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F Akai

Publications and source records attributed to F Akai.

34 records · Page 2Linked to original sources

Neurotrophic factor-like effect of FPF1070 on septal cholinergic neurons after transections of fimbria-fornix in the rat brain.

FPF1070 is an aqueous protein-free solution, which consists of 85% free amino acids and 15% small peptides. Our previous study showed a potent neurotrophic factor-like activity in cultured embryonic cells of dorsal root ganglia. The present study investigated whether FPF1070 regenerated the cholinergic cells in the medial septal nucleus after axonal transections by cutting the fimbria-fornix. Fimbrial transection reduced the number of septal cholinergic cells by 30 +/- 3.6%, compared with the number on contralateral sides at 4 weeks. Intraperitoneal injections of FPF1070 caused 49.9 +/- 6.3% of the cholinergic neurons to survive. Furthermore, the cell sizes of the cholinergic neurons were significantly different: 16.4 +/- 4.2 microns, 14.3 +/- 3.8 microns in FPF1070 treatment and vehicle treatment, respectively. These results indicated that FPF1070 prevents the degeneration and atrophy of impaired cholinergic neurons by systemic administration.

Amino Acids↗

Intense immunoreactivity for Mn-superoxide dismutase (Mn-SOD) in cholinergic and non-cholinergic neurons in the rat basal forebrain.

The immunohistochemical localization of manganese (Mn)-superoxide dismutase (Mn-SOD) was studied in the rat basal forebrain using polyclonal antibodies to Mn-SOD. Neurons of the basal forebrain exhibit a high density of Mn-SOD immunoreactivity. Double immunostaining with a monoclonal antibody to choline acetyltransferase demonstrated that both cholinergic and non-cholinergic neurons in the basal forebrain are intensely immunoreactive for Mn-SOD.

Animals↗

Immunocytochemical localization of manganese superoxide dismutase (Mn-SOD) in the hippocampus of the rat.

The immunocytochemical distribution of manganese superoxide dismutase (Mn-SOD) was determined in the rat hippocampus. The enzyme was localized in the mitochondria. CA1 pyramidal cells were weakly immunostained, whereas CA3 pyramidal cells were strongly reactive. These differences in the intensity of the Mn-SOD immunostaining reactions may relate to variations in the sensitivity of subfields of the hippocampus to ischemia.

Animals↗

Ultrastructural investigation of the CA1 region of the hippocampus after transient cerebral ischemia in gerbils.

Ultrastructural damage leading to delayed neuronal death was investigated in the mid-CA1 region of the hippocampus from the stratum (str.) moleculare to oriens after transient bilateral forebrain ischemia in Mongolian gerbils. After ischemia for 5 min without recirculation, mild swelling of the peripheral part of the apical and basal dendrites was already apparent in the str. moleculare and str. oriens. Mitochondria in the dendrites were also swollen in the same area. During recirculation for 12 h to 3 days, swelling of the dendritic cytoplasm persisted with formation of microvacuoles, but swelling of mitochondria receded. Microvacuolation and loss of microtubules were also observed in the proximal part of the dendrites during this period, and swelling and disruption of internal cristae were observed in mitochondria after recirculation for 3 days. The dendrites became severely degenerated after recirculation for 4 days. In the pyramidal cell bodies, no abnormality was observed at the end of ischemia for 5 min, but disaggregation of polyribosomes and swelling of the endoplasmic reticulum were observed 12 h after recirculation. Proliferation of the endoplasmic reticulum in parallel arrays occurred after recirculation for 1 day and persisted. Severe degeneration of the pyramidal cell bodies was obvious after recirculation for 4 days. The findings observed in the present investigation suggested that the neuronal structure most vulnerable to ischemia was the peripheral part of the dendrites and postischemic neuronal damage occurred early in this part of the dendrites.

Animals↗

Prediction of stroke before and after unilateral occlusion of the common carotid artery in gerbils.

