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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
10                                     However, parallel fibres can also release transmitter directly in
11             In the cerebellum, tension along parallel fibres can explain why the cortex is highly elo
12 r of activated parallel fibres prolonged the parallel fibre EPSC, demonstrating an interaction betwee
13 n is made of an ascending portion and a long parallel fibre extending at right angles, an architectur
14 denosine is directly released in response to parallel fibre firing and does not arise from extracellu
15 nner portion of the molecular layer, whereas parallel fibres form synapses on the thin, distal Purkin
16  adenosine release evoked by stimulating the parallel fibres in the cerebellum.
17  layer, translating mossy fibre signals into parallel fibre input to Purkinje cells.
18                                The clustered parallel fibre input we observe is ideally suited for dr
19 ling them to act as coincidence detectors of parallel fibre input.
20     Here, we used trains of stimuli to study parallel fibre inputs to Purkinje cells in rat cerebella
21                                          The parallel fibres interact strongly with the substrate and
22 at repolarization of the action potential in parallel fibres is supported by at least three groups of
23 muli were applied, even to a small number of parallel fibres, knocking out GLAST or blocking GLT-1 in
24 ditions, single complex spikes do not induce parallel fibre long-term depression.
25 at genetic deletion of MAGL prolonged DSE at parallel fibre (PF) or climbing fibre (CF) to Purkinje c
26  to Purkinje cells (PC) via the granule cell/parallel fibre (PF) pathway.
27  photorelease of L-glutamate or by bursts of parallel fibre (PF) stimulation.
28 ial indications that ascending axon (AA) and parallel fibre (PF) synapse properties and modalities of
29 localization of GLAST away from the cleft of parallel fibre (PF) synapse.
30 cal supervised learning occurs at cerebellar parallel fibre (PF) to Purkinje cell synapses, comprisin
31 the bidirectional inversion of plasticity at parallel fibre (PF)-Purkinje cell (PC) synapses in cereb
32 alternate activation of two separate sets of parallel fibres (PF1 and PF2).
33 cerebellar cortex, brief, 8 Hz activation of parallel fibres (PFs) induces a cyclic adenosine 3'5'-mo
34                       Tetanic stimulation of parallel fibres (PFs) produces a slow EPSP (sEPSP) or sl
35 ype mice, increasing the number of activated parallel fibres prolonged the parallel fibre EPSC, demon
36                                       At the parallel fibre-Purkinje cell glutamatergic synapse, litt
37 ed in perisynaptic regions of the cerebellar parallel fibre-Purkinje cell synapse and is physically a
38 frame, and that synaptic transmission at the parallel fibre-Purkinje cell synapse remained functional
39 early stages of cerebellar development, when parallel fibre-Purkinje cell synapses have recently been
40 tude of excitatory post-synaptic currents at parallel fibre-Purkinje cell synapses in mice.
41 ynaptic membrane of many synapses, including parallel fibre-Purkinje cell synapses in the cerebellum,
42 se can be modulated by receptors that act on parallel fibre-Purkinje cell synapses, we suggest that t
43 otor learning, long-term depression (LTD) at parallel fibre-Purkinje cell synapses.
44 nosine release exerts feedback inhibition of parallel fibre-Purkinje cell transmission.
45 -Purkinje cell synapses, we suggest that the parallel fibres release adenosine.
46 interneurons and Purkinje cells activated by parallel fibre stimulation in slices of cerebellar corte
47 NMDAR-mediated component of EPSCs, evoked by parallel fibre stimulation or occurring spontaneously, w
48 ity to occur and having a greater effect for parallel fibre stimulation than for granular layer stimu
49 effective if imposed up to two seconds after parallel-fibre stimulation.
50 onnections, observed in neural circuits with parallel fibres such as the insect mushroom body, could
51 hippocampal mossy fibre synapses, cerebellar parallel fibre synapses and corticothalamic synapses, wh
52       We find that DSE is normally stable at parallel fibre synapses but, following 4 Hz stimulation,
53 ecular layer, spillover of glutamate between parallel fibre synapses can lead to activation of perisy
54 tors produced by glutamate diffusion between parallel fibre synapses in the cerebellar cortex of juve
55 abinoid type-1 (Cb1) receptors is reduced at parallel fibre synapses in the cerebellum following 4 Hz
56             We investigated this question at parallel fibre synapses in the cerebellum, which co-expr
57                                         Many parallel fibre synapses might be silent, however, and gr
58 asured presynaptic GABA receptor function at parallel fibre synapses onto stellate cells in the cereb
59 e Bergmann glial cell processes that envelop parallel fibre synapses, but the possible contribution o
60  other forms of Cb1R-dependent plasticity at parallel fibre synapses, priming or inhibiting the circu
61 tamate receptor activation and plasticity at parallel fibre synapses, providing a link between input
62 the cerebellum receive approximately 180,000 parallel fibre synapses, which have often been viewed as
63 tentiation and the striking number of silent parallel fibre synapses.
64 e images could be explained by plasticity at parallel fibre synapses.
65 cells, evoking complex spikes and depressing parallel fibre synapses.
66  to regulate the function of local groups of parallel-fibre synapses.
67 dly potentiates mGluR-mediated excitation at parallel-fibre synapses.
68  also contribute to dendritic integration of parallel fibre synaptic input.
69  InsP3 produces a long-lasting depression of parallel-fibre synaptic transmission that is limited to
70 ings demonstrate that glutamate release from parallel fibre terminals of the tottering mouse is contr
71 o terminate transmission at the climbing and parallel fibre to Purkinje cell synapses.
72 by Albus and Ito, synaptic depression at the parallel fibre to Purkinje cells synapse (pf-PC) is the
73  cause long-term depression of synapses from parallel fibres to Purkinje cells.
74 s, whereas predictive signals are relayed by parallel fibres to the apical dendrites of the same cell
75  induce long-term depression with an optimal parallel-fibre to first-complex-spike timing interval of
76 ing the subunit composition of AMPARs at the parallel fibre-to-cerebellar stellate cell synapse.
77                     When spatially separated parallel fibres were activated by granular layer stimula
78 sence of GLAST, prolonged the EPSC when many parallel fibres were stimulated but not when few were st
79        Spike-mediated adenosine release from parallel fibres will thus powerfully regulate cerebellar