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1 e associated with dendrite and synapse loss (deafferentation).
2 y to the hypertension caused by baroreceptor deafferentation.
3 vagal complex were increased following vagal deafferentation.
4 CN neurons to either death or survival after deafferentation.
5 uring swimming and jumping, before and after deafferentation.
6 l neurons leaves the terminals in a state of deafferentation.
7 loss of iGluR4 immunoreactivity by 24 h post-deafferentation.
8 ain was further investigated after olfactory deafferentation.
9 ion of Purkinje cells to episodic functional deafferentation.
10 with previous subdiaphragmatic vagal sensory deafferentation.
11 s which can be observed within 1 h following deafferentation.
12 y : fibre ratio at 7 days) was unaffected by deafferentation.
13 any kinds of injuries, including axotomy and deafferentation.
14 r remodeling and synaptogenesis initiated by deafferentation.
15 omplexity of responses to different forms of deafferentation.
16 n, and is balanced in the setting of chronic deafferentation.
17 cortex are quickly reduced within minutes of deafferentation.
18  reduction of amyloid plaques on the side of deafferentation.
19 s in Alzheimer's disease, namely hippocampal deafferentation.
20 ceptors, within 4 h of unilateral vestibular deafferentation.
21 g differences between central and peripheral deafferentation.
22       This facilitation was blocked by vagal deafferentation.
23 the IPSC equilibrium potential within 1 d of deafferentation.
24 ng animals are also more affected by sensory deafferentation.
25 mice during and after recovery from chemical deafferentation.
26 the mitotic behavior of astrocytes following deafferentation.
27 n the OB can be reconstituted after chemical deafferentation.
28 inished at 1 week and absent by 3 weeks post-deafferentation.
29 lse facilitation was nearly eliminated after deafferentation.
30  was examined in zebrafish, using peripheral deafferentation.
31 e its target, the olfactory bulb (OB), after deafferentation.
32 urons following lesions, target loss, and/or deafferentation.
33 zation that immediately follows a peripheral deafferentation.
34 ssentially the same regardless of the age of deafferentation.
35 ion resulting from the reversible peripheral deafferentation.
36 his disease may be the result of cholinergic deafferentation.
37 ells exhibit markedly different responses to deafferentation.
38  recovery that follows unilateral vestibular deafferentation.
39 -NA) following neonatal unilateral vibrissae deafferentation.
40 ge from piston impact, brain displacement or deafferentation.
41 ular changes in response to brain injury and deafferentation.
42 otion of topographic plasticity after visual deafferentation.
43  strength was not observed following partial deafferentation.
44 l hippocampus indicating relatively complete deafferentation.
45 ceps brachii muscle proximal to the level of deafferentation.
46 or rats that received subdiaphragmatic vagal deafferentation.
47 l cuneate nucleus within three months of the deafferentation.
48 ease of central gain attributable to sensory deafferentation.
49 ton are responsible for cell death following deafferentation.
50 a-actin mRNAs were not noticeably altered by deafferentation.
51 atory response to nigrostriatal dopaminergic deafferentation.
52 tional protein synthesis apparatus following deafferentation.
53 in the human following peripheral or central deafferentation.
54  memory deficits associated with hippocampal deafferentation.
55 d transient hypersensitivity consistent with deafferentation.
56 s that had earlier received a surgical vagal deafferentation.
57 vasion by ectopic visual inputs and not from deafferentation.
58 llowing lithium administration and following deafferentation.
59  determinant of Bcl-2 upregulation following deafferentation.
60 pregulated in 20-30% of NM neurons following deafferentation.
61 -2 and increases neuronal survival following deafferentation.
62 e over an approximately 14-week period after deafferentation.
63 mulation, in contrast, were unaffected after deafferentation.
64 s in normally innervated cells but not after deafferentation.
65 be produced by the brain related to auditory deafferentation.
66 ntial parameters were observed after chronic deafferentation.
67 ainstem circuitry selectively in response to deafferentation.
68 on of somatosensory cortex that follows such deafferentations.
69 imals injected with PHA-L after intracranial deafferentations.
