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Biomedical subjects

T Tsumoto

Publications and source records attributed to T Tsumoto.

At least 19 recordsLinked to original sources
PubMed2005

Endovascular treatment of unruptured cerebral aneurysms.

76 consecutive patients with 78 unruptured cerebral aneurysms underwent endovascular therapy from July 1999 to May 2004 in our institute. For the wide-necked aneurysms, the remodeling technique, double microcatheter technique, or stent-assisted coil embolization was used, while a parent artery occlusion or covered stent was applied for the giant or fusiform aneurysms. Immediate angiographical results demonstrated 33 complete occlusions, 26 neck remnants, and 14 dome fillings. Four cases were treated with parent occlusion or stenting only, and one case was not treated with embolization but with clipping due to the rupture of the aneurysm during coil embolization. Immediate angiographic findings demonstrated that in aneurysms between 5 to 10 mm, the rate of complete occlusion was 48%, that of neck remnants 33%, and that of dome fillings 27%. In aneurysms between 11 to 25 mm, the rate of complete occlusion was 14%, that of neck remnants 28%, and that of dome fillings was 58%. In the angiographic follow-up results, all aneurysms smaller than 5 mm showed complete occlusion. In aneurysms between 5 to 10 mm, 74% of the aneurysms showed complete occlusion, and 21% showed neck remnants, and 5% showed dome filling. In aneurysms between 10 to 24 mm, 25% showed complete occlusion, while 75% showed dome filling. The overall mortality rate was 0% and the morbidity rate was 3.7% (2 major strokes, 1 minor stroke) at 30-days after embolization. In the clinical follow-up study, one case of a large basilar tip aneurysm caused a fatal rupture 28 months after the initial embolization. Endovascular therapy was performed on the unruptured aneurysms and was found to be an acceptable treatment, except for durability in cases of large aneurysms.

Adult↗
PubMed2004

Brain-derived neurotrophic factor increases inhibitory synapses, revealed in solitary neurons cultured from rat visual cortex.

To elucidate chronic actions of brain-derived neurotrophic factor (BDNF) on GABAergic synapses, we examined effects of a long-term application of BDNF for 10-15 days on autapses (synapses) of solitary GABAergic neurons cultured from rat visual cortex. Solitary neuron preparations were used to exclude a possible contamination of BDNF actions on excitatory neurons in dissociated neuron culture or slice preparations. Neurons were confirmed to be GABAergic pharmacologically with bicuculline, a selective antagonist for GABAA receptors and immunocytochemically with antibody against glutamic acid decarboxylase 65, a GABA synthesizing enzyme. To evaluate GABAergic synaptic function, evoked and/or miniature inhibitory postsynaptic currents (IPSCs) were recorded in the whole-cell voltage-clamp mode. The treatment with BDNF at a concentration of 100 ng/ml enhanced the amplitude of evoked IPSCs and the frequency of miniature IPSCs. In contrast, BDNF did not have a detectable effect on the amplitude of miniature IPSCs and the paired pulse ratio of IPSCs evoked by two, successive activations. To evaluate morphological changes, neurons were immunocytochemically stained with antibodies against microtubule-associated protein 2, to visualize somatodendritic region and synapsin I, to visualize presynaptic sites. The quantitative analysis indicated that BDNF increased the area of soma, the numbers of primary dendrites and dendritic branching points, the total length of dendrites and the number of synaptic sites. Such an action of BDNF was seen in both subgroups of GABAergic neurons, parvalbumin-positive and -negative neurons. To visualize functionally active presynaptic sites, neurons were stained with a styryl dye, FM1-43. BDNF increased the number of stained sites that was correlated with the frequency of miniature IPSCs. These results suggest that the chronic treatment with BDNF promotes dendritic and synaptic development of GABAergic neurons in visual cortex.

Analysis of Variance↗
PubMed2003

Restenosis of the sigmoid sinus after stenting for treatment of intracranial venous hypertension: case report.

