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T Terashima

Publications and source records attributed to T Terashima.

At least 91 records · Page 5Linked to original sources
PubMed1995

Alpha calcium/calmodulin-dependent protein kinase II immunoreactivity in corticospinal neurons: combination of axonal transport method and immunofluorescence.

A combination of either retrograde or anterograde fluorescent tracer and immunofluorescence histochemistry using the monoclonal antibody specific for the alpha isoform of calcium/calmodulin-dependent protein kinase II (CaM kinase II alpha) was employed to test whether CaM kinase II alpha is expressed in somata of corticospinal neurons and their axons over their whole course. After the injection of carbocyanine dye DiI into the hindlimb area of the primary motor cortex of the rat, corticospinal axons and their terminal arbors were anterogradely labeled: DiI-labeled corticospinal fibers proceeded caudally in the ipsilateral internal capsule, cerebral peduncle and medullary pyramid, crossed at the pyramidal decussation and descended in the ventralmost area of the contralateral dorsal funiculus of the spinal cord. These DiI-labeled corticospinal axons expressed strong CaM kinase II alpha immunoreactivity along their course. However, their terminal arbors within the gray matter of the lumbar cord were very weakly immunostained. With the injection of Fast Blue into the lumbar enlargement of the rat, somata of corticospinal neurons in layer V of the motor cortex were retrogradely labeled. The subsequent immunofluorescent histochemistry revealed that more than 80% of Fast Blue-labeled corticospinal neurons were immunostained with CaM kinase II alpha antibody. The present immunohistochemical study demonstrated that CaM kinase II alpha is strongly expressed in both somata and axons of a majority of corticospinal neurons, although we could not detect this enzyme in the corticospinal terminals in the spinal target areas.

Amidines↗
PubMed1995

Anatomy, development and lesion-induced plasticity of rodent corticospinal tract.

In this review the current knowledge of the anatomy, development and plasticity of the rodent corticospinal tract is summarised. Recent technical advancements, especially in neuronal tracing methods, have provided much new data concerning the anatomy of the corticospinal tract. The rodent corticospinal axons project to the subcortical nuclei via collateral branches. These collateral branches of corticospinal axons are formed by delayed interstitial budding during early postnatal periods. Corticospinal neurons are generated in the ventricular zone during a short time lag, migrate into the cortical plate, and settle in layer V of the cerebral cortex. The migration of corticospinal neurons is experimentally deranged by prenatal exposure to alcohol or genetically affected by the reeler genetic locus (rl), resulting in generation of ectopic corticospinal neurons. Such experimentally or genetically induced ectopic corticospinal neurons are a good model for examining whether target recognition and path finding are affected by the intracortical position of corticospinal neurons. Some chemical molecules (e.g. L1 and B-50/GAP43) are transiently expressed in the corticospinal tract during the perinatal period, while others (e.g. protein kinase C gamma subspecies and alpha CaM kinase II) are permanently expressed in the adult corticospinal tract. The only chemical marker specific for layer V corticofugal neurons is an antibody to a soluble protein, protein 35. Since the corticospinal tract in the rodent is an easily identified group of fibers situated in the most ventral portion of the dorsal funiculus of the spinal cord and exhibits considerable postnatal development, it has often been utilized in the neurological studies on plasticity and regenerative capacity of the lesioned central nervous system. Recently, it has been clarified that growing corticospinal fibers have the ability to penetrate and traverse across the lesion sites under certain special conditions.

Animals↗
PubMed1995

Effects of pretreatment with SDZ MRL 953, a novel immunostimulatory lipid A analog, on endotoxin-induced acute lung injury in guinea pigs.

SDZ MRL 953 (SDZ), a novel immunostimulatory lipid A analog, has been reported to have immunopharmacological activities similar to those of lipopolysaccharide (LPS) but to have little of the toxicity of LPS. We investigated the effects of pretreatment with SDZ on Escherichia coli endotoxin-induced acute lung injury in guinea pigs. Four experimental groups consisted of saline control (n = 16), SDZ (-12 h) plus LPS (2 mg/kg of SDZ per kg of body weight injected intravenously 12 h before intravenous injection of 2 mg of LPS per kg; n = 15), SDZ (-10 min) plus LPS (SDZ injected 10 min before LPS injection; n = 10), and LPS alone (n = 16). The animals were sacrificed, and lung tissue was sampled 4 h after LPS or saline infusion. Lung injury was assessed by measuring the wet weight-to-dry weight ratio and the level of 125I-labeled albumin accumulation in bronchoalveolar lavage fluid relative to that in plasma. In the SDZ (-12 h) plus LPS group, these two parameters of acute lung injury were decreased compared with those in the LPS alone group. However, they were not decreased in the SDZ (-10 min) plus LPS group. We conclude that SDZ attenuates endotoxin-induced acute lung injury when it is administered 12 h before LPS injection. The attenuating effects of SDZ are speculated to be due to down regulation of the response to endotoxin rather than to receptor blocking.

