the Ca1 sector at 7 d after 5 min of ischemia, which was consistent with the extent of histological neuronal damage. When vinconate (100 and 300 mg/kg, ip) was administered 10 min before 5 min of ischemia, the abnormal calcium accumulation was not detected in the CA1 sector. These data indicate that suppression of abnormal neuronal activity may be owing to the antagonistic action of vinconate on calcium accumulation.

Animals↗
PubMed1989

Excitatory amino acid binding sites in the rat hippocampus after transient forebrain ischemia.

The influence of transient forebrain ischemia on the temporal alteration of glutamate receptors in the hippocampal formation was analyzed by means of in vitro quantitative receptor autoradiography. We compared the binding of N-methyl-D-aspartate (NMDA) receptors using [3H]3-[+/-)2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), noncompetitive NMDA antagonist binding sites using [3H]N-(1-(2-thienyl)-cyclohexyl)-3,4-piperidine (TCP), and kainate (KA) receptors. In the CA1 subfield of the hippocampus, the number of NMDA receptors and noncompetitive NMDA antagonist binding sites remained constant during the early stage of recirculation when the CA1 pyramidal cells remained histologically intact. A significant reduction of these receptor densities was observed 7 days following ischemia, when NMDA receptors and noncompetitive NMDA antagonist binding sites lost 64 and 29% of their binding sites in the stratum radiatum of the CA1, respectively. The KA receptor density in the CA1 subfield decreased by 44% 7 days after ischemia. Marked loss of the above-mentioned receptors in the CA1 after selective depletion of the CA1 pyramidal cells indicated that NMDA receptors, noncompetitive NMDA antagonist binding sites, and KA receptors in the CA1 are predominantly localized on the CA1 pyramidal cells. NMDA receptor density in the CA3 gradually decreased during the recirculation period. The stratum moleculare of the dentate gyrus, whose structure was histologically intact after ischemic insult, also showed a reduction of NMDA receptors 7 days following ischemia. [3H]KA receptor density in the stratum lucidum of the CA3 and in the hilus also decreased during recirculation. These

Amino Acids↗
PubMed1989

Effects of a new calcium channel blocker, KB-2796, on protein synthesis of the CA1 pyramidal cell and delayed neuronal death following transient forebrain ischemia.

The effects of a new calcium channel blocker, 1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)-piperazine dihydrochloride (KB-2796), on delayed neuronal death (DND) in the hippocampus were examined in gerbils in comparison with those of pentobarbital and flunarizine. The neuronal density in the hippocampal CA1 subfield was counted on the seventh day of recirculation following 5 min of bilateral carotid occlusion, and protein biosynthesis in the brain was also determined at 1, 2, 4, 24, and 72 h following occlusion. The drugs were intraperitoneally administered after recirculation. KB-2796 (10 mg/kg) significantly prevented DND in the CA1 subfield. Pentobarbital (40 mg/kg), but not flunarizine (3 and 10 mg/kg), inhibited DND. Protein synthetic activity in the CA1 subfield was reduced by ischemia and the reduction was not restored even at 72 h after recirculation. KB-2796 did not ameliorate the reduction of protein synthesis in the CA1 subfield by 24 h after recirculation, but in one of three animals restoration of protein synthesis was observed at 72 h of recirculation. Pentobarbital also restored the reduced protein synthesis in two of three animals at 72 h. These results suggest that calcium influx into neurons participates in the pathogenesis of DND, and also that KB-2796 might prevent both morphological and functional cell damage in CA1 neurons induced by transient ischemia.

Animals↗
PubMed1989

Prevention of ischemic neuronal damage by alpha 1-adrenoceptor agonist (methoxamine).

The effect of methoxamine, an alpha 1-adrenoceptor agonist, on ischemic neuronal damage was studied in the gerbil. The animals were subjected to 5 min of ischemia by bilateral common carotid arteries occlusion. Morphological changes and calcium accumulation were evaluated in the CA1 sector of the hippocampus after 7 days of survival. The degree of ischemic neuronal damage and calcium accumulation in the methoxamine-treated groups were significantly attenuated compared with the saline-treated ischemic group. The results suggest that alpha 1-adrenoceptor stimulation prevents ischemic neuronal damage.