70 nsory input was reduced by either a complete deafferentation, a genetic impairment of neurotransmitte
71                                          For deafferentation above this threshold, however, a slow pe
72               A comparison of the extents of deafferentation across the monkeys shows that even if th
73 sent a compensatory mechanism in response to deafferentation after callosotomy.
74                                  One week of deafferentation altered the pattern of cell genesis, wit
75                                   Peripheral deafferentation alters cortical function and such altera
76 amputees during the first 12 weeks following deafferentation and at 26 and 30 weeks post-amputation.
77 N-gamma blocking antibody prevented neuronal deafferentation and clinical disease without reducing CT
78 electrophysiologically mapped to define hand deafferentation and cortical reactivation further.
79 with NFT densities respectively suggest that deafferentation and intrinsic neurofibrillary degenerati
80 ecovery are dependent both on the vestibular deafferentation and on the activation of glucocorticoid
81            We developed an in vitro model of deafferentation and reactive hyperexcitability using org
82 ct persisted throughout the entire period of deafferentation and returned to baseline values afterwar
83 lfactory system during development and after deafferentation and suggest that the expression of Na be
84 dorsal mPFC was enhanced after noradrenergic deafferentation and was negatively correlated with stres
85  the morphology found in mental retardation, deafferentation, and prionoses.
86  inhibition of the ipsi-lesional cells after deafferentation, and thus promote the recovery of restin
87 g that these responses of the MVN neurons to deafferentation are discrete, parallel processes.
88 l maps in primate somatosensory cortex after deafferentation are poorly understood.
89 rse and nature of development are altered by deafferentation at birth; 2) reorganization of terminals
90 vation but, surprisingly, did increase after deafferentation at P21, when all neurons ultimately surv
91                     Furthermore, cholinergic deafferentation attenuated the frequency and amplitude o
92 lar topology and broadcast the presence of a deafferentation-based bottom-up prediction error as a re
93 , beneficial effects on cortical cholinergic deafferentation-based impairments in attention may remai
94 m limbs-whether resulting from amputation or deafferentation-became illustrated, and some reasons for
95 ytoskeleton is altered or degraded following deafferentation but that this process is not regulated a
96 stantially larger GFAP inductions than after deafferentation, but fewer effects of age.
97 tions correlates well with the extent of MGN deafferentation, but not with extent of removal of norma
98 it in recognition of target loss and partial deafferentation by aged granule cells and/or an impaired
99                                              Deafferentation by optic nerve section resulted in incre
100                             Functional vagal deafferentation by perineural capsaicin or CCK A recepto
101       These results indicate that acute hand deafferentation can elicit a focal increase in excitabil
102 ing rule to show that loss of input (partial deafferentation) can trigger network reorganization that
103 he degradation of the cytoskeleton following deafferentation could potentially lead to either atrophy
104                                          For deafferentation degrees below this value, homeostatic up
105                      In the long term, slow, deafferentation-dependent transneuronal atrophy at brain
106 , and that inhibition of axonal transport or deafferentation depletes BDNF.
107                                              Deafferentation did not immediately affect the dividing
108  to prevent microglial activation, olfactory deafferentation did not reduce adult neurogenesis, showi
109 bers) in response to target loss and partial deafferentation diminishes with age.
110 r volume of HG, which suggests that auditory deafferentation does not lead to cell loss within primar
111 nt and form of reorganization resulting from deafferentation early in life vs. adulthood are not the
112 s in the olfactory bulb, suggesting that the deafferentation effect is specific.
113 duced redox imbalance in the cochlea and the deafferentation effects upstream the acoustic pathway.
114                        After selective vagal deafferentation, EGLU was without effect, suggesting tha
115                               However, after deafferentation, EphA4-null mice had a significant, thre
116 d cells), but there was a critical degree of deafferentation for pathological network reorganization.