Adjuvants, Immunologic↗
PubMed1995

Attenuation of hyperoxic lung injury by the 21-aminosteroid U-74389G.

Hyperoxic lung injury is attributable to oxygen radicals produced under hyperoxic conditions. The 21-aminosteroid (AS), U-74389G, is a potent antioxidant. We examined the effect of U-74389G on lung injury in guinea pigs during exposure to 90% O2 for 48 h. We injected either vehicle or 10 mg/kg of U-74389G 30 min before the O2 exposure and injected the same dose 12, 24, and 36 h later. We performed two series of experiments after exposure. In the first series, we measured the clearance rate of 99mTc-labeled dialdehyde starch (DAS) from the lungs as an index of pulmonary epithelial damage in three experimental groups consisting of 1) control (n = 6) O2 alone (n = 6), and 3) O2 + AS (n = 6). In the second series, pulmonary endothelial injury was estimated by using 28 guinea pigs divided into four experimental groups consisting of 1) control (n = 8), 2) AS alone (n = 5), 3) O2 alone (n = 6), and 4) O2 + AS (n = 9). In the second series, we measured the wet-to-dry weight ratio (W/D) as an index of lung water and the concentration ratio of 125I-labeled albumin in lung tissue and bronchoalveolar lavage (BAL) fluid compared with plasma (T/P and BAL/P, respectively) as indexes of pulmonary endothelial damage. Cell accumulation in BAL fluid and lung tissue samples was also assessed in the second series.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Course and collaterals of corticospinal fibers arising from the sensorimotor cortex of the reeler mouse.

The reeler genetic mutation, occurring spontaneously in mice, affects migration of neuroblasts in the central nervous system at its last stage, causing severe cytoarchitectonic abnormalities in laminated structures, such as the cerebral and cerebellar cortex. In the reeler mouse, corticospinal (CS) neurons are malpositioned in association with the deranged laminar cytoarchitecture. To examine whether CS projections in the reeler mouse and their collaterals terminating with subcortical nuclei are normal or not, 5% biocytin was injected into the sensorimotor cortex of 2-month-old normal and reeler mice. Anterogradely labeled CS fibers of normal and reeler mice exited from the cortex and entered the internal capsule and the cerebral peduncle. They penetrated the basal pontine gray matter as longitudinal pontine fibers and entered the medullary pyramid. They continued caudally as a compact bundle along the ventral surface of the medulla, passed through the pyramidal decussation at the spinomedullary junction and entered the contralateral dorsal funiculus of the spinal cord. Both in normal and reeler mice, collaterals arising from these CS fibers projected to the ipsilateral red nucleus, basal pontine gray matter, inferior olivary complex, and the contralateral gracile nucleus. Thus, in the reeler mouse, the course and termination of CS fibers and their collaterals are identical to their normal counterparts, suggesting that radially malpositioned CS neurons in the sensorimotor cortex project to the subcortical nuclei in a manner similar to normal CS neurons.

Animals↗
PubMed1995

BCG priming enhances endotoxin-induced acute lung injury independent of neutrophils.

Bacillus Calmette Guérin (BCG) is known to increase susceptibility to endotoxin in some animal species. We investigated the effect of BCG-priming and the role of neutrophils in the priming process on the pathogenesis of acute lung injury caused by intravenously administered Escherichia coli endotoxin (LPS). Guinea pigs were divided into seven groups: (1) control (n = 8), (2) BCG-alone (n = 6), (3) cyclophosphamide (CPA)-alone (n = 6), (4) CPA+LPS (n = 6), (5) LPS-alone (n = 6), (6) BCG+LPS (n = 6), and (7) BCG+CPA+LPS (n = 6). A BCG dose of 8 mg/kg was injected subcutaneously 10 d before the study. CPA was administered intraperitoneally to induce peripheral neutropenia. Animals were observed for 4 h after intravenous administration of 0.2 mg/kg of LPS. The plasma TNF level was measured 2 h after LPS challenge. Lung wet-to-dry weight ratio, [125I] albumin leakage in lung tissue, differential cell count in bronchoalveolar lavage (BAL) fluid, and histopathologic features were examined immediately after death. Although the LPS-alone group showed PMN accumulation in lung tissue, neither excess lung water nor increased albumin leakage was induced by this dose of LPS. The BCG+LPS group showed increased lung water, histopathologic edema, and increases in BAL fluid cell counts and plasma TNF in comparison with the LPS-alone group. The BCG+CPA+LPS group also showed enhanced lung injury comparable to that seen in the BCG+LPS group. In both the CPA-alone and the CPA+LPS groups, no parameter was increased as compared with those in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis.

