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1 action (DE-3 motoneurons) and elongation (CV motoneurons).
2 orce potentiation performs best for the slow motoneuron.
3 a single twitch works less well for the fast motoneuron.
4 chanism of compensation on the medial rectus motoneuron.
5 ted for harboring proximal upper limb flexor motoneurons.
6 ecting between antagonistic amine actions on motoneurons.
7 and in both polar regions by efferent gamma-motoneurons.
8 d by VGLUT1 content) on retrogradely labeled motoneurons.
9 in addition to the directly back-labeled L6 motoneurons.
10 rminates inspiration and activates laryngeal motoneurons.
11 essing CD8(+) T lymphocytes selectively kill motoneurons.
12 d KCC2, respectively, in neonatal rat lumbar motoneurons.
13 tio to the decreased number of ChAT-positive motoneurons.
14 hibition (P-boutons) on retrogradely labeled motoneurons.
15 currents from inputs formed by the different motoneurons.
16 direct rhythmic activation of lumbar flexor motoneurons.
17 last-order interneurons that innervate hand motoneurons.
18 als from spinal cord neurons with a focus on motoneurons.
19 tor-mediated excitation prevails in Group II motoneurons.
20 s that make disynaptic connections with hand motoneurons.
21 n to the region of the medial rectus C-group motoneurons.
22 rons supplying horizontal extraocular muscle motoneurons.
23 function of L-type like calcium channels in motoneurons.
24 ociated slower recovery times than secondary motoneurons.
25 em that supports the firing of medial rectus motoneurons.
26 68 granules in microglia surfaces opposed to motoneurons.
27 nd the axonal compartment of larval crawling motoneurons.
28 T cells, concomitant with the signal to the motoneurons.
29 otor cells, with monosynaptic connections to motoneurons.
30 ar inputs to control spinal interneurons and motoneurons.
31 ries on microglia function around axotomized motoneurons.
32 e characteristics mature earlier in cervical motoneurons.
33 scle receives synaptic inputs from different motoneurons.
34 a long-lasting muscarinic cation current in motoneurons.
35 providing direct monosynaptic input to alpha-motoneurons.
36 trigger inspiratory bursts that propagate to motoneurons.
37 ubclass responding robustly compared with Is motoneurons.
38 a formed macroclusters associated with dying motoneurons.
39 , and two separate populations of protractor motoneurons.
40 f muscle activation via 'C-bouton' inputs to motoneurons.
41 Notably, lamina VIII also harbors axial motoneurons.
42 s were synaptically connected to respiratory motoneurons.
43 ons between leptin receptors and respiratory motoneurons.
44 ir voltage-activated calcium channels, vagal motoneurons acquire a stressless form of pacemaking that
45 extension show that orchestration of serial motoneuron activation does not rely on feed-forward mech
46 generating a set of fundamental patterns of motoneuron activation, each timed at a specific phase of
49 contribution of Kv2.1 channels to rat alpha-motoneuron activity, the Kv2 inhibitor stromatoxin was u
54 lations to increase the activity of only one motoneuron and recordings of postsynaptic currents from
56 creased the synaptic strength of respiratory motoneurons and acted to boost motor amplitude from the
57 rush of Ia afferent synapses on regenerating motoneurons and decreased presynaptic inhibitory control
58 ed a system to differentially manipulate the motoneurons and examined the effects of cell type-specif
59 of C-INs is synaptically coupled to phrenic motoneurons and excitatory inputs to these "pre-phrenic"
60 icits the expression of the MHC-I complex in motoneurons and exerts their cytotoxic function through
61 wn about the output properties of individual motoneurons and how they affect the translation of moton
62 hole-cell patch-clamp recordings from spinal motoneurons and interneurons, we describe a long-duratio
63 endritic-like muscle cell extensions towards motoneurons and is required to recruit type A GABA recep
65 citatory D(1)-mediated effect of dopamine on motoneurons and network output that also involves co-act
68 interneuron activity, which inhibits caudal motoneurons and pre-conditions their excitability prior
69 injured axons, dendrites, and synapses from motoneurons and sensory neurons is strongly inhibited.