Adrenergic alpha-Agonists↗
PubMed1989

Selective neuronal vulnerability following transient cerebral ischemia in the gerbil: distribution and time course.

An important feature of ischemic brain damage is the selective vulnerability of specific neuronal populations. We studied the distribution and time course of neuronal damage following transient cerebral ischemia in the gerbil, using light microscopy and 45Ca autoradiography. Following 5 min of ischemia, selective neuronal damage determined by abnormal 45Ca accumulation was recognized only in the hippocampal CA1 subfield and part of the inferior colliculus. Ischemia for 10 to 15 min caused extensive neuronal injury in the 3rd and 5th layers of neocortex, the striatum, the septum, the whole hippocampus, the thalamus, the medial geniculate body, the substantia nigra, and the inferior colliculus. Progression of the damage was rapid in the medial geniculate body and the inferior colliculus, moderate in the neocortex, striatum, septum, thalamus, and the substantia nigra, and was delayed in the hippocampal CA1 sector. However, the delayed damage of the hippocampus occurred earlier when the ischemia period was prolonged. Histological observation revealed neuronal loss in the identical sites of the 45Ca accumulation. This study revealed that the distribution and time course of selective neuronal damage by ischemia proceeded with different order of susceptibility and different speed of progression.

Animals↗
PubMed1989

Correlation between cerebral blood flow and histologic changes in a new rat model of middle cerebral artery occlusion.

We describe a new focal ischemia model consisting of unilateral middle cerebral artery occlusion with a silicone rubber cylinder attached to a nylon surgical thread inserted through the internal carotid artery in rats. Recirculation was accomplished by pulling the thread out of the artery. We evaluated the reliability of this model and studied the influence of reperfusion of the brain by measuring regional cerebral blood flow in 30 rats and by using conventional neuropathologic methods after different periods of occlusion in 48 rats. The anterior neocortex and the lateral part of the caudate putamen, which were supplied by the occluded middle cerebral artery, were the regions most frequently damaged. After 1 hour of occlusion in five rats, in the cortex supplied by the occluded artery mean +/- SD blood flow was 0.19 +/- 0.08 ml/g/min (approximately 15% of that in the corresponding region of five sham-operated control rats), and mild scattered ischemic cell change was observed. Three (n = 5) or six (n = 5) hours of occlusion reduced blood flow more severely and caused severe ischemic cell changes in the cortex supplied by the occluded artery in proportion to the duration of ischemia. Characteristically, in five rats subjected to 3 hours of occlusion followed by 3 hours of recirculation, blood flow was restored and spongy edematous change was observed in the cortex supplied by the recirculated artery. This change resulted in hypoperfusion of the neighboring cortical region surrounding the recirculated area. Our model should be useful in various investigations of the influence of reperfusion on focal ischemic brain injury.

Animals↗
PubMed1989

[Measurement of blood glucose variations due to surgical stress].

It has been confirmed that the oral surgical invasion not only arouses emotions, such as anxiety and fear, but causes physiological changes at the same time through 2 different pathways, the autonomic nervous system and endocrine system. The change in blood glucose concentration is known as one of representative vital reactions associated with these 2 functional systems. Although secure measurement manipulation producing errors as small as possible is essential to the comparison of blood glucose concentrations obtained from a same individual at different times, various errors are often made during specimen preparation and measurement. Resulting values of glucose concentration are known to be especially influenced by specimen pretreatment, kinds of specimens, meals, menstruation and anesthetics among factors affecting the measurement. Thus we determined these factors in order to establish a measurement procedure to produce the least errors. As a result, it was thought to be desirable that the measurement is performed using the following procedure: 1) blood is sampled more than 90 minutes after meal; 2) whole blood collected from the median basilic vein is used as a specimen; 3) measurement is performed as soon as possible, within 60 minutes after sampling; 4) quantitative values of blood glucose concentration are obtained using dextrosticks and a dextrometer; 5) every specimen is measured 5 time to obtain a mean value used as blood glucose concentration in that specimen through averaging 3 measurement values, omitting the highest and lowest values, and 6) as for female patients, measurement (as well as operation) is performed on a day 2 weeks after the beginning of menstruation. It was concluded that blood glucose concentration can be used as a highly reliable parameter for the observation of vital reactions to external stimulation and for the determination of internal environment at a certain point of time if the measurement is performed with careful consideration of the above-mentioned factors.

