Biomedical subjects

T Tsumoto

Publications and source records attributed to T Tsumoto.

At least 37 records · Page 2Linked to original sources

PubMed1999

Acetylcholine suppresses the spread of excitation in the visual cortex revealed by optical recording: possible differential effect depending on the source of input.

Optical recording with a voltage-sensitive dye was performed in visual cortical slices of the rat to determine the effect of acetylcholine (ACh) on the spread of excitation. In the presence of ACh, the spread of excitation initiated by stimulation at the white matter/layer VI (WM/VI) was greatly suppressed throughout the cortex, with less suppression in the middle layers. By comparing the effect of ACh with that of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the fraction of the synaptic component that was sensitive to ACh was evaluated. ACh suppressed approximately 40-50% (maximum 55.8%, n = 11) of the initial synaptic component in the superficial and deep layers. In the middle, however, the effect was weakest and only approximately 20-30% (minimum 20.9%, n = 11) of the initial synaptic component was suppressed. On the basis of histological analysis, the region with the weakest ACh effect extended from upper V to lower II/III. To identify the site of ACh action in terms of pre- versus postsynaptic localization, exogenous glutamate was applied. Because ACh did not suppress the excitation induced by glutamate, the site of the ACh action was indicated to be presynaptic. When layer II/III was stimulated instead of WM/VI, the suppression was uniform throughout the cortex. A muscarinic receptor antagonist, atropine, blocked the suppression by ACh. In conclusion, our results indicate the following two points. First, ACh strongly suppresses intracortical connectivity through presynaptic muscarinic receptors. Secondly, in contrast to the intracortical connection, some group(s) of fibres, possibly thalamocortical afferents that arise from white matter and terminate in the middle cortical layers are suppressed much less by ACh. While ACh has been reported to have confusingly diverse effects, e.g. direct depolarization and hyperpolarization as well as synaptic facilitation and suppression, its effect on the propagation of excitation is very clear; suppression on intracortical connection, leaving thalamocortical inputs rather intact. We postulate that cholinergic innervation enables the afferent input to have a relatively dominant effect in the cortex.

Acetylcholine↗

PubMed1999

[Acquired stuttering associated with callosal infarction: a case report].

A 66-year-old right-handed man with acquired stuttering was reported. He complained of paresis in his left leg and speech dysfluency. He was not aphasic in terms of comprehension and writing. His speech dysfluency was mainly characterized by initial syllable repetitions. He has apraxia with his left hand, but has neither agraphia with his left hand nor crossed optic ataxia. MRI showed cerebral infarction in the truncus of the corpus callosum, and angiography revealed occlusion of the right anterior cerebral artery. 99mTc HM-PAO SPECT showed decreased blood flow in the right frontal lobe. Within six months of its onset, the patient's speech dysfluency had diminished. As the causative lesion for acquired stuttering, we proposed a hemispheric lesion in addition to a callosal lesion.

Aged↗

PubMed1999

[Choroid plexus papilloma in the posterior third ventricle in infancy: a case report].

Choroid plexus papillomas represent approximately 0.5% of all intracranial tumors, but they are found in the third ventricle only infrequently. We report a case of choroid plexus papilloma in the third ventricle which is difficult to differentiate from a pineal region tumor. A 4-month-old female presented with bulging fontanelle and sunset phenomenon. A CT scan and MRI showed marked hydrocephalus caused by a tumor extending from the posterior third ventricle to the peneal body. Preoperatively, we diagnosed the lesion as a pineoblastoma. The tumor was totally removed through the occipital transtentorial approach. Pathological examination of the tumor revealed a typical choroid plexus papilloma. The operation was uneventful, and she has grown normally without recurrence of the tumor for three years since the operation. A sagittal gadolinium-enhanced MRI was useful in our case to differentiate a choroid plexus papilloma from a pineal region tumor, because the former extended into the aqueduct forming the shape of the letter V while the latter compressed the aqueduct downward.

Cerebral Ventricle Neoplasms↗

PubMed1998

Role of NMDA receptors in the propagation of excitation in rat visual cortex as studied by optical imaging.