71 paired recordings between identified spinal motoneurons and skeletal muscle cells in larval zebrafis
72 r junction (NMJ) is a synapse formed between motoneurons and skeletal muscle fibers that is covered b
73 Neuromuscular junction is a synapse between motoneurons and skeletal muscles, where acetylcholine re
74 amma isoforms are expressed in primary mouse motoneurons and their transcripts are translocated into
75 has been related to the hyperexcitability of motoneurons and to changes in spinal sensory processing.
77 verall reduced firing rate compared with SIF motoneurons, and had significantly lower recruitment thr
78 ervical motoneurons are born prior to lumbar motoneurons, and spinal cord development follows a seque
79 nic mutants, presynapses of this cholinergic motoneuron are mislocalized to the dendrite at the ventr
80 ding of synaptic currents, we also show that motoneurons are activated by out-of-phase peaks in excit
83 onstrate that Kv2.1 clustering properties in motoneurons are dynamic and respond to both high and low
88 gical studies have revealed that SIF and MIF motoneurons are segregated anatomically and receive diff
90 mputational modeling indicated that Group II motoneurons are the major contributor to actual eye move
93 e ATD pathway on the firing of medial rectus motoneurons, as well as the plastic mechanisms by which
94 e significance of activated microglia around motoneurons axotomized after nerve injuries has been int
95 ingled within the abducens nucleus, with MIF motoneurons being smaller and having a lesser somatic sy
96 communication between the cortex and spinal motoneurons, but the neurophysiological basis of this co
97 paired recordings, we confirm that a single motoneuron can release both transmitters on a single pos
98 Moreover, expressing HuD in SMN-deficient motoneurons can rescue the motoneuron development and mo
100 rved an increase in synaptic coverage around motoneuron cell bodies compared with short-term data, wh
101 revealed increased microglia coverage of the motoneuron cell body surface with time after injury and
104 evidence that the excitability of peripheral motoneurons contributes to the pathophysiology of restle
106 y connections were relatively common between motoneurons controlling muscles that act at different jo
108 silencing assays we identify the individual motoneurons controlling the five major sequential steps
109 ccur in cervical motoneurons prior to lumbar motoneurons, correlating with the maturation of premotor
115 t SMN:HuD complexes are essential for normal motoneuron development and indicate that mRNA handling i
116 in SMN-deficient motoneurons can rescue the motoneuron development and motor defects caused by low l
117 eraction between SMN and HuD is critical for motoneuron development and point to a role for RBPs in S
118 t that in addition to autonomous mechanisms, motoneuron development depends on activity resulting fro
119 rding the mechanisms that control vertebrate motoneuron development, particularly the later stages of
123 ords expressing ChR2, illumination increased motoneuron discharge and transiently accelerated the rhy
125 rch in ChAT(+) or Isl1(+) neurons, depressed motoneuron discharge, transiently decreased the frequenc
126 FICANCE STATEMENT In zebrafish models of the motoneuron disease spinal muscular atrophy (SMA), motor
127 inactivation in mice results in a late-onset motoneuron disease, characterized by degeneration of axo
128 utant SOD1 produces long-term suppression of motoneuron disease, including near-complete preservation
129 observed 4 typical presentations: (1) lower motoneuron disorder responsible for proximal lower limb
130 d may appear before clinical presentation of motoneuron disorders such as amyotrophic lateral scleros
131 ed whether Drosophila tonic Ib and phasic Is motoneurons display competitive or cooperative interacti
133 amine neurons in the substantia nigra, vagal motoneurons do not enhance their excitability and oxidat
134 nes of embryonic spinal commissural neurons, motoneurons, dorsal root ganglion neurons, retinal gangl
138 We show that the conductance increase in motoneurons during functional network activity is mainly
142 with laser-capture microdissection of spinal motoneurons during the myelinogenic phase of development
144 erator (CPG) is symmetrical, with antagonist motoneurons each firing with an approximately 50% duty c
147 distinctly different mechanisms to regulate motoneuron excitability and behavioral plasticity, and t
154 stigates whether different types of abducens motoneurons exist that become active during different ty
155 ctivity is associated with increased phrenic motoneuron expression of glutamatergic N-methyl-D-aspart
157 on of voluntary electromyography) and spinal motoneurons (F-waves) in an intrinsic hand muscle during
158 At the basis of this hierarchy, we find the motoneurons, few neurons at the top control global aspec
162 ilar short-term alterations in medial rectus motoneuron firing pattern, which were more drastic in ML
163 al electrophysiological properties of spinal motoneurons follows the same rostro-caudal sequence.
