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1 olive and therefore may be correlated across climbing fibres.
2 uration of electrically controlled bursts in climbing fibres.
3 s, and excitatory collaterals from mossy and climbing fibres.
4 nation of relative strengths among competing climbing fibres.
5 f conditioned eyelid responses by activating climbing fibres.
6 reover, developmental elimination of surplus climbing fibres--a model for activity-dependent synaptic
7                                              Climbing fibre activity elicited by an unconditioned sti
8     These results, combined with analysis of climbing fibre activity in a computer simulation of the
9      Several anatomical reports suggest that climbing fibre afferents contact Golgi cells, and electr
10 of cerebellar learning theories asserts that climbing fibre afferents from the inferior olive provide
11 ht to be a key feature of how inferior olive climbing fibre afferents make their vital contribution t
12 rtant because non-synchronous stimulation of climbing fibres and peripheral afferents failed to alter
13 ast a proportion of the fibres that activate climbing fibres are corticospinal fibres.
14 system, suggest that transient inhibition of climbing fibres below their background level is the sign
15 rkinje cells remained multiply innervated by climbing fibres beyond the normal developmental time fra
16  Golgi cell peripheral responses mediated by climbing fibres can potentially contribute to cerebellar
17                 Pairing PF1 stimulation with climbing fibre (CF) activation at 1 Hz for 5 min produce
18                        EPSCs from individual climbing fibre (CF) inputs were identified on the basis
19 4) to investigate changes in transmission in climbing fibre (CF) pathways during motor learning.
20                                Reflex evoked climbing fibre (CF) responses (33 units) were recorded a
21 MAGL prolonged DSE at parallel fibre (PF) or climbing fibre (CF) to Purkinje cell (PC) synapses.
22 e imaged post-lesion sprouting of cerebellar climbing fibres (CFs) in mice using in vivo time-lapse m
23 hen they receive synaptic inputs solely from climbing fibres (CFs).
24       In vivo and in vitro data suggest that climbing fibre collateral excitation is weak in adult mi
25                        We therefore examined climbing fibre collateral input to large premotor CbN ce
26 res in the cerebellar cortex, implicates the climbing fibre collateral pathway in early postnatal dev
27                                   Activating climbing fibre collaterals evoked well-timed increases i
28                           The convergence of climbing fibre collaterals onto CbN cells decreases from
29 with intracellular D-aspartate prolonged the climbing fibre EPSC.
30 g fibre-Purkinje cell synaptic density, more climbing fibres extending to the outer portion of the mo
31 rts of the contralateral motor cortex evoked climbing fibre field potentials at the same cerebellar r
32                                              Climbing fibre field potentials evoked by low intensity
33                                    Normally, climbing fibres form synapses mainly on the thick, proxi
34 AG to cerebellar cortex, which terminates as climbing fibres in lateral vermal lobule VIII (pyramis).
35 ptic strength coinciding with the pruning of climbing fibres in the cerebellar cortex, implicates the
36  that attributes the persistence of multiple climbing fibre innervation to an obscured discrimination
37 eneration of proximal dendrites, the site of climbing fibre innervation, most pronounced.
38 hen painful signals are involved, and as the climbing fibre input to zone C3 is extremely responsive
39  into question the widely held view that the climbing-fibre input is an 'all-or-none' event.
40 r Purkinje cells, a single activation of the climbing-fibre input markedly potentiates mGluR-mediated
41 lex spike (CS) caused in Purkinje cells by a climbing-fibre input.
42 grating diverse afferent signals to generate climbing fibre inputs to the cerebellar cortex.
43 grating diverse afferent signals to generate climbing fibre inputs to the cerebellar cortex.
44 rning relies on movement errors signalled by climbing-fibre inputs to cause long-term depression of s
45 ggest that during learning, longer bursts in climbing fibres lead to longer-duration CS responses in
46 We reinvestigated this issue and, given that climbing fibres mediate synaptic plasticity in the cereb
47 that the conduction velocities of cerebellar climbing fibre (olivocerebellar) axons are tuned accordi
48 tive stimulation of peripheral afferents and climbing fibres on Golgi cell responses.