To examine the role of the N-methyl-D-aspartate (NMDA) type of glutamate receptors in the propagation of information in visual cortex, optical imaging with high spatial and temporal resolution of neuronal activity was used in cortical slices of rats. Single-shock stimulation of the white matter elicited a vertical propagation of excitation toward the cortical surface simultaneously with a horizontal spread of excitation in lower layers. The horizontal spread in upper layers occurred subsequent to the vertical spread reaching these layers. The results from perfusion of Ca2+-free medium and application of an antagonist of non-NMDA receptors indicated that this intracortical propagation of signals is due mostly, if not exclusively, to the postsynaptic excitation of cortical neurons. Blockade of NMDA receptors attenuated the rising and peak phases of the upper horizontal spread, but did not affect those of the lower horizontal or vertical propagation of excitation. Perfusion with Mg2+-free solution enhanced the upper horizontal spread, but in most cases did not significantly change the spread of excitation in the other pathways. These results indicate that NMDA receptors are involved in the flow of information in the upper layers of visual cortex, and further suggest that this propagation of activity is mediated mainly by horizontal connections intrinsic to the upper layers.

2-Amino-5-phosphonovalerate↗

PubMed1998

Localized contribution of N-methyl-D-aspartate receptors to synaptic input-induced rise of calcium in apical dendrites of layer II/III neurons in rat visual cortex.

To examine the role of N-methyl-D-aspartate receptors in the synaptic input-induced increase in Ca2+ in layer II/III neurons of visual cortex, Ca2+ imaging with a relatively low-affinity indicator was carried out simultaneously with whole-cell recordings of synaptic activity in cortical slices of young rats. Electrical stimulation of layer IV elicited excitatory postsynaptic potentials that generated action potentials concomitantly with a marked rise of Ca2+ signal in apical dendrites of 24 pyramidal cell-like neurons. Dendritic regions about 50 microm from the soma (peak regions) consistently showed the strongest increase in signal. The application of an N-methyl-D-aspartate receptor antagonist, DL-2-amino-5-phosphonovalerate, reduced the Ca2+ signal in peak regions but did not in other regions in nine of the 15 neurons tested. In all the dendritic regions in which Ca2+ signal was measured, the magnitude of the increase in signal was related linearly to the number of action potentials, suggesting that voltage-dependent Ca2+ channels activated by action potentials may also be involved in the increase. In 25 of 33 neurons which were voltage-clamped at 80 mV and perfused with the Mg2+-free solution, layer IV stimulation could induce a local rise in Ca2+ signal in apical dendrites. This rise was blocked by the N-methyl-D-aspartate receptor antagonist almost completely. Such an antagonist-sensitive Ca2+ rise was still seen even when the membrane potential was held at +10 mV when voltage-dependent Ca2+ channels were expected not to be activated by excitatory synaptic inputs. These results suggest that N-methyl-D-aspartate receptors are involved in the synaptic input-induced rise in Ca2+ at postsynaptic sites in apical dendrites of layer II/III neurons, and the increase may be boosted through voltage-dependent Ca2+ channels activated by action potentials.

Action Potentials↗

PubMed1998

[Thoracic arachnoid cyst presenting incomplete features of Brown-Séquard syndrome: a case report].

Spinal intradural arachnoid cyst presenting incomplete features of Brown-Séquard syndrome is very rare. Only 6 cases have been reported. We report one in a thoracic lesion. A 42-year-old man noticed thermohypesthesia in his right leg, and monoparesis in his left leg. On admission, he presented incomplete features of Brown-Séquard syndrome below the Th7 level. MRI showed the spinal cord to be displaced antero-laterally to the right at Th6-7 level. Myelography and CT myelography failed to show the cyst wall, but an arachnoid cyst was totally removed with T5-8 osteoplastic laminotomy. Sensory disturbance has not changed postoperatively, but motor weakness in his left leg recovered within one month after the operation. No cystic lesion has been detected by MRI during the ten months since the operation. We investigated all seven cases in the literature including our case which showed incomplete features of Brown-Séquard syndrome. As regards to the location of the cyst, all cases were at the mid-thoracic level. And four cases were at the midline. These results suggest that the mechanism of Brown-Séquard syndrome associated with spinal arachnoid cyst may be related not only to the laterality of the lesion but also to the asymmetrical circulation in the watershed area.