We report what we believe to be the first case of restenosis of the sigmoid sinus after stenting, in a 42-year-old man with an arteriovenous malformation with progressive right hemiparesis secondary to venous hypertension. Angiography revealed severe stenosis of the left sigmoid sinus, which was dilated with a self-expandable stent. Six months after the procedure, however, the sinus was again severely stenosed. Intravascular sonography revealed intimal proliferation in the stented sinus. It was dilated percutaneously, and the venous pressure decreased from 51 to 33 mmHg. On sonography, the intimal tissue decreased in thickness and the diameter of the stent enlarged a little.

Adult↗
PubMed2003

Low-frequency depression of synaptic responses recorded from rat visual cortex.

To characterize the low-frequency depression (LFD) of synaptic transmission in the visual cortex, we recorded field potentials and minimal excitatory postsynaptic potentials (EPSPs) from layer II/III following intracortical stimulation at various frequencies in cortical slices of rats. Field potentials were stable at 0.017 Hz, but showed an amplitude depression at 0.033-0.1 Hz at stimulus intensity of 1.5 times the threshold for induction of the postsynaptic component and at 0.1-0.2 Hz at intensity of 1.2 times the threshold. The LFD was input-specific and its magnitude correlated with the stimulus frequency. An interruption of stimulation for 15 min yielded a nearly complete recovery from LFD. Minimal EPSPs tested at 0.1-1.7 Hz often showed LFD with similar features. However, some inputs were stable or even facilitated during repeated stimulation. At 0.1 and 0.2 Hz, >50% of inputs were stable, whereas 10% and 25% were depressed, respectively. At 0.5 and 1.7 Hz, LFD was observed in >60% and 80% of inputs, respectively. The magnitude of LFD strongly varied across inputs. In 3 of the 41 inputs analyzed, LFD was so strong that these inputs became virtually silent. Occurrence of responses to the second pulse in the paired-pulse paradigm when the first response was absent and recovery of depressed EPSPs following stimulus interruption or shift to a lower frequency suggest that these synapses were presynaptically silent due to a lowered probability of transmitter release. Altogether, the results indicate that testing intervals of <10 or even < or =30 s cannot be regarded as completely neutral. At the single-cell level, frequency-dependent changes were strongly heterogeneous across different inputs. LFD and its spontaneous recovery may underlie the previously described "post-rest" potentiation, and should be taken into account when considering information processing in cortical networks.

Animals↗
PubMed2003

Activity-dependent change in the protein level of brain-derived neurotrophic factor but no change in other neurotrophins in the visual cortex of young and adult ferrets.

Neurotrophins are suggested to play a role in activity-dependent plasticity of visual cortex during the critical period of postnatal development. Thus, the concentration of neurotrophins in the cortex is expected to change with development and/or with alteration in neuronal activities. To test this, we measured protein levels of nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 in visual cortex of young (postnatal day 38-46, at the peak of the critical period) and adult ferrets with two-site enzyme-immunoassay systems. Measurements were carried out also in somatosensory cortex, hippocampus and cerebellum as control. With development the level of brain-derived neurotrophic factor did not significantly change, while those of the other neurotrophins changed in the visual cortex. A blockade of visual inputs for 24 h by an injection of tetrodotoxin into both eyes significantly decreased brain-derived neurotrophic factor protein level in the visual cortex, but not in the other regions in both young and adult ferrets. On the other hand, no significant decrease was seen in the protein level of the other neurotrophins in the visual cortex of young and adult ferrets. A monocular injection of tetrodotoxin in young ferrets resulted in the reduction of brain-derived neurotrophic factor by approximately half that by binocular injection. The degree of the decrease in the contralateral cortex to the injected eye was significantly larger than that in the ipsilateral cortex, reflecting that the contralateral eye is dominantly represented in the cortex in ferrets. Blockade of cortical neuronal activities by a GABA(A) receptor agonist led to a remarkable reduction of brain-derived neurotrophic factor protein in the visual cortex. These results suggest that the level of brain-derived neurotrophic factor protein in visual cortex is regulated by activities of cortical neurons.