A method was developed to predict the severity of cerebral ischemia before permanent occlusion of a common carotid artery in gerbils by observing the diameter and appearance of the artery after temporary occlusion and observing clinical signs after permanent occlusion. The severity of cerebral ischemia was confirmed by a sensitive immunohistochemical method and measurement of focal cerebral blood flow after 30 minutes' ischemia. All gerbils with greater than 40% reduction of the diameter and a white arterial margin distal to temporary occlusion developed severe neurologic signs following permanent occlusion, but no gerbils with reduction of less than 30% and a red arterial margin developed neurologic signs. With the cumulative neurologic score, gerbils could be divided into classes with no, mild, moderate, and severe symptoms, mostly after 10 minutes. Severely symptomatic gerbils were identified in 3 minutes. Extensive ischemic damage was observed in severely symptomatic gerbils, but no immunohistochemical lesion was detected in mildly symptomatic gerbils. Cerebral blood flow was markedly reduced in severely symptomatic gerbils but more selectively reduced in the cortical structures of moderately symptomatic gerbils. This prediction method is useful for investigating early cerebral ischemia and for evaluating the effectiveness of pharmacologic agents.

Animals↗

Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils.

Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving the neuropil, neuronal perikarya, and dendrites. The earliest lesion in the caudoputamen evolved after 30 minutes of ischemia. After reestablishment of cerebral circulation, the immunohistochemical ischemic lesions in the neuronal structure disappeared if the ischemic period was 10 minutes or less and partially disappeared even after ischemia for 15 minutes in the cerebral cortex, while the postischemic lesion in the caudoputamen disappeared even after ischemia for 15 minutes. Reactive astrocytes were detected in the cerebral cortex and caudoputamen as early as 24 hours after reperfusion, both in the areas with and without the neuronal lesions. No lesion was identified in the hippocampus or thalamus. This experimental model is suitable for investigation of rapidly progressive regional ischemia in the cerebral cortex and for comparison with other regional or global cerebral ischemia in the gerbil or other animal species.

Animals↗

A morphological study on the effects of collagen gel matrix on regeneration of severed rat sciatic nerve in silicone tubes.

The present study is a chronological morphological examination on the effects of collagen gel matrix on regeneration of severed sciatic nerves. The nerves (5 mm length) were resected, and both the distal and proximal stumps were inserted into a silicone tube with 5 mm gap in between. In the test side, the gap in the tube was then injected with liquid collagen which gels in the tissue when reconstructed with a certain buffer solution. The gap space in the tube of the control side was left empty. In a chronological examination of the tissue in the tube, considerably more rapid growth of sprouting axons toward the distal stump in the test side was revealed in comparison with the control side. The cells, including both fibroblasts and larger Schwann cells, were less in number. More orderly directions were observed in the collagen matrix than in the control tube. The result indicates that regeneration of the peripheral nerves in the silicone tube can be improved, by using appropriate exogenous fine materials, collagen matrix.

Animals↗

Experimental study of WGA binding on the endothelial cell surface in cerebral ischemia.

The relationship between the saccharide chain on the endothelial cell surface and the permeability of intracerebral blood vessels has been studied. In the present study, wheat germ agglutinin (WGA) was perfused into capillaries in the area postrema of the normal Mongolian gerbil, where the blood brain barrier (BBB) is known to lack, and into intracerebral blood vessels, the BBB of which had been destroyed by experimentally induced brain ischemia. The light microscopic features of the sections from WGA-perfused brain tissues of the normal gerbil revealed that most of the blood vessels, including capillaries in the brain parenchyma, showed positive findings (the reaction induced a very distinct staining of the vascular wall) from which the course and structure of the fine vessels could be determined. The reaction to WGA on the diaphragma fenestra (DF) in capillaries in the area postrema was relatively weak, and DF without the reaction were occasionally revealed by electron microscopy. The gerbil, in which cerebral ischemia had been induced, also showed partial defect of the reaction with WGA on the luminal side of the endothelial cells. The results of the present experiment suggest some degree of correlation between the saccharide chains, including the specific monosaccharide of WGA, on the endothelial cell surface and permeability. It was considered that lectin can be used as an index for morphological observations, suggesting an alteration in function of the endothelial cell membrane. In addition, the perfusion method in this experiment suggested the possibility of distinguishing pinocytotic vesicles from pits of cell membranes.