Adult↗

PubMed1997

Brain-derived neurotrophic factor enhances long-term potentiation in rat visual cortex.

Brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), members of the nerve growth factor (NGF) gene family, have been suggested to play a role in experience-dependent modification of neural networks in the developing nervous system. In this study we addressed the question of whether these neurotrophins are involved in long-term potentiation (LTP) in developing visual cortex. We recorded layer II/III field potentials and whole-cell currents evoked by test stimulation of layer IV at 0.1 Hz in visual cortical slices prepared from young rats (postnatal day 15-25) and observed effects of BDNF, NT-3, and NGF on these responses. Then we analyzed the effects of these neurotrophins on LTP induced by tetanic (Theta-burst type) stimulation of layer IV. We found that BDNF at 200 ng/ml potentiated field potentials and EPSCs in most cases and that this potentiation lasted after cessation of the BDNF application. At the concentration of 20 ng/ml, BDNF did not show such an effect, but it enhanced the magnitude of expressed LTP. On the other hand, NT-3 and NGF had none of these effects. Immunohistochemical staining of slices with antibody against BDNF showed that exogenous BDNF penetrated into the whole slice within approximately 5 min of its application. The actions of BDNF were blocked by preincubation of slices with TrkB-IgG fusion protein, a BDNF scavenger, or coapplication of K252a, an inhibitor for receptor tyrosine kinases. TrkB-IgG or K252a itself completely blocked LTP, suggesting that endogenous BDNF or another TrkB ligand plays a role in LTP in the developing visual cortex.

Action Potentials↗

PubMed1997

Quantal analysis suggests presynaptic involvement in expression of neocortical short- and long-term depression.

Long-term depression together with long-term potentiation represent popular experimental models to study synaptic plasticity. However, analyses of the mechanisms underlying the expression of cortical long-term depression are in their infancy and have been confined to the hippocampus. Short- and long-term depression in neocortex is not well understood. Here we recorded small excitatory postsynaptic potentials intracellularly from rat visual cortex slices. The responses fluctuated between several amplitude levels suggesting a quantal nature of the synaptic transmission. Consistent changes in the quantal steps accompanied neither paired-pulse depression (50 ms interval within the pair) nor long-term depression (induced by 1 Hz, 5 min stimulation). The amplitude distributions shifted to smaller values suggesting decreases in the number of quanta released without essential changes in the postsynaptic quantal efficiency. Both the coefficient of variation of response amplitudes and the number of response failures increased; cases were encountered suggesting a very low release probability after depression. Changes in quantal content estimated from the deconvolution analysis were correlated with the magnitude of depression. The findings suggest predominantly presynaptic loci for expression of short- and long-term neocortical depressions. The likely underlying mechanism is a decrease in transmitter release probability. Long-term depression decreased the probability so strongly that some inputs became virtually silent.

Animals↗

PubMed1997

Presynaptically silent synapses: spontaneously active terminals without stimulus-evoked release demonstrated in cortical autapses.

