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1 need to characterize the spatial pattern of parallel fibre activity evoked by physiological stimuli,
2 n brain's grey matter.We used rat cerebellar parallel fibres, an example of typical grey matter axons
3 repetitive activation of the synapse between parallel fibres and Purkinje cells causes InsP3-mediated
4 e studied glutamatergic transmission between parallel fibres and Purkinje cells in cerebellar slices.
5 tested whether synaptic transmission between parallel fibres and Purkinje cells in tottering mice was
6 ith 0.2 microm diameter (matching cerebellar parallel fibres) axonal noise alone can explain half of
7 llar granule cells fire in bursts, and their parallel fibre axons (PFs) form approximately 180,000 ex
8 imaging of multiple neighbouring cerebellar parallel fibre axons, we find evidence for clustered pat
9 rted to show plasticity when stimulating the parallel fibres, but not when granule cell axons are sti
12 r of activated parallel fibres prolonged the parallel fibre EPSC, demonstrating an interaction betwee
13 denosine is directly released in response to parallel fibre firing and does not arise from extracellu
14 nner portion of the molecular layer, whereas parallel fibres form synapses on the thin, distal Purkin
19 Here, we used trains of stimuli to study parallel fibre inputs to Purkinje cells in rat cerebella
21 at repolarization of the action potential in parallel fibres is supported by at least three groups of
22 muli were applied, even to a small number of parallel fibres, knocking out GLAST or blocking GLT-1 in
23 at genetic deletion of MAGL prolonged DSE at parallel fibre (PF) or climbing fibre (CF) to Purkinje c
27 cerebellar cortex, brief, 8 Hz activation of parallel fibres (PFs) induces a cyclic adenosine 3'5'-mo
29 ype mice, increasing the number of activated parallel fibres prolonged the parallel fibre EPSC, demon
31 ed in perisynaptic regions of the cerebellar parallel fibre-Purkinje cell synapse and is physically a
32 frame, and that synaptic transmission at the parallel fibre-Purkinje cell synapse remained functional
33 early stages of cerebellar development, when parallel fibre-Purkinje cell synapses have recently been
34 se can be modulated by receptors that act on parallel fibre-Purkinje cell synapses, we suggest that t
38 interneurons and Purkinje cells activated by parallel fibre stimulation in slices of cerebellar corte
39 NMDAR-mediated component of EPSCs, evoked by parallel fibre stimulation or occurring spontaneously, w
40 ity to occur and having a greater effect for parallel fibre stimulation than for granular layer stimu
42 hippocampal mossy fibre synapses, cerebellar parallel fibre synapses and corticothalamic synapses, wh
43 ecular layer, spillover of glutamate between parallel fibre synapses can lead to activation of perisy
44 tors produced by glutamate diffusion between parallel fibre synapses in the cerebellar cortex of juve
47 asured presynaptic GABA receptor function at parallel fibre synapses onto stellate cells in the cereb
48 e Bergmann glial cell processes that envelop parallel fibre synapses, but the possible contribution o
49 tamate receptor activation and plasticity at parallel fibre synapses, providing a link between input
50 the cerebellum receive approximately 180,000 parallel fibre synapses, which have often been viewed as
57 InsP3 produces a long-lasting depression of parallel-fibre synaptic transmission that is limited to
58 ings demonstrate that glutamate release from parallel fibre terminals of the tottering mouse is contr
61 s, whereas predictive signals are relayed by parallel fibres to the apical dendrites of the same cell
64 sence of GLAST, prolonged the EPSC when many parallel fibres were stimulated but not when few were st
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