164 During horizontal head movements, abducens motoneurons form the final element of the reflex arc tha
167 Microglia behaviors close to axotomized motoneurons greatly differ from those within uninjured m
169 arkably, mutation of lamin A/C in muscles or motoneurons had no effect on NMJ formation in either sex
170 Similarly, peripheral octopamine action on motoneurons has been reported to be required for increas
171 AIH-induced neuroplasticity have focused on motoneurons; however, most midcervical interneurons (C-I
175 functional participation of both MIF and SIF motoneurons in fixations and slow and phasic eye movemen
178 , we made intracellular penetrations into 89 motoneurons in the cervical enlargement of four terminal
181 s revealed previously unknown connections of motoneurons in the neonatal mouse cord that are likely t
182 ts with the RNA binding protein (RBP) HuD in motoneurons in vivo during formation of axonal branches
184 , fluorescence was observed in contralateral motoneurons, in motoneurons innervating adjacent ventral
185 t its own synapses, but the coinnervating Ib motoneuron increased the number of synaptic boutons and
186 ythmic synaptic drive to flexor and extensor motoneurons, increased the spiking in each cycle, and sl
188 as observed in contralateral motoneurons, in motoneurons innervating adjacent ventral roots, and in C
190 As in the cat, connections were minimal for motoneurons innervating the most distal intrinsic hand m
191 tions often spanned joints, for example from motoneurons innervating wrist and digit muscles to those
192 tyramine is released into the CNS to reduce motoneuron intrinsic excitability and responses to excit
195 the mSOD1 model of ALS, the excitability of motoneurons is poorly controlled, oscillating between hy
196 of signals modulating the activity of alpha motoneurons is required for Ia afferent-based co-contrac
198 quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes induced by
199 n of preBotC network activity, ultimately to motoneurons, is dependent on the strength of input synch
203 ration-causing mutant background accelerated motoneuron loss and disease progression to twice the rat
204 s part of the dynamic changes that accompany motoneuron loss in amyotrophic lateral sclerosis (ALS).
205 bsence of protein aggregation or significant motoneuron loss, questioning its validity to study ALS.
207 f the spinal cord demonstrated a significant motoneurons loss, accompanied by axonal degeneration, as
208 s legs syndrome, an increased HCN current in motoneurons may play a pathophysiological role, such tha
209 xcessive excitation is hypothesized to cause motoneuron (MN) degeneration in amyotrophic lateral scle
212 elopment of proprioceptive afferent input to motoneurons (MNs) and Renshaw cells (RCs) is disrupted b
213 a fatal neurodegenerative disease affecting motoneurons (MNs) in a motor-unit (MU)-dependent manner.
214 central nervous system, including in spinal motoneurons (MNs) where they aggregate as distinct membr
215 of the NMJ, focusing on communications among motoneurons, muscles and SCs, and underlying mechanisms.
222 el after distinct patterns of stimulation in motoneurons of Drosophila We found that the spacing effe
224 compensatory events take place in surviving motoneurons of SOD1-G93A mice, which sustain motor perfo
225 s widely expressed in the sexually dimorphic motoneurons of the L6 segment, suggesting that the dye-c
228 suggested that the high-conductance state in motoneurons originated from balanced inhibition and exci
229 ing augments the muscular response evoked by motoneuron output and that this effect survives a sciati
230 ns, regulation of Kv2.1 channels and greater motoneuron output due to an increase in the inter-spike
232 h and activity (sensory afferent), to modify motoneuron output to achieve graded muscle contraction (
234 nd show that the strength and reliability of motoneuron outputs are inversely correlated with motoneu
236 ing motor behavior in leeches indicated that motoneurons participate as modulators of this rhythmic m
237 undergo low-pass filtering that limits neck motoneuron phase-locking in response to stimuli >75 Hz.