Blood Glucose↗
PubMed1989

[Thermal sudomotor deficits in Parkinson's disease].

In order to evaluate sympathetic functions in Parkinson's disease (PD), thermal sweating was examined with colorimetric method in 50 cases of PD (22 males & 28 females, mean age at examination: 58 +/- 9.6 ys, mean duration of illness: 5.3 +/- 3.6 years, Hoehn and Yahr's stage: II-IV, patients without drugs: 15), and following results were obtained; normal sweating in 20 (A), possible generalized hyperhidrosis in 5 (B), localized hyperhidrosis in 4 (C), unilateral hypohidrosis in 7 (D), hypohidrosis over the trunk and legs in 7 (E), and anhidrosis over the trunk and lower extremities in 7 (F). In group F, acetylcholine- or pilocarpine-sweating was also defective, suggesting that postganglionic sympathetic fibers were also impaired. The results were analyzed with respect to age, duration and severity of illness, predominant somatic symptoms, postural changes of blood pressure or subjective dysuria. Abnormal sweating appeared to be related to higher age, severity of PD, and to rigid akinesia as the predominant symptoms. Group B appeared to involve relatively young patients without orthostatic hypotension or dysuria. Group B and C included 5 tremor-dominant patients. But, these features were not statistically significant. Patients in group F had rigid akinesia as the predominant feature (p less than 0.01), and showed higher incidence of dysuria (p less than 0.05). They appeared to have severe PD symptoms in spite of relatively shorter duration of the disease. An administration of drugs including anticholinergics had no significant influence upon the present results. It has been reported by several authors that the rapid progression of PD symptoms and early deterioration of mental status are related to rigid akinesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Differential localization of adenosine A1 receptors in the rat hippocampus: quantitative autoradiographic study.

[3H]Cyclohexyladenosine ([offCHA) was used to label adenosine A1 receptors in the rat hippocampus by quantitative autoradiography, and selective lesions in the neurons intrinsic to CA1 and CA3 subfields were chemically produced to determine the cellular localization of A1 receptors. Lesioning the CA3 subfield by intracerebroventricular kainic acid injection caused a 50% reduction in the maximal binding capacity of [3H]CHA in the CA3 subfield with no alteration in binding affinity. Five days after unilateral CA3 lesioning, a reduction of [3H]CHA binding by 10-30% of ipsi- and contralateral was observed in the dendritic fields in the CA1 region, though a significant reduction was restricted to the ipsilateral stratum radiatum. Thirty-five days after CA3 lesioning, [3H]CHA binding in the stratum radiatum in the CA1 subfield ipsilateral to the CA3 lesion revealed a small reduction in Bmax values but no alteration in Bmax in other sublayers of the CA1. The Kd values in all regions of the hippocampus were not different from the control values. Selective CA1 pyramidal cell lesioning by transient ischemia caused a 70% reduction of [3H]CHA binding sites in the CA1 subfield. Neither CA1 nor CA3 lesions altered [3H]CHA binding in the stratum moleculare of the dentate gyrus. These results suggest that only a small population of adenosine A1 receptors are associated with the terminals of the CA3 pyramidal cells (Schaffer collaterals and commissural fibers) in the CA1 subfield. A1 receptors in the CA1 and CA3 subfields are predominantly located on intrinsic pyramidal cells.

Adenosine↗
PubMed1988

The effect of transient ischemia on 2-[14C]deoxyglucose metabolism in the rat hippocampus pretreated with kainic acid.

CA1 pyramidal neurons are selectively vulnerable to ischemia. 2-[14C]Deoxyglucose (2-DG) autoradiography was employed to measure local glucose utilization in the rat hippocampus after transient ischemia, under the condition of unilateral prevention of ischemic CA1 pyramidal cell necrosis by unilateral lesioning of Schaffer collaterals (left side). Columnar 2-DG uptake patterns in the CA1 region with intact Schaffer collaterals (right side) was observed 19-22 h after recirculation, though no laterality was noted 3 and 8 h after recirculation. In the right subiculum, higher 2-DG uptake was observed 19-22 h after recirculation in 5 out of 8 animals. These results suggest that Schaffer collaterals play a role in modulating glucose metabolism in the CA1 and subiculum during recirculation.