117 etwork target firing rate for all degrees of deafferentation (fraction of deafferented cells), but th
118 in the control situation and after selective deafferentation from cats with unilateral transection of
119                  Three days after peripheral deafferentation, functional synapses become silent, lack
120                                              Deafferentation had no detectable effects on Na alpha I
121                             Finally, retinal deafferentation had no significant effect on the number
122                          SGN death following deafferentation has an early phase in which apoptosis is
123                         Cortical cholinergic deafferentation has been considered to be a major neurop
124 rmine if NPY-containing neurons that survive deafferentation have any distinguishing morphological an
125                                              Deafferentation, however, did not alter Gsk-3beta or NFk
126                                  Cholinergic deafferentation, however, resulted in a decrease in the
127 , nucleus magnocellularis (NM) die following deafferentation (i.e., deafness produced by cochlea remo
128 Bergmann gliosis, and signs of Purkinje cell deafferentation; (iii) selective striatal cholinergic in
129 the capacity of this map to reorganize after deafferentation in adults and animals late in developmen
130                                After chronic deafferentation in amputees, MEP amplitudes and motor ou
131                            Septo-hippocampal deafferentation in both groups of lesioned animals faile
132 radation of responses to surgical vestibular deafferentation in humans, skew deviation only occurring
133 perceptual and cortical reorganization after deafferentation in humans.
134 n this study we delayed the onset of retinal deafferentation in rats and mice in order to determine t
135 tal cortical plasticity induced by vibrissae deafferentation in the rat.
136 of the inhibitory synaptic conductance after deafferentation, indicating that driving force was not s
137 -based transfer to new cell populations, and deafferentation induced degeneration are part of a proce
138             Our study also suggests that the deafferentation-induced alterations of the sleep slow os
139  Inhibition of NFAT significantly attenuates deafferentation-induced apoptosis of AVCN neurons and ab
140 FAT-mediated gene expression plays a role in deafferentation-induced apoptosis of cochlear nucleus ne
141 functional auditory-limbic connectivity, and deafferentation-induced atrophy in frontal brain regions
142 d whether the chloramphenicol enhancement of deafferentation-induced cell death reveals the same ultr
143 hibitor, results in a pronounced increase in deafferentation-induced cell death.
144 served, however, at times that coincide with deafferentation-induced cell loss (3 and 7 days).
145  that underlie AVCN neuron susceptibility to deafferentation-induced death remain unknown.
146  against subsequent programmed cell death or deafferentation-induced death.
147          We conclude that in CN neurons, the deafferentation-induced increase in calcium activates at
148  in regulating programmed neuronal death and deafferentation-induced neuronal death in the brainstem
149                                          The deafferentation-induced plastic changes can be up-regula
150 teral vs. contralateral target choice during deafferentation-induced plasticity.
151 al dendrites is a significant contributor to deafferentation-induced reactive hyperexcitability.
152 whether it is possible to purposely modulate deafferentation-induced reorganization.
153 of MMP inhibition during the early phases of deafferentation-induced sprouting, characterizing compon
154                   To more precisely quantify deafferentation-induced structural plasticity of excitat
155 l elements accounts for at least part of the deafferentation-induced volume decrease in the zebrafish
156                                              Deafferentation induces rapid plastic changes in the cer
157                         Long-term peripheral deafferentation induces representational map changes in
158              The present model suggests that deafferentation injury in sensory systems can cause apop
159     Although the process can be triggered by deafferentation, intense activation of glutamate recepto
160 n of Bcl-2 gene expression by lithium and by deafferentation involves different molecular pathways.
161                          Ipsilaterally, both deafferentation (IoN transection) and deprivation (whisk
162  in a phantom limb after partial or complete deafferentation is an important problem.
163  that is seen immediately after a peripheral deafferentation is dependent upon both descending cortic
164 he adult somatosensory system as a result of deafferentation is elusive.
