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1 tracts susbserving motor control (mainly the pyramidal tract).
2 lateral funiculi, which comprise the crossed pyramidal tract.
3 gradely, BDA3k was injected into the pontine pyramidal tract.
4 plasia and severe hypoplasia/agenesis of the pyramidal tracts.
5 f the arm (median, radial and ulnar) and the pyramidal tract: (1) increased excitability of corticosp
6 ons responded to both intratelencephalic and pyramidal tract activation, arguing that these cortical
7              The cephalic decussation of the pyramidal tract, an enlarged hypoglossal nucleus, an add
8 autonomic dysfunction, cognitive impairment, pyramidal tract and cerebellar dysfunction, and white ma
9 er, and those that send their main axon into pyramidal tract and have a collateral projection to stri
10                                       In the pyramidal tract and lateral corticospinal tract, fibres
11 ed by stimulating the unlesioned ipsilateral pyramidal tract and the medial longitudinal fasciculus w
12 ns predominated in the basal ganglia and the pyramidal tracts and included fine, diffuse cytoplasmic
13 bria, and internal capsule in the brain, and pyramidal tracts and lateral columns of the spinal cord.
14 ernal capsule, the external capsule, and the pyramidal tracts and medial lemniscus of the pons and me
15 observed in association with the ipsilateral pyramidal tract as it descended ventromedially through t
16 n (cTMS) or by electrical stimulation of the pyramidal tract at the level of the pyramidal decussatio
17  of the contralesional, but not ipsilesional pyramidal tract at the level of the red and facial nucle
18  by collaterals of thick and fast conducting pyramidal tract axons originating from the frontal corte
19 genetic activation of intratelencephalic and pyramidal tract axons.
20 to the assertion that intratelencephalic and pyramidal tract cortical neurons innervate different str
21 ramidal neurons but morphologically resemble pyramidal tract, D2R-expressing pyramidal neurons.
22 sive early-onset ataxia, cognitive deficits, pyramidal tract damage and optic atrophy, thus demonstra
23 xhibit hypoplasia of the corpus callosum and pyramidal tracts, dilated ventricles, and extensive dege
24  0.025-0.080) and bilateral corticospinal or pyramidal tract (eg, right hemisphere: beta = 0.042; 95%
25 associated with an eye movement disorder and pyramidal tract features.
26 ransport of GDNF was evident in axons in the pyramidal tract from the cerebral peduncle to the caudal
27  labeled axons in the ipsilateral descending pyramidal tract in both species.
28 umulating evidence against somatotopy in the pyramidal tract in the lower brainstem and in the spinal
29 he parapyramidal area and just dorsal to the pyramidal tract in the raphe magnus.
30 h, cerebello-thalamic fibres, as well as the pyramidal tract, in the pathogenesis of SID in STN-DBS.
31              Conditioning stimulation of the pyramidal tract increased both the terminal excitability
32 anced axonal sprouting from the ipsilesional pyramidal tract into the brainstem was observed in vehic
33 ed genetic and retrograde labeling to target pyramidal tract, intratelencephalic and corticostriatal
34  a global developmental delay accompanied by pyramidal tract involvement, microcephaly, short stature
35                               Lesions of the pyramidal tract just rostral to the inferior olive subst
36 eral responses following M1 inactivation and pyramidal tract lesion could be evoked after systemic ad
37 hemisphere using reversible inactivation and pyramidal tract lesion.
38  three top classes (intratelencephalic [IT], pyramidal tract-like [PT-like], and corticothalamic [CT]
39 ge of a major class of M1 output neuron, the pyramidal tract neuron (PTN), is modulated during observ
40 ns both corticocollicular neurons, a type of pyramidal-tract neuron projecting to the inferior collic
41 de of local field potential (slow waves) and pyramidal tract neurone (PTN) discharge from pairs of si
42                       The firing patterns of pyramidal tract neurones (PTNs) and unidentified neurone
43  the pericruciate cortex, and commoner among pyramidal tract neurones (PTNs) than non-PTNs.
44 ; 39 cells were antidromically identified as pyramidal tract neurones (PTNs).