We evaluated the contribution of interleukin-8 (IL-8) to the pathogenesis of idiopathic pulmonary fibrosis (IPF) by studying bronchoalveolar lavage fluid (BALF) in eight patients with IPF in the chronically progressive phase, five patients with IPF in the subacutely progressive phase, eight patients with sarcoidosis (SAR), and eight control (CTL) subjects. IL-8 levels were not increased in the BALF of the patients with IPF in the chronic phase (11.3 +/- 8.8 pg/ml), nor in that of the SAR patients (13.8 +/- 7.8 pg/ml), whereas they were increased in the BALF of patients with IPF in the subacutely progressive phase (1.93 +/- 1.10 ng/ml). We then investigated extracellular and cell-associated IL-8 in lipopolysaccharide (LPS)-stimulated BALF cells to determine the IL-8-producing potential of alveolar macrophages (AM). Following LPS stimulation of BALF cells from patients with IPF in the chronic phase, both the extracellular IL-8 in culture fluid and the cell-associated IL-8 in AM were increased as compared with those for the CTL subjects (p < 0.05 and p < 0.05, respectively). These results suggest that AM of patients with IPF are primed for IL-8 production. We conclude that IL-8 may play a role in neutrophilic alveolitis, especially during the subacute phase of IPF.

Acute Disease↗
PubMed1995

Neutrophil-induced lung protection and injury are dependent on the amount of Pseudomonas aeruginosa administered via airways in guinea pigs.

We investigated the roles of neutrophils in mediating both the protective effect against bacterial infection and the harmful effect of lung injury induced after the intratracheal instillation of live bacteria. We examined the mortality rate, lung injury, and bacterial clearance following the intratracheal instillation of Pseudomonas aeruginosa in low (10(4) colony-forming units [CFU]) and high doses (10(8) CFU) in normal (control) guinea pigs, others made neutropenic with cyclophosphamide (CPA), and guinea pigs made neutrophilic with recombinant granulocyte colony-stimulating factor (rG-CSF). Lung injury was assessed by the ratio of the concentration of 125I-labeled albumin in lung tissue to that in plasma (T/P) and the animals' lung weight-to-body weight (LW/BW) ratio. With 10(4) CFU, the CPA group showed an increased T/P ratio of 0.22 +/- 0.03 versus 0.14 +/- 0.01 in the control and 0.11 +/- 0.01 (mean +/- SEM) in the rG-CSF groups (p < 0.01). Viable bacteria were recovered from bronchoalveolar lavage fluid (BALF) in the CPA group. Neutrophil recruitment was observed in the lungs of animals in the control and rG-CSF groups. With 10(8) CFU, the mortality rate was increased in the rG-CSF group (7 of 10) as compared with the control (0 of 9) and CPA groups (1 of 9) (p < 0.05), which reflected an increased LW/BW (g/kg) ratio (16 +/- 2 versus 12 +/- 1) in the CPA group (p < 0.05). We conclude that neutrophils protect against lung injury during low-level bacterial challenge, but enhance lung injury and contribute to mortality during high-level bacterial challenge.

Animals↗
PubMed1995

Neutrophils activated by granulocyte colony-stimulating factor suppress tumor necrosis factor-alpha release from monocytes stimulated by endotoxin.

We investigated the in vitro effects of granulocyte colony-stimulating factor (G-CSF) on tumor necrosis factor-alpha (TNF-alpha) release from monocytes. Peripheral blood monocytes and neutrophils were obtained from healthy donors (n = 8). Neutrophils alone, neutrophils plus monocytes, and monocytes alone were incubated with and without G-CSF (10 ng/ml) and were studied for TNF-alpha release; monocytes subsequently were stimulated by endotoxin (lipopolysaccharide [LPS] at 10 and 1,000 ng/ml). Neutrophils alone did not produce TNF-alpha after LPS stimulation irrespective of G-CSF treatment. TNF-alpha release from monocytes was suppressed significantly by pretreatment with G-CSF in the presence of neutrophils (P < 0.01). Suppression of TNF-alpha release after LPS was not observed when monocytes were preincubated with G-CSF in the absence of neutrophils. TNF-alpha release from monocytes stimulated by LPS was not inhibited when monocytes were incubated with the supernatant from G-CSF-activated neutrophils. Pretreatment with G-CSF inhibited intracellular TNF-alpha production, as measured by flow cytometry, of monocytes stimulated by LPS (P < 0.05). These data suggest that neutrophils activated by G-CSF directly suppress TNF-alpha release from monocytes stimulated by LPS.