165 ccupancy of the vacant synaptic space due to deafferentation is the base for the mechanism of compens
166                                              Deafferentation leads to cortical reorganization that ma
167                                              Deafferentation led to a 24 mV depolarizing shift in the
168        We wished to test the hypothesis that deafferentation lesions cause changes in the regulation
169 pothesis that broad functional (or anatomic) deafferentation may combine to reduce central thalamus a
170 (SDA), the most complete and selective vagal deafferentation method existing to date, to study the co
171                        One day after sensory deafferentation, microglial cells proliferate in the olf
172 l experiments revealed that, following vagal deafferentation, mu-opioid receptors were colocalized on
173 ted pathological features of neuronal system deafferentation, NFT progression and propagation, and ne
174 ter 2 weeks in all animals, neither striatal deafferentation nor in vitro induction of differentiatio
175 s in neuronal latency induced by the sensory deafferentation occurred as often in the thalamus as in
176                        This suggests that if deafferentation occurs, synapses other than recurrent ex
177 us studies have indicated that amputation or deafferentation of a limb induces functional changes in
178                                        Acute deafferentation of a limb results in bilateral cortical
179 citatory perforant path results in the acute deafferentation of a segregated zone on the distal dendr
180 n area CA1 of hippocampus, septo-hippocampal deafferentation of adult gerbils was performed.
181  In a control group of animals with neonatal deafferentation of auditory thalamus but without redirec
182 ux was determined in rats sustaining partial deafferentation of cortical cholinergic inputs.
183 S lesions derive from the resulting combined deafferentation of dorsal and ventral hippocampal region
184 viously been suggested to indicate a partial deafferentation of epileptic neurons, but this interpret
185          We also found that, after extensive deafferentation of MGN, other axonal systems in addition
186                                              Deafferentation of motor neurons is an early event in SM
187 e show that only during this critical period deafferentation of mouse AVCN neurons by in vivo cochlea
188                                              Deafferentation of neural tissue can result in cell deat
189             ZnSO(4) produced a near complete deafferentation of OB within 3 days following intranasal
190                                              Deafferentation of OBs did not eliminate nicotine-stimul
191 ytochrome oxidase (CO) histochemistry, after deafferentation of one eye or even by leaving afferent i
192 tion', the behavioural recovery that follows deafferentation of one inner ear, are largely unknown.
193    The current data suggest that cholinergic deafferentation of prefrontal cortex alters top-down and
194        The effects of restricted cholinergic deafferentation of prefrontal cortex in rats on sustaine
195 he presence of primary cortical pathology or deafferentation of striato-cortical projections.
196 injury to the CNS results in chronic partial deafferentation of subsets of surviving neurons.
197 erent models of chronic synaptic inhibition: deafferentation of the barrel cortex and administration
198                                The degree of deafferentation of the bulb by treatment with 3-MI was a
199 not appear to enter the cell cycle following deafferentation of the chicken auditory brainstem.
200 se phenotype in HD mice, we examined whether deafferentation of the corticostriatal and nigrostriatal
201 f mice, suggesting that the ensuing state of deafferentation of the DA terminals may contribute to th
202                                The extent of deafferentation of the dorsal hippocampus was determined
203 in these nuclei during development and after deafferentation of the excitatory auditory nerve (nVIII)
204 otoxin, which leads to selective cholinergic deafferentation of the infused cortex, yielded recogniti
205 ptor loss and often result in remodeling and deafferentation of the inner retina.
206 ects of CL-316,243 in mice with the chemical deafferentation of the intra-scapular BAT pads.
207 activity was still observed even after total deafferentation of the laryngeal and pharyngeal areas in
208 e essential for odor discrimination and that deafferentation of the majority of bulbar glomeruli may
209  To this end, the effects of either surgical deafferentation of the mediobasal hypothalamus or admini
210  in DOPAC in the nucleus accumbens; surgical deafferentation of the mediobasal hypothalamus prevented
211 duction of normal retinal targets along with deafferentation of the MGN are two concurrent factors re
212                                  Cholinergic deafferentation of the mPFC, but not motor cortex, impai
213                                              Deafferentation of the olfactory bulb resulted in a tran
214 ed in ankle flexors of rats with and without deafferentation of the stimulated side.
215                                   Additional deafferentation of the transected animals did not alter
216 the cerebellar hemispheres reorganizes after deafferentation of the upper lip in neonatal rats (postn
217 g in older persons with vision impairment or deafferentation of the visual cortex.