Animals↗
PubMed1988

A tissue culture assay for tetrodotoxin, saxitoxin and related toxins.

In the presence of ouabain, veratridine enhances sodium influx in the mouse neuroblastoma cell line Neuro-2A (ATCC, CCL131), causing cellular swelling and subsequent death. Tetrodotoxin (puffer fish toxin) or saxitoxin (paralytic shellfish poison), both of which block the sodium channel of excitable membranes, antagonize this effect, enabling cell growth to continue. This phenomenon was used as the basis of a new assay for these toxins. It is also possible to estimate the quantity of TTX from the relationship between TTX concentration and percentage of living cells. This new method is simple, inexpensive, and sensitive, and may replace the conventional mouse bioassay.

Animals↗
PubMed1988

Neurotransmitter receptors of the rolling mouse Nagoya: a quantitative autoradiographic study.

The distribution of neurotransmitter and neuromodulator receptors was studied in the brain of the rolling mouse Nagoya (RMN) and in controls, using in vitro receptor autoradiography. Quantitative autoradiography was used to map adenosine A1 (labeled with [3H]cyclohexyladenosine), GABAA [( 3H]muscimol), opiate [( 3H]naloxone), L-glutamate [( 3H]L-glutamate), benzodiazepine [( 3H]flunitrazepam), and muscarinic cholinergic [( 3H]quinuclidinyl benzilate) receptors. In the cerebellar cortex, GABAA and adenosine A1 binding sites were significantly reduced in the RMN, whereas other transmitter binding sites were not significantly altered. Adenosine A1 binding sites were also reduced in the cerebral cortex and caudate-putamen. Benzodiazepine binding was significantly decreased in the cerebral cortex and increased in the CA1 subfield of the hippocampus. These results suggest that neurochemical alterations in the caudate-putamen as well as in the cerebellar cortex play important roles in the ataxia and motor dysfunction of the RMN.

Animals↗
PubMed1988

Prevention of ischemic and postischemic brain edema by a novel calcium antagonist (PN200-110).

The effect of PN200-110, a novel calcium antagonist, on the formation of brain edema was examined with rats using a middle cerebral artery (MCA) occlusion model. PN200-110 was effective in preventing the formation of brain edema in 6-h ischemia and in 3-h reperfusion following 3-h ischemia, which were cases in which great accumulations of calcium were autoradiographically observed. Furthermore, PN200-110 diminished the excessive accumulation of calcium in the MCA area involved. These results indicate that an inhibition of the massive influx of calcium into brain cells by PN200-110 may partially ameliorate cell damage, resulting in prevention of brain edema.

Animals↗
PubMed1988

Autoradiographic localization of opioid and spirodecanone receptors in the gerbil hippocampus as compared with the rat hippocampus.

Opioid ([3H]naloxone) and spirodecanone ([3H]spiperone) binding sites in the hippocampus were visualized in the Mongolian gerbil and in the rat using in vitro autoradiography. In the hippocampus, marked differences were noted in the stratum (sr.) pyramidale of the CA1 subfield where opioid and spirodecanone (assayed in the presence of mianserin and sulpiride) binding activities were very low in gerbils, but high in rats. Gerbils exhibited a high concentration of [3H]naloxone binding sites in the sr. pyramidale of the CA3 subfield, as observed in the rat. In addition, the gerbil has a very high opioid receptor density in the hilar region and in the sr. moleculare of the dentate gyrus. The cellular localization of opioid and spirodecanone receptor sites was studied in the rat hippocampus using selective neuronal damage to CA1 and CA3 neurons by means of ischemia and kainic acid treatment, respectively. The results suggest that the gerbil differs from the rat with respect to the characteristic pyramidal cells (spirodecanone binding site) and interneurons (opioid receptor) in the CA1 subfield of the hippocampus. Distinct localization of opioid and spirodecanone receptors in the gerbil provides a good model with which to investigate the electrophysiological and biochemical roles of opioid peptides and butyrophenone spirodecanone drugs.

Animals↗