Adult↗
PubMed1995

[Pulmonary alveolar proteinosis associated with myelodysplastic syndrome].

A 57-year-old man with myelodysplastic syndrome developed dyspnea on exertion in September 1993. Chest X-ray film showed diffuse infiltrative shadows in the middle and lower lung fields on both sides. The infiltrates were prominent in the perihilar regions but less so in the periphery, consistent with a "bat wing pattern." Milky fluid was obtained by bronchoalveolar lavage. The specimens obtained from transbronchial lung biopsy were compatible with the pathological findings of pulmonary alveolar proteinosis with amorphous periodic acid-Sciff-positive materials in the alveolar spaces. Impaired function of alveolar macrophages was demonstrated from their abnormally low phagocytosis of FITC-labeled latex beads. Whole lung lavage under general anesthesia was done twice, but the patient died because of progression of respiratory failure.

Fatal Outcome↗
PubMed1994

Musculotopic organization in the motor trigeminal nucleus of the reeler mutant mouse.

We examined the musculotopic organization in the motor trigeminal nucleus and the somatotopical arrangement in the trigeminal ganglion of the normal and reeler mice. To determine whether or not masticatory motoneurons are malpositioned in the reeler mouse, we injected horseradish peroxidase (HRP) into the masticatory muscles of normal and reeler mice. Injections of HRP into the jaw-closing muscles, i.e., the masseter and temporalis muscles, labeled large multipolar neurons in the dorsolateral division of the motor trigeminal nucleus of both normal and reeler mice. Similar injections into the jaw-opening muscles, i.e., the anterior belly of the digastric muscle and mylohyoid muscle, labeled large multipolar neurons in the ventromedial division of the motor trigeminal nucleus of both mouse strains. Thus, the normal myotopical arrangement of the masticatory muscles on the motor trigeminal nucleus is preserved in the reeler mouse. However, detailed analysis revealed that jaw-opening motoneurons were more widely scattered in the reeler mouse than in the normal control. To examine the somatotopical arrangement of the first-order sensory neurons in the trigeminal ganglion of the normal and reeler mice, we subcutaneously injected Fast blue (FB) into the mental region and Diamidino yellow (DY) into the vibrissal region of the same animals. No differences in distribution patterns of FB-labeled and DY-labeled neurons in the whole-mounted trigeminal ganglion could been seen between these two strains, suggesting that migration of trigeminal ganglion cells, which are derived from the neural crest and placode, is not deranged by the reeler genetic locus.

Animals↗
PubMed1994

An electrophysiological and immunohistochemical study of the hippocampus of the reeler mutant mouse.

The pyramidal cell layer in the CA1 subfield of the hippocampus of the reeler mouse is split into two laminae, the deep and the superficial. We examined the electrophysiological properties of double-layered CA1 pyramidal neurons in the reeler mouse hippocampal slice in vitro. We also studied cytoarchitectonic abnormalities in the hippocampus of this mutant by immunohistochemical methods using anti-parvalbumin and anti-F3/F11-protein antibodies. Laminar analysis of the postsynaptic field potentials in the CA1 subfield of the reeler hippocampus revealed broad negative field potentials with double negative peaks. In the CA1 subfield of the reeler mouse, tetanic stimulation of Schaffer collateral/commissural fibers induced long-term potentiation (LTP) in the majority of the deep layers (near alveus) examined, but very rarely in the superficial layer (near the molecular layer). Immunohistochemical study showed that parvalbumin-immunopositive neurons were densely concentrated in the hippocampus of the reeler mouse, especially in the stratum radiatum and the stratum lacunosum-molecular, in which only a few parvalbumin-immunoreactive neurons were seen in the normal mouse. Abnormal trajectories of axons arising from malpositioned pyramidal cells in the CA1 subfield of the reeler mouse were identified by F3/F11 immunohistochemistry. Interestingly, F3/F11-immunoreactive Schaffer collaterals were misdirected in the CA1 subfield of this mutant. The present electrophysiological and immunohistochemical data suggest that impairment of LTP in the superficial layer of the CA1 pyramidal neurons appears to be mainly due to strong inhibitory inputs to this malpositioned population of neurons.

Animals↗
PubMed1994

Specific distribution of Ca2+/calmodulin-dependent protein kinase II alpha and beta isoforms in some structures of the rat forebrain.