Aging↗
PubMed2001

Activity-dependent transfer of brain-derived neurotrophic factor to postsynaptic neurons.

Neurotrophins such as brain-derived neurotrophic factor (BDNF) are thought to be transferred from post- to presynaptic neurons and to be involved in the formation and plasticity of neural circuits. However, direct evidence for a transneuronal transfer of BDNF and its relation to neuronal activity remains elusive. We simultaneously injected complementary DNAs of green fluorescent protein (GFP)-tagged BDNF and red fluorescence protein into the nucleus of single neurons and visualized expression, localization, and transport of BDNF in living neurons. Fluorescent puncta representing BDNF moved in axons in the anterograde direction, though some moved retrogradely, and transferred to postsynaptic neurons in an activity-dependent manner.

Animals↗
PubMed2001

Brain-derived neurotrophic factor induces long-lasting potentiation of synaptic transmission in visual cortex in vivo in young rats, but not in the adult.

Brain-derived neurotrophic factor (BDNF) rapidly enhances excitatory synaptic transmission in cortical slices. To date, however, a question of how long such an action persists remains unanswered as it is hard to record synaptic responses longer than several hours in slice preparations. To address this question and to investigate possible age-dependency of the action, we analysed effects of a brief application of BDNF and nerve growth factor (NGF) on field potentials of visual cortex in rats of postnatal days 13-17 and 19-24 and in the adulthood for 10-24 h. Evoked potentials to stimulation of the lateral geniculate nucleus were recorded simultaneously from two cortical sites into which the neurotrophin and control solution were injected. An application of BDNF induced a slowly developing increase in the field potential amplitude in young rats. The amplitude attained a plateau level 3-4 h after the infusion; 139 +/- 26% (mean +/- SD) and 132 +/- 21% of the baseline in the rats at P13-17 and P19-24, respectively. This potentiation remained stable from 4 to 8 h, then gradually decreased to the baseline 15-16 h after the infusion. NGF applied in the same way did not induce potentiation. An inhibitor of BDNF receptors blocked the potentiation when it was applied immediately after the BDNF application, but was not effective about 2 h later. In the adults, BDNF did not potentiate field potentials. These results indicate that BDNF induces synaptic potentiation lasting for several hours only in the developing cortex through processes downstream of receptor activation.

Aging↗
PubMed2001

Induction of brain-derived neurotrophic factor by convulsant drugs in the rat brain: involvement of region-specific voltage-dependent calcium channels.

A high level of hippocampal brain-derived neurotrophic factor (BDNF) in normally aged as compared with young rats suggests that it is important to maintain a considerable level of hippocampal BDNF during aging in order to keep normal hippocampal functions. To elucidate possible mechanisms of endogenous BDNF increase, changes in levels of BDNF were studied in the rat brain following systemic administration of various convulsant agents; excitotoxic glutamate agonists, NMDA, kainic acid and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA); GABA receptor antagonists, picrotoxin, pentylenetetrazole (PTZ) and lindane (gamma-hexachlorocyclohexane); and L-type voltage-dependent calcium channel agonist, BAY-K 8644. Kainic acid and AMPA, but not NMDA, caused remarkable increases in BDNF protein in the rat hippocampus and entorhinal cortex. Picrotoxin, PTZ and lindane stimulated BDNF production in the entorhinal cortex and also in the hippocampus of rats showing very severe convulsions. On the other hand, BAY-K 8644 treatment increased BDNF levels in the neocortex and entorhinal cortex. Maximal levels of BDNF protein were observed at 12--24 h, 8--16 h and 6 h following administration of kainic acid, PTZ and BAY-K 8644, respectively. Kainic acid stimulated BDNF synthesis in presynaptic hippocampal granule neurons, but not in postsynaptic neurons with its receptors, while PTZ and BAY-K 8644 produced the same effects in postsynaptic neurons in the entorhinal cortex (in granule neurons in the hippocampus) and in the whole cortex, respectively. Nifedipine inhibited almost completely BAY-K 8644, but not PTZ, effects. omega-Conotoxin GVIA and DCG-IV partially blocked kainic acid-induced enhancement of BDNF, indicating involvement of L-type and N-type voltage-dependent calcium channels, respectively. In addition, BDNF levels in the hippocampus of mice deficient in D-myo-inositol-1,4,5-triphosphate receptor gene were scarcely different from those in the same region of controls, suggesting little involvement of intracellular calcium increase through this receptor. BAY-K 8644, but not kainic acid or PTZ, stimulated the phosphorylation of cyclic AMP responsive element binding protein. Our results indicate convulsant-dependent stimulation of BDNF production and involvement of region-specific voltage-dependent calcium channels.