This study addresses the question of whether synapses that are capable of releasing transmitters spontaneously can also release them in an excitation-dependent manner. For this purpose, whole cell patch recordings were performed for a total of 48 excitatory solitary neurons in a microisland culture to observe excitatory autaptic currents elicited by spontaneous transmitter release as well as by somatic excitation. A somatic Na+-spike, induced in response to a short voltage step, evoked excitatory postsynaptic currents (EPSCs) of various amplitudes through the autapses; in some cases, no response was noticeable. To make sure that the recorded autaptic spontaneous EPSCs (sEPSCs) under a voltage clamp resulted from independent release of transmitters and were not associated with action potentials, sEPSCS in the presence and absence of tetrodotoxin (TTX) were compared in six cells. In the presence of TTX the evoked EPSCs were completely eliminated, whereas the sEPSCs were still observed and the amplitude distribution histograms were statistically not different from those recorded in the absence of TTX. A quantitative analysis of the sEPSCs (presumably miniature EPSCs) showed that the amplitude of stimulus-evoked EPSCs did not correlate with either the frequency or median amplitudes of the sEPSCs or the age of the culture. To identify whether the absence of stimulus-evoked response was caused either by conduction failure of excitation along the axons or by impairment of the release machinery that links the terminal depolarization to vesicle exocytosis, we examined whether high K+ and hypertonic solutions could facilitate the spontaneous release of transmitters. Although the hypertonic solution increased the spontaneous release in all cells tested (n = 18), the high K+ solution had a differential effect in increasing spontaneous release, i.e., the cells with larger evoked responses were more readily facilitated by the high K+ solution. Because the high K+ solution induced depolarization of presynaptic terminals, the present results indicated that the smaller evoked responses were due to the larger number of impaired or "silent" presynaptic terminals that were unable to link presynaptic depolarization to transmitter release. In summary, the present experiments provided evidence that at least some of the presynaptic terminals are silent in response to stimuli, while remaining spontaneously active at the same time. Because this phenomenon is due to the lack of sensitivity to depolarization at the terminals, these synaptic terminals seem incapable of linking terminal depolarization to transmitter release.

Animals↗

PubMed1997

Iatrogenic arteriovenous fistula of the middle meningeal artery caused during embolization for meningioma--case report.

A 73-year-old female developed middle meningeal arteriovenous fistula during embolization of a falx meningioma. The cause of this complication was thought to be perforation by the guide wire during catheterization at the sharp bend in the sphenoidal portion of the middle meningeal artery. Embolization of the fistula and the feeding artery to the meningioma with polyvinyl alcohol particles 250-355 microns size resulted in complete obliteration of the fistula. Computed tomography showed no epidural or subdural hematoma. Introduction of the microcatheter beyond the sharp bend in the middle meningeal artery should not be attempted to avoid the possibility of iatrogenic middle meningeal arteriovenous fistula.

Aged↗

PubMed1996

Mechanisms underlying orientation selectivity of neurons in the primary visual cortex of the macaque.

1. Effects of blocking intracortical inhibition by microiontophoretic administration of bicuculline methiodide (BMI), a selective antagonist for GABAA receptors, on orientation selectivity of 109 neurones were studied in the primary visual cortex (V1) of anaesthetized and paralysed monkeys. 2. The averaged orientation tuning of visual responses of cells was poor in cytochrome oxidaserich blobs of layer II/III and in layer IVc beta, moderate in layers IVb, IVc alpha and V, and sharp in the interblob region of layer II/III and in layers IVa and VI. 3. Iontophoretic administration of BMI reduced the sharpness of orientation tuning of cells to a varying extent in each layer. In most cells, furthermore, the originally ineffective stimuli induced visual responses during the BMI administration, suggesting that excitatory inputs evoked by the non-optimally oriented stimuli were masked by GABAergic inhibition. Nevertheless, the maximal facilitation was observed in the response to the optimally or near-optimally oriented stimuli. 4. There was a difference in such an effect of BMI among layers. Orientation selectivity of cells in interblobs in layer II/III and in layer IVb was sensitive to BMI whereas that of cells in layer VI was relatively insensitive to BMI, suggesting a larger contribution of excitatory mechanisms to the orientation selectivity in this layer. 5. In the orientation-selective cells, an analysis of the magnitude of excitation and inhibition evoked by stimuli at various orientations suggests that both inputs tune around the optimal orientation and their magnitudes are almost proportional to each other except at the optimal orientation. This analysis also indicates that the orientation tuning of inhibition had a less prominent peak around the optimal orientation than that of excitation. This dominance of excitation over inhibition around the optimal orientation may function to accentuate the response to the optimally oriented stimulus. 6. These results suggest that, in the monkey V1, the orientation selectivity of cells is largely dependent on the orientation-biased excitatory and inhibitory inputs which have a broader tuning profile, covering from the optimal to null-orientation, than that observed in extracellularly recorded responses at the control level.