45 ted rhythmicity of motor cortical (including pyramidal tract) neurones.
46 ly and callosally projecting) in layers 2-6, pyramidal tract neurons (corticocollicular, corticoponti
47 l limbs to the posture-related modulation of pyramidal tract neurons (PTNs) arising in the primary mo
48     Here, we investigated whether identified pyramidal tract neurons (PTNs) in area F5 of two adult m
49 .5-6 kg weights and recorded from identified pyramidal tract neurons (PTNs) in primary motor cortex a
50  we found that the intrinsic excitability of pyramidal tract neurons (PTNs) in the primary motor cort
51 re the activity of fast- and slow-conducting pyramidal tract neurons (PTNs) of the motor cortex in ca
52 phologically distinct populations of layer 5 pyramidal tract neurons (PTNs) that exhibit specific tuf
53                                              Pyramidal tract neurons (PTNs) within macaque rostral ve
54 ths between the activated neuron type and L5 pyramidal tract neurons (PTNs).
55 al neurons were identified antidromically as pyramidal tract neurons (PTNs).
56 Some cells were antidromically identified as pyramidal tract neurons (PTNs).
57 he major output cell type of the neocortex - pyramidal tract neurons (PTs) - send axonal projections
58 main output neurons of the cerebral cortex - pyramidal tract neurons (PTs) - to associate inputs that
59                                              Pyramidal tract neurons (PTs) represent the major output
60    In addition, the initial state of layer 5 pyramidal tract neurons contained a memory trace of the
61                                              Pyramidal tract neurons had abnormal event rates, while
62 of the auditory stimulus, but, surprisingly, pyramidal tract neurons had the largest causal role.
63 is larger on the somatic membrane surface of pyramidal tract neurons in comparison with those project
64                  We recorded the activity of pyramidal tract neurons in the motor cortex of the cat b
65 s in the motoneuron inputs (e.g., 20 Hz from pyramidal tract neurons) would be filtered out by the mu
66 expressing Fezf2 (aIC(Fezf2)), which are the pyramidal tract neurons, signal motivational vigor and i
67 hyl-d-aspartate receptor activity in layer 5 pyramidal tract neurons, unmasking previously unknown fe
68 ore efficient at controlling the activity of pyramidal tract neurons, which are embedded deep in the
69 l contribution of subcortical projections by pyramidal tract neurons.
70 ctive connectivity with intratelecephalic or pyramidal tract neurons.
71 uts excited neurons mainly in L5B, including pyramidal tract neurons.
72  of CM cells includes both "fast" and "slow" pyramidal tract neurons.
73 ing to reduction in the excitability of mPFC pyramidal-tract neurons and deficits in social memory in
74                   Our data further show that pyramidal-tract neurons in the cortex collateralized wit
75  connectivity of intratelencephalic, but not pyramidal tract, neurons with direct and indirect pathwa
76 osite hemisphere was inactivated or when the pyramidal tract on the nonstimulated side was sectioned.
77 e matter tracts were involved, including the pyramidal tract, optic radiation, and corpus callosum, l
78 tribution across different subsectors of the pyramidal tract or lateral corticospinal tract, arguing
79  separated cortical sites, and encompass the pyramidal tract output neurones.
80 phage accumulation, increased contralesional pyramidal tract plasticity, and reduced brain atrophy.
81 s with proximal RFs (upper arm/shoulder) and pyramidal tract-projecting neurons (PTNs) with fast-cond
82  subtypes of Fezf2(+) neurons that resembled pyramidal tract projection neurons (PT-PNs) and intratel
83 halic projection neurons (Tlx3-Cre), layer 5 pyramidal tract projection neurons (Sim1-Cre), layer 5 p
84 of the brainstem branching patterns of these pyramidal tract projections, we used MAPseq, a molecular
85 f contralesional rather than of ipsilesional pyramidal tract projections.