Animals↗
PubMed2001

Bone defect associated with middle meningeal arteriovenous fistula treated by embolization--case report.

A 57-year-old male presented with a frontal bone defect associated with a middle meningeal arteriovenous fistula (AVF) manifesting as headache. The patient had a history of head injury 19 years previously. Skull radiography and computed tomography demonstrated a left frontal bone defect. Left external carotid angiography demonstrated a middle meningeal AVF at the frontal region, at the same location as the bone defect. The AVF was fed by the bilateral middle meningeal and left deep temporal arteries, and drained by the superior sagittal and ipsilateral cavernous sinuses. The minor feeding artery, the left deep temporal artery, was embolized with polyvinyl alcohol particles, then 0.4 ml of a 1:3 mixture of n-butyl cyanoacrylate and lipiodol was injected from the left middle meningeal artery. Follow-up angiography 3 months after the embolization revealed complete obliteration of the fistula. The bone defect may have been caused by erosion of the frontal bone by the pulsating effect of the feeding and draining vessels of the fistula, or by inadequate nutrition to the bone tissue because of the arteriovenous shunt.

Arteriovenous Fistula↗
PubMed2000

Actions of brain-derived neurotrophic factor on evoked and spontaneous EPSCs dissociate with maturation of neurones cultured from rat visual cortex.

To address the question of whether brain-derived neurotrophic factor (BDNF) directly enhances excitatory synaptic transmission, we recorded excitatory postsynaptic currents (EPSCs) from solitary neurones cultured on glial microislands for 7-38 days, and observed changes in EPSCs after the application of BDNF. In this preparation the possible action of BDNF on GABAergic inhibition was not involved, and evoked and spontaneous (miniature) EPSCs were derived from the same group of synapses (autapses). The application of BDNF at a concentration of 200 ng ml-1 rapidly enhanced the frequency of miniature EPSCs (mEPSCs) in almost all the neurones tested. On the other hand, the amplitude of mEPSCs did not change at all, suggesting that the site of BDNF action is presynaptic. In contrast to the enhanced frequency of mEPSCs, evoked EPSCs were not potentiated in 61 % of the cells tested. Most of these BDNF-insensitive EPSCs had a peak amplitude larger than 1 nA, while most of the other BDNF-sensitive EPSCs had a smaller amplitude. The former EPSCs had smaller coefficients of variation (CVs) of amplitude, while the latter had larger CVs, suggesting the possibility that the presynaptic release probability for the former groups of EPSCs might have beeen saturated so that the BDNF action was occluded. To test this possibility we applied a low Ca2+ solution to 17 cells and reduced the amplitude of their evoked EPSCs to less than or near to 1 nA. It was found, however, that BDNF did not enhance these EPSCs. Rather, evoked EPSCs of almost all the cells cultured for less than 15 days were enhanced by BDNF, while those of most of the cells cultured for longer than 16 days were not enhanced. These results suggest that BDNF enhances transmitter release from presynaptic sites through its action on the release machinery, which can be differentiated into a BDNF-insensitive form for evoked release and a BDNF-sensitive form for spontaneous release with maturation of synapses.