Animals↗

PubMed1996

Long-term depression in rat visual cortex is associated with a lower rise of postsynaptic calcium than long-term potentiation.

To test the hypothesis that an input-associated rise of Ca2+ at postsynaptic sites beyond a certain threshold leads to the induction of long-term potentiation (LTP) while a lower rise below the threshold leads to long-term depression (LTD), the method of microscopic Ca2+ fluorometry was employed simultaneously with recordings of synaptic activity from layer II/III of visual cortical slices prepared from young rats. The conventional Ca2+ indicators, such as fura-2 or fluo-3, may interfere with intracellular processes for the induction of LTP/LTD because of their strong Ca(2+)-chelating action. To minimize such a problem, another Ca2+ indicator, rhod-2, was used since it has a much weaker Ca(2+)-chelating action than those indicators. In 16 slices loaded with rhod-2 through the perfusion medium, tetanic stimulation of theta-burst type was applied to layer IV of the cortex and changes in Ca2+ concentration were analyzed in layer II/III from which field potentials to test stimulation of layer IV were recorded simultaneously. In 7 slices in which weak tetanic stimulation consisting of 0.1 ms duration pulses was applied to layer IV, LTD of field responses was induced, while LTP was induced in 6 of the 9 slices in which strong tetanus consisting of 0.2 ms pulses was applied. In the 6 slices in which LTP was induced, the peak rise of fluorescence intensity during tetanus was 13.9 +/- 0.2 (S.E.M.) %, which was significantly (t-test, P < 0.01) higher than that (10.4 +/- 0.3%) in the 9 slices in which LTD was induced. In another series of experiments, rhod-2 was injected directly into 12 pyramidal cell-like neurons in layer II/III through patch pipettes, and changes in Ca2+ concentration in apical dendritic areas during tetanus were measured simultaneously with recordings of excitatory postsynaptic potentials (EPSPs) evoked by test stimulation of layer IV. It was found that LTP of EPSPs was induced in 4 cells which exhibited a strong rise of dendritic Ca2+ signal (197.1 +/- 18.5%) while LTD was induced in other 5 cells which showed a weak rise of the signal (31.0 +/- 4.1%). These results seem consistent with the above-mentioned, Ca(2+)-switching hypothesis for the induction of LTP and LTD in visual cortex.

Animals↗

PubMed1996

Lateral suprasylvian visual cortex is activated earlier than or synchronously with primary visual cortex in the cat.

To explore functional connectivity between area 17 and posteromedial lateral suprasylvian (PMLS) area of the cat cerebral cortex, we carried out cross-correlation analysis of spike trains of neurons recorded simultaneously from both areas of anesthetized, paralyzed cat. Most of correlated pairs had peaks which indicate that PMLS cells were activated earlier than or simultaneously with their partners in area 17, suggesting that 'backward' as well as synchronous activation operates between these cortical areas.

Animals↗

PubMed1996

Postsynaptic calcium and calcium-dependent processes in synaptic plasticity in the developing visual cortex.

In this paper we describe some of the results obtained from recent experiments on mechanisms underlying long-term potentiation (LTP) and long-term depression (LTD) in the visual cortex of young rats. In particular, we focus on experiments which tested the hypotheses that the induction of LTP in the visual cortex is of Hebbian type and that an input-associated Ca2+ rise at postsynaptic sites and subsequent activation of protein kinases or protein phosphatases may play roles in the induction of LTP or LTD in the developing visual cortex.

Animals↗

PubMed1996

Less segregated processing of visual information in V2 than in V1 of the monkey visual cortex.

To test the possibility of cross-talk between parallel pathways dealing with different aspects of visual information such as orientation, direction of motion and colour in cortical area V2, we quantitatively analysed visual responses of 121 V2 cells recorded from anaesthetized and paralysed macaques and compared them with those of 147 V1 cells. A selectivity index of visual responses was calculated for each neuron, which was then classified as selective or not to a particular attribute of visual stimuli. Twenty-one percent of the V2 neurons had dual selectivity to both colour and direction of stimulus motion (C&D cells). In V1, only 5% of the cells were C&D cells. Thus, the proportion of C&D cells significantly increased from V1 to V2. We also carried out cross-correlation analysis of spike trains recorded simultaneously from pairs of V2 neurons or pairs of V1 neurons. In V2, correlated firings could be observed between cells with completely different optimal orientation, such as orthogonal, while it was never observed in V1. The cross-correlation analysis further indicted that functional interactions in V2 were more widespread than those in V1. These results suggest that neurons which have different functional properties become less segregated, and that functional interactions become more widespread in V2 than in V1.

