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Takuya Yasui

Publications and source records attributed to Takuya Yasui.

5 recordsLinked to original sources
PubMed2005

Dynamic synapses as archives of synaptic history: state-dependent redistribution of synaptic efficacy in the rat hippocampal CA1.

Plastic modifications of synaptic strength are putative mechanisms underlying information processing in the brain, including memory storage, signal integration and filtering. Here we describe a dynamic interplay between short-term and long-term synaptic plasticity. At rat hippocampal CA1 synapses, induction of both long-term potentiation (LTP) and depression (LTD) was accompanied by changes in the profile of short-term plasticity, termed redistribution of synaptic efficacy (RSE). RSE was presynaptically expressed and associated in part with a persistent alteration in hyperpolarization-activated I(h) channel activity. Already potentiated synapses were still capable of showing RSE in response to additional LTP-triggering stimulation. Strikingly, RSE took place even after reversal of LTP or LTD, that is, the same synapse can display different levels of short-term plasticity without changing synaptic efficacy for the initial spike in burst presynaptic firing, thereby modulating spike transmission in a firing rate-dependent manner. Thus, the history of long-term synaptic plasticity is registered in the form of short-term plasticity, and RSE extends the information storage capacity of a synapse and adds another dimension of functional complexity to neuronal operations.

Action Potentials↗
PubMed2003

Activity-evoked capacitative Ca2+ entry: implications in synaptic plasticity.

The Ca2+ influx controlled by intracellular Ca2+ stores, called store-operated Ca2+ entry (SOC), occurs in various eukaryotic cells, but whether CNS neurons are endowed with SOC capability and how they may operate have been contentious issues. Using Ca2+ imaging, we present evidence for the presence of SOC in cultured hippocampal pyramidal neurons. Depletion of internal Ca2+ stores by thapsigargin caused intracellular Ca2+ elevation, which was prevented by SOC channel inhibitors 2-aminoethoxydiphenyl borate (2-APB), SKF96365, and La3+. Interestingly, these inhibitors also accelerated the decay of NMDA-induced Ca2+ transients without affecting their peak amplitude. In addition, SOC channel inhibitors attenuated tetanus-induced dendritic Ca2+ accumulation and long-term potentiation at Schaffer collateral-CA1 synapses in hippocampal slice preparations. These data suggest a novel link between ionotropic receptor-activated SOC and neuroplasticity.

Animals↗
PubMed2003

Mossy fibre synaptic NMDA receptors trigger non-Hebbian long-term potentiation at entorhino-CA3 synapses in the rat.

Hippocampal CA3 pyramidal cells receive two independent afferents from the enthorinal cortex, i.e. a direct input via the temporoammonic pathway (TA, perforant path) and an indirect input via the mossy fibres (MF) of dentate granule cells. In spite of past suggestions that the TA is assigned an important role in exciting the pyramidal cells, little is known about their physiological properties. By surgically making an incision through the sulcus hippocampi and a small part of the dentate molecular layer, we succeeded in isolating TA-mediated monosynaptic responses in CA3 stratum lacunosum-moleculare. The TA-CA3 synaptic transmission was completely blocked by a combination of D,L-2-amino-5-phosphonopentanoic acid (AP5) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), NMDA and non-NMDA receptor antagonists, respectively, and displayed paired-pulse facilitation and NMDA receptor-dependent long-term potentiation, which are all typical of glutamatergic synapses. We next addressed the heterosynaptic interaction between TA-CA3 and MF-CA3 synapses. The TA-CA3 transmission was partially attenuated by single-pulse MF pre-stimulation at inter-pulse intervals of up to 70 ms. However, surprisingly, burst stimulation of the MF alone induced long-lasting facilitation of TA-CA3 synaptic efficacy. This non-Hebbian form of synaptic plasticity was efficiently prevented by local application of AP5 into the MF synapse-rich area. Therefore, MF-activated NMDA receptors are responsible for the heterosynaptic modification of TA-CA3 transmission, and thereby, the history of MF activity may be etched into TA-CA3 synaptic strength. Our findings predict a novel form of spatiotemporal information processing in the hippocampus, i.e. a use-dependent intersynaptic memory transfer.

Animals↗
PubMed2002

Auditory behaviors and auditory brainstem responses of infants with hypogenesis of cerebral hemispheres.

Three infants with an almost complete absence of the cerebral hemispheres as a result of brain anomalies were studied both audiologically and neurologically. The brain anomalies were diagnosed by means of MRI and CT scans. Behavioral audiometry revealed reactions only to loud sound stimulations but auditory brainstem responses showed wave configurations and thresholds compatible with the ages of the infants. There were significant differences in the thresholds obtained by behavioral audiometry and auditory brainstem responses. It can be considered that these auditorily stimulated behavioral responses are evoked by auditory motor reflexes originating in the brainstem, but not by auditory perception.

Audiometry↗