Animals↗
PubMed2000

Brain-derived neurotrophic factor blocks long-term depression in solitary neurones cultured from rat visual cortex.

1. To address questions of whether long-term depression (LTD) in the visual cortex is expressed in pre- or postsynaptic sites, whether brain-derived neurotrophic factor (BDNF) exerts its LTD-blocking action without involvement of GABAergic inhibition, and whether the action of BDNF is pre- or postsynaptic, we observed excitatory postsynaptic currents (EPSCs) from solitary neurones cultured on glial microislands. In this preparation GABAergic inhibition is not involved and a group of synapses (autapses) which generate evoked EPSCs is thought to be the same as those generating spontaneous EPSCs. 2. A short depolarising voltage step to the soma generated Na+ spikes which were followed by autaptic EPSCs. When this somatic activation was paired with prolonged depolarisation for 100 ms to -30 mV and repeated at 1 Hz for 5 min, LTD was induced in all of the nine cells tested. Then, the frequency of spontaneous EPSCs decreased, but the amplitude did not change, suggesting that the site of LTD expression is presynaptic. 3. Application of BDNF at 50 ng ml-1 blocked the depression of evoked EPSCs and the decrease in the frequency of spontaneous EPSCs. An inhibitor for receptor tyrosine kinases, K252a, antagonised the action of BDNF, suggesting an involvement of BDNF receptors, TrkB. 4. These results suggest that BDNF prevents low-frequency inputs from inducing LTD of excitatory synaptic transmission through presynaptic mechanisms in the developing visual cortex.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2000

Brain-derived neurotrophic factor expands ocular dominance columns in visual cortex in monocularly deprived and nondeprived kittens but does not in adult cats.

Segregation and stabilization of thalamocortical afferents to eye-specific patches, so-called "ocular dominance (OD) columns," in visual cortex are hypothesized to be based on activity-dependent competition for trophic factors such as brain-derived neurotrophic factor (BDNF) between afferents representing the two eyes during the critical period of postnatal development. To test this hypothesis we observed effects of an intracortical infusion of BDNF on OD columns in monocularly deprived kittens and also compared effects between normal kittens and adult cats. BDNF had a hypertrophic action on afferents irrespective of visual inputs so that it desegregated OD columns in the visual cortex of deprived and normal kittens, but this action was not seen in the adults, substantiating its hypothesized trophic role in plasticity of OD columns in the developing visual cortex.

Animals↗
PubMed1999

Brain-derived neurotrophic factor prevents low-frequency inputs from inducing long-term depression in the developing visual cortex.

Brain-derived neurotrophic factor (BDNF) is reported to enhance synaptic transmission and to play a role in long-term potentiation in hippocampus and neocortex. If so, a shortage or blockade of BDNF might lead to another form of synaptic plasticity, long-term depression (LTD). To test this possibility and to elucidate mechanisms if it is the case, EPSCs evoked by test stimulation of layer IV were recorded from layer II/III neurons in visual cortical slices of young rats in the whole-cell voltage-clamp mode. LTD was induced by low-frequency stimulation (LFS) at 1 Hz for 10-15 min if each pulse of the LFS was paired with depolarization of neurons to -30 mV but was not induced if their membrane potentials were kept at -70 mV. Such an LTD was blocked by exogenously applied BDNF, probably through presynaptic mechanisms. Suppression of endogenous BDNF activity by the anti-BDNF antibody or an inhibitor for BDNF receptors made otherwise ineffective stimuli (LFS without postsynaptic depolarization) effective for LTD induction, suggesting that endogenous BDNF may prevent low-frequency inputs from inducing LTD in the developing visual cortex.

Aging↗
PubMed1999

Estimation of single channel conductance underlying synaptic transmission between pyramidal cells in the visual cortex.