Acetylglucosaminidase↗

Lectin (UEA-1) reaction of capillary endothelium with reference to permeability in autopsied cases of cerebral infarction.

The relationship between endothelial reactivity to Ulex europaeus agglutinin-1 (UEA-1) and the permeability of the vascular wall in human autopsied cases of cerebral infarction was studied. Sections from the cerebral cortex were reacted with horseradish peroxidase UEA-1 to demonstrate the surface membrane of endothelial cells. Albumin in the neuropil of sections was demonstrated for the estimation of increased vascular permeability. The results showed that endothelial reactivity to UEA-1 was reduced in cases where death had occurred 3 to 5 days after onset of cerebral infarction. Reactivity was also diminished in cases where death had occurred after 13 and 25 days; these cases showed fresh ischemic lesions caused by re-attacks of infarction. Albumin extravasation into the neuropil was demonstrated in these intermediate cases. Chronic cases, dying after more than 52 days, showed no reduction of endothelial reactivity to UEA-1 and no albumin extravasation was proved. It was concluded that UEA-1 can be employed as a useful morphological marker for evaluation of endothelial function and vascular permeability.

Aged↗

Light and electron microscopic studies of calcitonin gene-related peptide-like immunoreactive neurons and axon terminals of the nucleus of the tractus solitarius of the rat.

This study was an examination of the ultrastructural characteristic features of calcitonin gene-related peptide (CGRP)-like immunoreactive neurons and their axon terminals in the nucleus of the tractus solitarius of the rat. Some axon terminals were identified as receiving synaptic inputs from non-immunoreactive axon terminals. This may suggest that part, if not all, CGRP containing afferents are affected presynaptically by other afferents.

Animals↗

The synaptic relationship between vasoactive intestinal polypeptide (VIP)-like immunoreactive neurons and their axon terminals in the rat small intestine: light and electron microscopic study.

The present study demonstrates synaptic contacts between vasoactive intestinal polypeptide (VIP)-like immunoreactive neurons and immunoreactive axon terminals in the submucous and myenteric plexuses of the rat small intestine. Our observations suggest that VIP afferents directly affect the VIP neurons in the small intestine via synapses.

Animals↗

Neuronal changes of hypokalemic myopathy. A light- and electron-microscopic study on muscle biopsy.

Hypokalemic myopathy has been observed in various clinical conditions. There are many studies of the pathomorphological changes of muscle fibers but alterations in intramuscular nerves and motor end-plates are seldom mentioned. The present authors observed biopsied muscle from a 51-year-old housewife who had suffered from gradually increasing muscle weakness. Laboratory examinations revealed a severe hypokalemia of 1.5 mEq/1, 18304 U/1 of CPK, 1300 U/1 of LDH, 343 U/1 of SGOT and 297 IU/1 of adolase. Light-microscopic examination showed changes previously described, including twin-peaked distribution in the histogram of type I, IIA and IIB fibers, ballooning and thickening of terminal axon, and 2 or 3 end-plates closely spaced along the length of muscle fibers. The electron-microscopic examination revealed empty folds of basement membrane in end-plate regions, reduced secondary synaptic clefts, interposition of Schwann cell processes between nerve ending and primary synaptic cleft, and an increase of disarranged microtubules and neurofilaments in terminal axons. The findings suggest that severe hypokalemia primarily produces structural alterations of intramuscular peripheral nerves and motor end-plates as well as of muscle fibers.

Axons↗