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

 
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