Axon collaterals originating from pyramidal cells are one of the most abundant presynaptic elements in the neocortical circuits. To understand a quantitative aspect of synaptic transmission between pyramidal cells, we attempted to estimate single channel conductance by applying non-stationary noise analysis to unitary excitatory postsynaptic currents. Simultaneous recordings were carried out in two pyramidal cells of superficial layers in visual cortical slices. Unitary postsynaptic currents, which were evoked by action potentials of presynaptic cells impaled with conventional sharp electrodes, were recorded from postsynaptic cells with whole-cell patch clamp techniques. Estimated single channel conductance was 12.8 3.8(S.D.) pS for kittens and 10.4 +/- 1.5 pS for rats. Dividing these values by the conductance for unitary postsynaptic currents, we calculated the number of non-N-methyl-D-aspartate receptor channels activated during the postsynaptic currents. The obtained estimates were 52 (kittens) and 41 (rats). To further estimate the number of channels involved in each quantal event, we analysed amplitude histograms of miniature and spike-evoked excitatory postsynaptic currents. The derived number of estimates from these two kinds of histograms agreed quite well; about 20 channels were required for individual quantal events. Assuming open probability of non-N-methyl-D-aspartate receptor channels to be 0.7, our results suggest that the number of channels available for synaptic transmission between individual pyramidal cells would be 74 (kittens) and 59 (rats). We propose that at pyramidal-pyramidal synapses, the number of open channels is several times smaller than that previously reported for the synapses between geniculo-cortical afferent and layer IV spiny stellate cells.

Action Potentials↗
PubMed1999

Effects of blocking non-N-methyl-D-aspartate receptors on visual responses of neurons in the cat visual cortex.

To elucidate the function of non-N-methyl-D-aspartate types of glutamate receptors in the primary visual cortex of the adult cat, we studied the effects of the iontophoretically applied glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and D-amino-5-phosphonovalerate. Antagonists were applied with ejecting currents that selectively blocked non-N-methyl-D-aspartate receptors. Among 93 cells in which stable recordings were obtained, 6-cyano-7-nitroquinoxaline-2,3-dione reduced the visual response in all cells. The average response magnitude during 6-cyano-7-nitroquinoxaline-2,3-dione administration was reduced to 11.7% of the control (average ejecting current: 41.2 nA). The effect of 6-cyano-7-nitroquinoxaline-2,3-dione was obvious throughout all cortical layers. The effect of D-amino-5-phosphonovalerate on the visual response was tested in 14 cells and it was also effective in blocking the visual response: the average response magnitude during D-amino-5-phosphonovalerate administration was 45.0% of the control (average ejecting current: 41.4 nA). The effect of 6-cyano-7-nitroquinoxaline-2,3-dione on the response was compared in individual cells at both high and low firing rates in order to determine whether a differential effect exists on the level of firing activity of cells due to secondary inactivation of voltage-dependent N-methyl-D-aspartate receptors. However, no indication of response dependency on firing rate was seen with 6-cyano-7-nitroquinoxaline-2,3-dione. We suggest that excitatory transmission at the geniculocortical and corticocortical synapses seems to be strongly dependent on non-N-methyl-D-aspartate receptors throughout the primary visual cortex of the adult cat, and that both non-N-methyl-D-aspartate and N-methyl-D-aspartate type glutamate receptors function additively.

2-Amino-5-phosphonovalerate↗
PubMed1999

Selective pruning of more active afferents when cat visual cortex is pharmacologically inhibited.

Activity-dependent competition is thought to guide the normal development of specific patterns of neural connections. Such competition generally favors more active inputs, making them larger and stronger, while less active inputs become smaller and weaker. We pharmacologically inhibited the activity of visual cortical cells and measured the three-dimensional structure of inputs serving the two eyes when one eye was occluded. The more active inputs serving the open eye actually became smaller than the deprived inputs from the occluded eye, which were similar to those in normal animals. These findings demonstrate in vivo that it is not the amount of afferent activity but the correlation between cortical and afferent activity that regulates the growth or retraction of these inputs.

Animals↗