49                                   Cerebellar climbing fibres originate in the inferior olive (IO).
50 ations for the regulation of transmission in climbing fibre pathways during voluntary movements and m
51 tory synaptic transmission from parallel and climbing fibres (PFs, CFs) to PCs in acute cerebellar sl
52 o show that blocking inhibitory input to the climbing fibres prevents extinction of the conditioned r
53                           This suggests that climbing fibres projecting to different parts of the cer
54 ate significant gating of cutaneous input to climbing fibres projecting to the C1, C2 and C3 zones du
55 k-dependent modulation of cutaneous input to climbing fibres projecting to the C1, C2 and C3 zones in
56                            The activation of climbing fibres projecting to the posterior lobe cerebel
57                                          The climbing fibre projection from the motor cortex to the c
58                           The inferior olive climbing fibre projection to two somatotopically corresp
59 tive motor signals to the cerebellum via the climbing fibre projection, which sends collaterals direc
60                                              Climbing fibres provide one of the major excitatory inpu
61 r TrkB plays a role in the maturation of the climbing fibre-Purkinje cell (CF-PC) synapse.
62 tionship between the altered distribution of climbing fibre-Purkinje cell connections and tremor.
63 jor excitatory inputs to Purkinje cells, and climbing fibre-Purkinje cell connections are essential f
64         These findings suggest that abnormal climbing fibre-Purkinje cell connections could be of imp
65 ter type 2 immunohistochemistry, we labelled climbing fibre-Purkinje cell synapses of 12 essential tr
66                          The distribution of climbing fibre-Purkinje cell synapses on Purkinje cell d
67 ter portion of the molecular layer, and more climbing fibre-Purkinje cell synapses on the thin Purkin
68 ential tremor, the increased distribution of climbing fibre-Purkinje cell synapses on the thin Purkin
69 s to examine the density and distribution of climbing fibre-Purkinje cell synapses using post-mortem
70 nge during frequency-dependent depression at climbing fibre-Purkinje cell synaptic connections.
71 ntrols, essential tremor cases had decreased climbing fibre-Purkinje cell synaptic density, more clim
72    We have re-evaluated this issue using the climbing fibre reflex.
73 ntial shape and may contribute to the unique climbing fibre response.
74                By comparison of latencies of climbing fibre responses evoked from different locations
75  the dorsal column nuclei did not affect the climbing fibre responses evoked in crus II, and produced
76                                              Climbing fibre responses resulting from low intensity (n
77                                        Large climbing fibre responses were evoked in parts of crus II
78                          Corticofugal evoked climbing fibre responses were mapped across the cerebell
79                        This implies that the climbing fibre responses were not exclusively mediated v
80                                              Climbing fibre responses with similar form and cerebella
81 nje cells were identified by the presence of climbing fibre responses.
82  brainstem stimulation that did not activate climbing fibres, responses were not depressed.
83                 Additionally, however, these climbing fibres send collaterals to the cerebellar nucle
84             Here, we show that inhibition of climbing fibres serves as a teaching signal for extincti
85 precision is not an important element of the climbing fibre signal.
86            While it is well established that climbing fibre signals are important for motor coordinat
87  central role in control of olivo-cerebellar climbing fibre signals.
88 In control experiments using either the same climbing fibre stimulation alone, or peripheral afferent
89                     The results confirm that climbing fibre stimulation depresses Golgi cell firing a
90 MDA receptor-mediated EPSCs can be evoked by climbing fibre stimulation, and appear to be mediated ma
91          Theories concerning the role of the climbing fibre system in motor learning, as opposed to t
92            Soma-to-dendrite translocation of climbing fibre terminals was unaffected.
93 e cells are initially innervated by multiple climbing fibres that are subsequently culled to assume t
94 iring and after conjunctive stimulation with climbing fibres these were significantly reduced.
95 cells that had axons that branched to supply climbing fibres to both regions of the zone.
96 Where overlaps occurred, cells that provided climbing fibres to one or the other region were intermin
97 stral levels of DAO, the territory providing climbing fibres to the anterior lobe was centred more la
98 r olivary neurons transmit their signals via climbing fibres, which powerfully excite Purkinje cells,
99 ts thus show that conjunctive stimulation of climbing fibres with other inputs to Golgi cells can ind

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