218                                 Furthermore, deafferentation of the wiping limb did not significantly
219 tween brain and body and the effects of this deafferentation on body representation are poorly unders
220 e interactive effects of age and cholinergic deafferentation on synaptic connectivity in frontal cort
221               For most synergies, effects of deafferentation on the activation coefficients were not
222 amined both normal growth and the effects of deafferentation on the bulb from hatching to adulthood.
223 investigate the effects of very early visual deafferentation on the functional organization of the br
224 study evaluated the effects of total cardiac deafferentation on the reflex control of efferent renal
225 in cortical topography in primates following deafferentation or amputation, and this review will atte
226 e expression induced by peripheral olfactory deafferentation or naris blockade confirms that function
227                   Here we report that either deafferentation or reduction of sensory input by nares o
228                                              Deafferentation or sensory deprivation decreases TH expr
229 enervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cyst
230 electroporation, live cell imaging, in vitro deafferentation, pharmacology, and electrophysiological
231                                After partial deafferentation postsynaptic sites are reinnervated by l
232                                              Deafferentation produced a 298% increase in the metaboli
233                                    Vibrissae deafferentation produced a small but not statistically s
234 ted that less extensive cortical cholinergic deafferentation, produced by intracortical infusions of
235                To determine whether cortical deafferentation produces similar effects, we examined th
236                             Contralaterally, deafferentation reduced more complex dendritic trees, an
237                                              Deafferentation remains the best available pathophysiolo
238 on is comparable with that induced by direct deafferentation resulting from transection of NM axons.
239                 To test whether or not early deafferentation results in changes in calretinin immunos
240 ohistochemistry of the mouse CN to show that deafferentation results in strikingly different sets of
241 arlier study suggest that septal cholinergic deafferentation results in: (a) the loss of a distinct s
242 e used a rat model of subdiaphragmatic vagal deafferentation (SDA), the most complete and selective v
243 sh a role for MMP-dependent processes in the deafferentation/sprouting cycle.
244 t shared synergies, however, were altered by deafferentation, suggesting that sensory inflow modulate
245 pression of these glial factors in fields of deafferentation suggests the possibility of additive or
246 ress normally associated with the vestibular deafferentation syndrome.
247 rd section (approximately T8) and unilateral deafferentation (T12-S2) to answer the following questio
248 al studies suggest that temporary functional deafferentation (TFD) of parts of the stroke-affected up
249                      Following chronic vagal deafferentation, the opioid agonist methionine-enkephali
250                          Sixty minutes after deafferentation, the surviving neurons show increased ph
251  clearly demonstrate that peripheral sensory deafferentation triggers a system-wide reorganization, a
252 vity before and after unilateral cholinergic deafferentation using intracortical infusion of the immu
253 r the expression of GATs changes after nerve deafferentation using the rat superior colliculus (SC) a
254  subjects and six with unilateral vestibular deafferentation (UVD) underwent binocular eye and head m
255 on of these factors in unilateral vestibular deafferentation (UVD) was examined.
256                          Rats undergoing PMV deafferentation via capsaicin, celiac-superior mesenteri
257 ase in average firing rate in the network by deafferentation was compensated by homeostatic synaptic
258                            Transient forearm deafferentation was induced by ischemic nerve block (INB
259 in [3H]CP55,940 binding contralateral to the deafferentation were largely absent at all post-lesion d
260 changes in the motor cortex contralateral to deafferentation were probed with TMS, measuring motor th
261 ical cholinergic and/or caudate dopaminergic deafferentation were produced by bilateral infusions of
262                           However, bilateral deafferentation, when performed in a single-stage proced
263 he somatosensory hand area of primates after deafferentation where cortex can become activated by a m
264 amina ganglion mother cells ceased following deafferentation, whereas cell death in the lamina cortex
265 tic spines may be a compensatory response to deafferentation, which is lost with advancing age.
266                                        After deafferentation, which was induced by dissection of the
267  phenotype was produced by chronic "chemical deafferentation" with glutamate receptor antagonists.
268               Both are also more affected by deafferentation, with at least a 35% reduction in lamina
269                             In spite of this deafferentation, ZK 93,426 produced a transient potentia

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