86 c spines in both the subcortical-projecting, pyramidal tract (PT) and intratelencephalic (IT) cell ty
87 CK+ interneurons make stronger synapses onto pyramidal tract (PT) cells over nearby intratelencephali
88 ells also inhibit the apical dendrites of L5 pyramidal tract (PT) cells to suppress action potential
89   We investigated whether stimulation of the pyramidal tract (PT) could reset the phase of 15-30 Hz b
90 esponses in both intratelencephalic (IT) and pyramidal tract (PT) dendrites, whereas monosynaptic hip
91 cal layer 5 (L5) intratelencephalic (IT) and pyramidal tract (PT) neurons are embedded in distinct in
92 rons in PL, whereas cBLA drives layer 5 (L5) pyramidal tract (PT) neurons in IL.
93 ing the postsynaptic excitability of layer 5 pyramidal tract (PT) neurons relative to neighboring int
94 cortex neurons, intra-telencephalic (IT) and pyramidal tract (PT) neurons, convey the resulting corti
95 ovide input to many subcortical motor areas: pyramidal tract (PT) neurons, which project throughout t
96 cal populations: intratelencephalic (IT) and pyramidal tract (PT) neurons.
97 cific reduction of thalamic excitation to M1 pyramidal tract (PT) neurons.
98  with the structural integrity of either the pyramidal tract (PT) or alternate motor fibers (aMF).
99 ording from CT, intratelencephalic (IT), and pyramidal tract (PT) projection neurons, we found strong
100 two major types (intratelencephalic (IT) and pyramidal tract (PT)), with distinct inputs and projecti
101  the intratelencephalic (IT) type to adopt a pyramidal tract (PT)-type identity.
102 rd via axons that project to and through the pyramidal tract (PT).
103 jection to the ipsilateral brainstem via the pyramidal tract (PT-type); and 2) one that projects intr
104 n studies of TAI focused on limited areas of pyramidal tract (Py) but not its entire length.
105 vement of cerebellar pathways as well as the pyramidal tract, remains a matter of debate.
106 r distribution were evoked from sites in the pyramidal tract rostral and caudal to the inferior olive
107 eral spinal CST connections after unilateral pyramidal tract section (PTx), which models CST loss aft
108 ng the OPA3 -linked phenotype by early-onset pyramidal tract signs and marked lower limb dystonia.
109 low progression, distal limb amyotrophy, and pyramidal tract signs associated with severe loss of mot
110                                              Pyramidal tract signs were described in 13 patients and
111 ded chorea, cerebellar ataxia, dystonia, and pyramidal tract signs.
112 ancement produced by the second of a pair of pyramidal tract stimuli, or a higher stimulus multiple o
113 etic interrogation of intratelencephalic and pyramidal tract synapses with principal striatal spiny p
114 usly defined IT (intratelencephalic) and PT (pyramidal tract) synapses.
115 c EPSPs and disynaptic IPSPs evoked from the pyramidal tract that were present in the intact monkey s
116                   In the corpus callosum and pyramidal tracts, the ratio of parallel to perpendicular
117        Eight weeks after injury, produced by pyramidal tract transection, half of the rats received f
118 ivity of antidromically-identified lamina 5b pyramidal-tract type neurons (n = 153) and intratelencep
119  corticothalamic (CT) neurons in layer 6 and pyramidal tract-type (PT) neurons in layer 5B.
120        This reduced activation was strong in pyramidal tract-type neurons (-50%) but essentially abse
121                                   Given that pyramidal tract-type neurons form the primary efferent p
122  dysfunction of movement-related activity in pyramidal tract-type neurons is likely to be a central f
123       DTT was performed to segment bilateral pyramidal tracts using semiautomated fiber tracking soft
124                   Input from the ipsilateral pyramidal tract was rare and weak in both lesioned and c
125 of the medullary corticospinal fibres in the pyramidal tract were made in three adult macaque monkeys
126 vity (D(av)) (median, -2.0% per week) in the pyramidal tract were measured in infants without brain i
127  electrical stimulation of the contralateral pyramidal tract were measured in intracellular recording
128 the SC and pons but avoid ventral SC and the pyramidal tract, whereas cells transplanted deep into th
129 e first being the rostral decussation of the pyramidal tract, which instead of occurring at the spino

 
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