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1  both transmitters on a single post-synaptic Renshaw cell.
2 e close contacts or puncta were observed per Renshaw cell.
3 with the soma and/or dendrites of individual Renshaw cells.
4 synaptic connection between motoneurones and Renshaw cells.
5 motoneurons, Ia inhibitory interneurons, and Renshaw cells.
6 y and organization of motor inputs on mature Renshaw cells.
7  is no reduction in the number of V1-derived Renshaw cells.
8 inhibitory amino acid transporter (VIAAT) in Renshaw cells.
9 nnectivity emerges during the development of Renshaw cells.
10 te the development of inhibitory synapses on Renshaw cells.
11 inhibitory circuit between motor neurons and Renshaw cells.
12 contribute to strengthen inhibitory input on Renshaw cells.
13 al support for the peptidergic modulation of Renshaw cells.
14 tes at both early and late postnatal ages on Renshaw cells.
15 he gephyrin/glycine receptor cluster size on Renshaw cells.
16 owth reached a plateau in 25- and 60-day-old Renshaw cells (0.45 +/- 0.43 microm(2); 0.56 +/- 0.55 mi
17 or expression in gephyrin patches located on Renshaw cells, a type of spinal interneuron that receive
18              Whole-cell recordings in P9-P15 Renshaw cells after P5 TeNT injections showed increases
19 ibitory glycinergic synapses may explain why Renshaw cells, although capable of firing at very high f
20                                  Group 1 are Renshaw cells and intensely express calbindin and coexpr
21                                   Early born Renshaw cells and late born Foxp2-V1 interneurons are ti
22 adapted to increase inhibitory efficacy over Renshaw cells and mature postnatally by mechanisms that
23 e cholinergic motoneuronal terminals on both Renshaw cells and motoneurons were enriched in glutamate
24 the formation of inhibitory synapses between Renshaw cells and motor neurons.
25 ter-IR motor axon synapses contact embryonic Renshaw cells and proliferate postnatally matching Rensh
26 oreactivity was used to identify 129 and 171 Renshaw cells and their dendrites in cat and rat lumbar
27 m from the soma in calbindin D28k-identified Renshaw cells and up to 184 microm in gephyrin-identifie
28 e receptor cluster size maturation that sets Renshaw cells apart from other interneurons is discussed
29               Our results suggest that while Renshaw cells are not directly required as an integral p
30                       Like other V1 neurons, Renshaw cells are thus competent to receive sensory syna
31 hrna2 was correlated with disconnection from Renshaw cells as well as major structural abnormalities
32 ron inputs were sufficient to depolarize the Renshaw cell beyond threshold for firing.
33 atal day 0 (P0) and this input spread to all Renshaw cells by P10-P15.
34          In neonatal mice motoneurons excite Renshaw cells by releasing both acetylcholine (ACh) and
35                        Using two markers for Renshaw cells (calbindin and cholinergic nicotinic recep
36                    The responses from single Renshaw cells demonstrate that motoneuron synapses elici
37 roliferation coupled with the enlargement of Renshaw cell dendrites.
38                               Concomitantly, Renshaw cells developed with increased excitability and
39 ox gene 6) is necessary for an early step in Renshaw cell development, whereas Engrailed 1 (En1), whi
40 the question of whether they interact during Renshaw cell development.
41 N-related transcription factor genes play in Renshaw cell development.
42   Loss of VIAAT from Chrna2(Cre) -expressing Renshaw cells did not impact any aspect of drug-induced
43                    By 10 and 15 days of age, Renshaw cells exhibited gephyrin-immunoreactive clusters
44 ack-coupling loops similar to the well-known Renshaw cells explain the deterioration of synergy due t
45                              Adult mammalian Renshaw cells express large and complex postsynaptic gep
46                         In neonatal animals, Renshaw cells expressed small punctate gephyrin-immunore
47 ted that this input is functional and evokes Renshaw cell firing.
48 eptors were almost always colocalized inside Renshaw cell gephyrin clusters.
49 ajority (60-75%) of terminals presynaptic to Renshaw cell gephyrin patches contained immunocytochemic
50 ters contained inside boutons presynaptic to Renshaw cell gephyrin patches were also investigated.
51 w cells and proliferate postnatally matching Renshaw cell growth.
52 ht coupling with motor neurons suggests that Renshaw cells have an integral role in movement, a role
53                                              Renshaw cells, Ia inhibitory interneurons (IaINs), and p
54 ecting, inhibitory interneurons that include Renshaw cells, Ia inhibitory interneurons, and other uni
55                                              Renshaw cells, identified in human postmortem cervical s
56  The populations of clusters over developing Renshaw cells immunoreactive to gephyrin or glycine rece
57 the plasticity to compensate for loss of the Renshaw cell in adult circuit function.
58 rovide immunohistochemical identification of Renshaw cells in lamina VII of the ventral horn.
59  the recurrent circuitry indicates a role of Renshaw cells in modulating motor outputs that may be co
60 ent work has revealed novel ways to identify Renshaw cells in situ and this in turn has promoted a ra
61  the repercussions for the possible role for Renshaw cells in speed and force control.
62 ent of experimental strategies to manipulate Renshaw cells in spinal circuits and clarify their role
63 tions, the average gephyrin cluster areas on Renshaw cells increased by 18.4% at P15 and 28.4% at P20
64                  VGLUT1-IR bouton density on Renshaw cells increased until P15 but thereafter decreas
65 elopment of inhibitory synapse properties on Renshaw cells, influencing recruitment of postsynaptic g
66 n this group receive convergent calbindin-IR Renshaw cell inputs.