Animals↗

PubMed1996

Brain-derived neurotrophic factor blocks long-term depression in rat visual cortex.

1. Brain-derived neurotrophic factor (BDNF) has been reported to play a role in long-term potentiation (LTP) in hippocampus, but whether it is involved also in long-term depression (LTD) is not yet known. In this study, we tested whether BDNF and its gene family, nerve growth factor (NGF), have any effect on synaptic transmission and LTD in visual cortical slices of young rats. 2. An application of BDNF at the concentration of 20 ng/ml did not significantly change layer II/III field responses evoked by layer IV stimulation at 0.1 Hz, although at 200 ng/ml it enhanced responses. BDNF at 20 ng/ml prevented LTD of field responses from being induced by low-frequency stimulation (1 Hz for 15 min) of layer IV. NGF did not have such effects in the same concentration range as that of BDNF. 3. The action of BDNF was antagonized by K252a, an inhibitor of receptor tyrosine kinases. When K252a alone was applied to slices, LTD of stronger magnitude than in control slices was induced by low-frequency stimulation. 4. These results suggest that endogeneous BDNF may prevent synapses from being depressed by low-frequency inputs in the developing visual cortex.

Animals↗

PubMed1995

An inhibitor for calcineurin, FK506, blocks induction of long-term depression in rat visual cortex.

Long-term depression (LTD) of synaptic transmission, often used as an essential component in synaptic models for learning, memory and forgetting, can be produced in layer II/III of the visual cortex by a prolonged, low-frequency stimulation (LFS) of layer IV. The activation of Ca2+/calmodulin-dependent protein phosphatase, calcineurin, has been postulated to play a role in the induction of LTD. The recent introduction of a specific inhibitor for calcineurin, FK506, prompted the investigation of the involvement of this phosphatase in the induction of LTD in visual cortex. Thus, we administered FK506 at 1 microM to visual cortical slices of young rats, and found that it did not significantly affect field responses of layer II/III evoked by test stimulation of layer IV at 0.1 Hz, but prevented LTD of the responses from being induced by LFS (1 Hz for 15 min) in all the 10 slices tested. Without FK506, significant LTD was induced by the same parameters of LFS in 8 of the 12 slices. These results suggest the critical involvement of calcineurin in producing LTD in visual cortex.

Animals↗

PubMed1995

Metabotropic glutamate receptors and visual cortical synaptic plasticity.

Two forms of use-dependent synaptic plasticity, called long-term potentiation (LTP) and long-term depression (LTD), can be elicited in the visual cortex following different paradigms of electrophysiological stimulation. These neurobiological phenomena often are considered as necessary components of models for the alteration in function of the nervous system that must occur at some level for the establishment and (or) maintenance of memory engrams, for learning processes, or for the consolidation of active neural connections and regression of inactive contacts in the developing brain. It has been postulated that for LTP and LTD to be produced in the hippocampus, activation of a particular subtype of excitatory amino acid receptor, the metabotropic receptor, is a critical requirement. Only recently has it become possible to test this hypothesis directly, as a new compound, (+/-)-alpha-methyl-4-carboxyphenylglycine (MCPG), has been introduced and the suggestion made that it selectively antagonizes the metabotropic receptor. This substance has been tested in the present study on responses recorded from slices of rat visual cortex and has been found both to block the activation of the metabotropic receptor and to interfere selectively with the form of synaptic plasticity called LTD. It thus appears from the experiments reported in this paper as though the metabotropic receptor subtype that is blocked by MCPG is required for the expression of LTD but not for the expression of LTP, in the visual cortex of adult rats.

Animals↗