238 that the temporal development of extraocular motoneurons plays a key role in assembling a functional
240 gative, putative interneurons outside of the motoneuron pools in addition to the directly back-labele
241 layers are supplied by anatomically discrete motoneuron pools, we injected tracer into the orbital la
242 network and the intrinsic properties of the motoneuron population driving each target was largely si
244 these maturative processes occur in cervical motoneurons prior to lumbar motoneurons, correlating wit
249 urons and how they affect the translation of motoneuron recruitment to the strength of muscle contrac
251 urons leads to activation of M2 receptors on motoneurons, regulation of Kv2.1 channels and greater mo
254 indings indicate that tonic Ib and phasic Is motoneurons respond independently to changes in activity
255 including those identified as projecting to motoneurons, responded to the perturbation; the timing o
256 f recurrent inhibition in primate upper limb motoneurons, revealing that it is more flexibly organize
259 dy bends, more ventral, higher-Rin secondary motoneurons (SMns) are recruited during weaker and slowe
261 del of ALS-like degeneration, we generated a motoneuron-specific deletion of Scnn1a, encoding the ENa
266 ies differences exist in the location of the motoneurons supplying multiply innervated fibers (MIFs)
267 processes that end in phagocytic cups at the motoneuron surface, then they closely attach to the moto
268 tral roots, timed GDNF-gene therapy enhanced motoneuron survival up to 45 weeks and improved axonal o
269 ChABC gene therapy alone did not enhance motoneuron survival, but led to improved muscle reinnerv
271 ment pattern and output properties of spinal motoneurons that can together generate appropriate inten
272 tions of tonic Ib or phasic Is glutamatergic motoneurons that coinnervate postsynaptic muscles of mal
273 induce a rhythmic antiphasic activity of the motoneurons that control contraction (DE-3 motoneurons)
274 c transmission during REM sleep, hypoglossal motoneurons that control the upper airway muscles are in
277 to some of the A- and B- group medial rectus motoneurons that supply singly innervated fibers was obs
278 ist for vertebrate muscle innervated by many motoneurons, there is no agreement on a parametric model
279 ptor-activated sacral CPGs and lumbar flexor motoneurons, thereby providing novel insights into mecha
280 erentially control elbow flexor and extensor motoneurons; therefore, it is possible that reorganizati
282 w cholinergic signaling inhibits hypoglossal motoneurons through presynaptic and postsynaptic muscari
283 (NMJ), a synapse that transmits signals from motoneurons to muscle fibers to control muscle contracti
284 regulated complement system in AD, mediating motoneuron toxicity in ALS, and stimulating peripheral l
285 etween corticospinal tract fibres and spinal motoneurones undergo activity-dependent reorganization.
286 gy of synaptic vesicles in axon terminals of motoneurons via its function as a guanine exchange facto
287 was paralleled by a marked ~50% increase in motoneuron volume and a near-normal density of acetylcho
288 ere manipulation of the activity of specific motoneurons was performed in the course of fictive crawl
289 y, single-unit recordings from medial rectus motoneurons were obtained in the control situation and a
292 ine acetyl-transferase (ChAT)-immunoreactive motoneurons which remained virtually unchanged in SOD1-G
293 earity, however, was not transmitted to neck motoneurons, which instead showed minimal phase-locking
294 ron surface, then they closely attach to the motoneuron while extending filopodia over the cell body.
295 reased with synaptic volume in both types of motoneurons, with larger synapses having slower recovery
296 h includes a protractor muscle innervated by motoneurons within the protractor nucleus that also has
298 on hypothesis' predicted that neonatal mSOD1 motoneurons would be much more sensitive to such perturb
299 n the whole repertoire of eye movements, MIF motoneurons would contribute only to slow eye movements
300 tion, when less force is needed, whereas SIF motoneurons would contribute to increase muscle tension
301 certain afferents, suggesting that while SIF motoneurons would participate in the whole repertoire of