The immunohistochemical distribution of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) alpha and beta isoforms in the rat forebrain was examined by using monoclonal antibodies specific to each isoform. The present study confirmed that alpha and beta immunoreactivities are localized only in neuronal elements. At the light microscopic level, specific distribution patterns of these isoforms and staining characteristics were recognized in some regions of the forebrain as follows. Firstly, alpha-immunoreactive neurons were more homogeneously distributed throughout the cellular layers of the cerebral cortex (i.e., layers II-VI) than beta-immunoreactive ones. Secondly, neurons in the globus pallidus were immunostained by the anti-beta antibody, but not by the anti-alpha antibody. Thirdly, neurons in the medial habenular nucleus, the subthalamic nucleus and the reticular thalamic nucleus were more densely stained with the anti-beta antibody than with the anti-alpha antibody. However, marked differences were not observed in the hippocampal formation at the light microscopic level. The electron microscopic analysis of the cerebral cortex demonstrated that subcellular localizations of alpha- and beta-immunoreactive products within the cortical neurons were quite dissimilar: (i) the nucleus was stained only with the anti-alpha antibody, but not with the anti-beta antibody, and (ii) beta-immunoreactive products were more sporadically localized in the cytoplasms of the perikarya and dendrites than the alpha-immunoreactive ones. These regional and subcellular differences between the distribution patterns of alpha and beta immunoreactivities suggest the functional diversity of CaM kinase II alpha and beta isoforms in the central nervous system.

Animals↗
PubMed1994

Immunocytochemical localization of calcium/calmodulin-dependent protein kinase II isoforms in the ganglion cells of the rat retina: immunofluorescence histochemistry combined with a fluorescent retrograde tracer.

To determine whether or not calcium/calmodulin-dependent protein kinase II (CaM kinase II) is localized in the ganglion cells in the rat retina, we labeled ganglion cells by injection of Fast blue (FB) into the lateral geniculate nucleus and then stained the retina immunohistochemically with monoclonal antibodies which react specifically with the alpha and beta isoforms of CaM kinase II. Eighty and 90% of the FB-labeled ganglion cells in the ganglion cell layer were immunoreactive with the alpha and beta antibodies, respectively, suggesting that both alpha and beta isoforms of CaM kinase II are expressed in most ganglion cells which project to the lateral geniculate nucleus.

Animals↗
PubMed1994

Immunohistochemical detection of calcium/calmodulin-dependent protein kinase II in the spinal cord of the rat and monkey with special reference to the corticospinal tract.

Calcium/calmodulin-dependent protein kinase II is a prominent enzyme in the mammalian brain that phosphorylates a variety of substrate proteins. In the present study, monoclonal antibodies that specifically recognize either the alpha or the beta isoforms of this enzyme were used to determine the distribution of these isoforms within the rat and monkey spinal cord. In the rat, the corticospinal tract consists of two components: the dorsal corticospinal tract, which occupies the ventralmost aspect of the dorsal funiculus; and the ventral corticospinal tract, which occupies an area adjacent to the ventral median fissure. Both dorsal and ventral corticospinal tract fibers were strongly immunopositive for the alpha-antibody. Unilateral ablation of the sensorimotor cortex of the rat eliminated the alpha-immunoreactive staining in the contralateral dorsal corticospinal tract. The neuropil in the superficial laminae of the dorsal horn (Rexed's laminae I and II) was densely stained with the alpha-antibody, whereas the neuropil in laminae IV-X was immunonegative. Dense alpha-immunopositive neurons were also distributed in the head of the dorsal horn (laminae I-IV). In contrast to the strong alpha-immunoreactivity seen in the dorsal corticospinal tract fibers, only very weak beta-immunoreactivity was observed in this tract. Moderate beta-immunoreactive products were distributed homogenously throughout the neuropil of the gray matter, although the neuropil of the superficial laminae of the dorsal horn (laminae I and II) was stained more strongly than the other regions of the gray matter (laminae III-X). Neuronal components in all laminae were immunopositive for the beta-antibody. Thus, motoneurons in the ventral horn, which were immunonegative for the alpha-antibody, were immunopositive for the beta-antibody. This selective distribution pattern of immunoreactivity of alpha- and beta-antibodies in the rat was also present in the monkey spinal cord, although the alpha-immunopositive corticospinal tract fibers in the monkey descended in the lateral funiculus as the lateral corticospinal tract instead of passing through the dorsal funiculus, as is the case in the rat. The differential distribution of immunoreactivity in the spinal cord suggests that these two isoforms of calcium/calmodulin-dependent protein kinase II may have different functional roles in the spinal cord.

Animals↗