Tohoku University · Neuroscience
Professor Ko Matsui's research lab focuses on the cellular and synaptic mechanisms underlying neurotransmission in the central nervous system, with a particular emphasis on neuron-glia interactions. The lab investigates the roles of glutamate receptors and transporters in both neuronal and astrocytic signaling, especially in retinal and cerebellar circuits. Using advanced electrophysiological techniques such as patch-clamp recordings and quantitative electron microscopy, the lab explores how synaptic and ectopic release mechanisms contribute to neural communication and synaptic plasticity. A central theme is the functional integration of astrocytes in synaptic transmission, challenging the traditional view of neurons as the sole contributors to synaptic currents.
Figures are computed from collected data and may differ slightly.
Until recently, communication from neurons to astrocytes was thought to be mediated by low-concentration transients of glutamate caused by spillover from the synaptic cleft. However, quantal events recorded in rat cerebellar Bergmann glial cells (BGs) have fast kinetics, comparable with those recorded in neurons. By combining outside-out patch recordings of BG AMPA receptors and quantitative electron microscopic analysis of glutamate receptor subunit 1 (GluR1) and GluR4 immunogold labeling measu
Properties of glutamatergic synaptic transmission were investigated by simultaneously voltage-clamping a pair of connected bipolar cells and cells in the ganglion cell layer (GLCs) in the newt retinal slice preparation. Activation of the Ca2+ current in a single bipolar cell was essential for evoking the glutamatergic postsynaptic current in the GLC. Depolarization for as short as 15 msec activated both NMDA and non-NMDA receptors. On the other hand, analysis of the spontaneous glutamatergic syn
Exocytosis of synaptic vesicles occurs not only at synaptic active zones but also at ectopic sites. Ectopic exocytosis provides a direct and rapid mechanism for neurons to communicate with glia that does not rely on transmitter spillover from the synaptic cleft. In the cerebellar cortex the processes of Bergmann glia cells encase synapses between presynaptic climbing fiber varicosities and postsynaptic Purkinje cell spines and express both AMPA receptors and electrogenic glutamate transporters.
We examined the role of glutamate uptake in the synaptic transmission of graded responses from newt retinal bipolar cells (BCs) to ganglion layer cells (GLCs). In dissociated Müller cells (retinal glia), glutamate evoked an uptake current that was effectively inhibited by L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC). PDC had no effect on the non-NMDA receptors of dissociated spiking neurons. In the retinal slice preparation, dual whole-cell recordings were performed from a pair of BC and GLC.
In many vertebrate CNS synapses, the neurotransmitter glutamate activates postsynaptic non-N-methyl-D-aspartate (NMDA) and NMDA receptors. Since their biophysical properties are quite different, the time course of excitatory postsynaptic currents (EPSCs) depends largely on the relative contribution of their activation. To investigate whether the activation of the two receptor subtypes is affected by the synaptic interaction in the inner plexiform layer (IPL) of the mouse retina, we analyzed the
Transmitter released from presynaptic neurons has been considered to be the sole generator of postsynaptic excitatory signals. However, astrocytes of the glial cell population have also been shown to release transmitter that can react on postsynaptic receptors. Therefore, we investigated whether astrocytes take part in generation of at least a part of the synaptic current. In this study, mice cerebellar acute slices were prepared and whole cell patch clamp recordings were performed. We found tha
It is usually assumed that individuals rest during sleep. However, coordinated neural activity that presumably requires high energy consumption is increased during REM sleep. Here, using freely moving male transgenic mice, the local brain environment and astrocyte activity during REM sleep were examined using the fibre photometry method with an optical fibre inserted deep into the lateral hypothalamus, a region that is linked with controlling sleep and metabolic state of the entire brain. Optica
Plastic change of the neuronal system has traditionally been assumed to be governed primarily by the long-term potentiation/depression mechanisms of synaptic transmission. However, a rather simple shift in the ambient ion, transmitter and metabolite concentrations could have a pivotal role in generating plasticity upon the physiological process of learning and memory. Local brain environment and metabolic changes could also be the cause and consequences of the pathogenesis leading to epilepsy. G
Unlike an electrical circuit, the hardware of the brain is susceptible to change. Repeated electrical brain stimulation mimics epileptogenesis. After such "kindling" process, a moderate stimulus would become sufficient in triggering a severe seizure. Here, we report that optogenetic neuronal stimulation can also convert the rat brain to a hyperexcitable state. However, continued stimulation once again converted the brain to a state that was strongly resistant to seizure induction. Histochemical
Actions from glial cells could affect the readiness and efficacy of learning and memory. Using a mouse cerebellar-dependent horizontal optokinetic response motor learning paradigm, short-term memory (STM) formation during the online training period and long-term memory (LTM) formation during the offline rest period were studied. A large variability of online and offline learning efficacies was found. The early bloomers with booming STM often had a suppressed LTM formation and late bloomers with
The potential role of astrocytes in lateral habenula (LHb) in modulating anxiety was explored in this study. The habenula are a pair of small nuclei located above the thalamus, known for their involvement in punishment avoidance and anxiety. Herein, we observed an increase in theta-band oscillations of local field potentials (LFPs) in the LHb when mice were exposed to anxiety-inducing environments. Electrical stimulation of LHb at theta-band frequency promoted anxiety-like behavior. Calcium (Ca<
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