67 he number of functional contacts on a single Renshaw cell is more than halved when the nicotinic rece
68 howed that most embryonic (embryonic day 18) Renshaw cells lack dorsal root inputs, but more than hal
69  neurones, and some interneurones, including Renshaw cells, lacked demonstrable Kv2.1-IR.
70                  We have recently shown that Renshaw cells mediate powerful shunt inhibition on moton
71                                              Renshaw cells mediate recurrent inhibition between moton
72 omeric nicotinic receptors at the motoneuron-Renshaw cell (MN-RC) synapse.
73 ings from identified, synaptically connected Renshaw cell-motoneuron pairs in the mouse lumbar spinal
74                           Calbindin-positive Renshaw cell number was decreased significantly at 12 we
75  the loss of presynaptic motor axon input on Renshaw cells occurs at early stages of ALS and disconne
76  stimulation was used to evoke currents from Renshaw cells or motoneurons to characterize responses o
77  in close apposition to lateral motoneurons, Renshaw cells, other GFP(+) INs, and unidentified neuron
78 y synapses between identified motoneuron and Renshaw cell pairs.
79 rging inputs from presynaptic motoneuron and Renshaw cell populations.
80                                 In parallel, Renshaw cell postsynaptic densities apposed to VGLUT1-IR
81  large size of many cholinergic terminals on Renshaw cells presumably correlates with the strong syna
82 increasing the strength of sensory inputs on Renshaw cells prevents their deselection and reduces mot
83      In this review we illustrate how mature Renshaw cell properties and connectivity arise through a
84                                              Renshaw cell properties have been studied extensively fo
85  to be the avian equivalent of the mammalian Renshaw cell (R-interneurons).
86  circuit formation, and the mature mammalian Renshaw cell raises the possibility that R-interneuronal
87 tudy focuses on the differentiation of adult Renshaw cells (RCs) and Ia inhibitory interneurons (IaIN
88 n 100 mum of the ventral white matter, where Renshaw cells (RCs) are located, (2) interneurons inters
89                                              Renshaw cells (RCs) are one of the most studied spinal i
90 e Ia inhibitory interneurons (IaINs) and all Renshaw cells (RCs) derive from embryonic V1 interneuron
91 tive afferent input to motoneurons (MNs) and Renshaw cells (RCs) is disrupted by thoracic spinal cord
92                                              Renshaw cells (RCs) receive excitatory inputs from moton
93                                     Although Renshaw cells (RCs) were discovered over half a century
94 program that controls the differentiation of Renshaw cells (RCs), an anatomically and functionally di
95                                              Renshaw cells receive a high density of inhibitory synap
96 INs and other V1-derived interneurons, adult Renshaw cells receive motor axon synapses and lack propr
97                                 For example, Renshaw cells receive, at least in the neonate, converge
98  neurons from neonatal mice lacking VIAAT in Renshaw cells received spontaneous inhibitory synaptic i
99                         Here we examined the Renshaw cell recurrent circuit that exerts inhibitory fe
100                                              Renshaw cells represent a fundamental component of one o
101 of 4.4 and 2.8 close contacts on cat and rat Renshaw cells, respectively.
102                                        Thus, Renshaw cells shift from integrating sensory and motor i
103        Our data suggest an integral role for Renshaw cell signaling in shaping the excitability and s
104                                     Further, Renshaw cell signaling is closely associated with the mo
105 in rat using gephyrin-immunoreactivity, as a Renshaw cell specific marker, in combination with substa
106           Most calbindin-immunoreactive (IR) Renshaw cells survive to end stage but downregulate post
107                                              Renshaw cell synapses on motor neurons underwent more co
108 glutamatergic and calbindin-labeled putative Renshaw cell synapses on their soma and proximal dendrit
109 okes depolarizing monosynaptic potentials in Renshaw cells that are depressed, but not abolished, by
110 ow that a subset of V1 INs differentiates as Renshaw cells, the interneuronal cell type that mediates
111  generate exclusively cholinergic actions on Renshaw cells, their intraspinal synaptic targets.
112                                              Renshaw cells (V1(R)) are excitable as soon as they reac
113    VAChT-immunoreactive terminals apposed to Renshaw cells varied in size from 0.6 to 6.9 microm in d
114 s in regard to GABA release sites onto adult Renshaw cells was also found.
115 mine the relationships of these terminals to Renshaw cells, we used dual immunolabelling with antibod
116 s modulate synaptic maturation on developing Renshaw cells, we used three animal models in which affe
117                                A total of 50 Renshaw cells were analysed quantitatively using a compu
118                    Peptidergic influences on Renshaw cells were assessed in rat using gephyrin-immuno
119                                              Renshaw cells were identified by their calbindin immunor
120                                              Renshaw cells were special in that they displayed an abu
121 tion of quadriceps motor neurons mediated by Renshaw cells which had been activated by soleus motor n
122 tor neurons in the spinal cord also activate Renshaw cells, which provide recurrent inhibitory feedba
123 30 cholinergic terminals were observed on 50 Renshaw cells, with a range of 21-138 terminal appositio
124 rved in close contact with the immunolabeled Renshaw cells, with an average of 4.4 and 2.8 close cont

 
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