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1 insonian-like motor deficits in a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model us
2 n, and sensorimotor neglect after unilateral nigrostriatal 6-hydroxydopamine lesion in mice.
3      Here, we show that phasic activation of nigrostriatal afferents in a mouse striatal slice prepar
4                                          The nigrostriatal and histological perspectives are not inco
5 of intravenous cocaine, and dopamine in both nigrostriatal and mesocorticolimbic terminal fields part
6 y tracing viruses simultaneously illuminates nigrostriatal and mesolimbic circuitry and shows no over
7               Thus, the similarities between nigrostriatal and mesolimbic dopamine systems can be as
8      The anatomical evidence for independent nigrostriatal and mesolimbic dopamine systems has, howev
9 tions are responsible for the segregation of nigrostriatal and mesolimbic dopaminergic pathways.
10                                              Nigrostriatal and ventral tegmental area (VTA) midbrain
11  maraviroc treatment also protected both the nigrostriatal axis and neurotransmitters and improved mo
12 progressing to bilateral degeneration of the nigrostriatal axis with aging.
13 ostriatal nerve terminals is associated with nigrostriatal axonal dysfunction in mild to moderate PD.
14 e development of degenerative changes in the nigrostriatal axons and terminals.
15 ilarly, neither unilateral 6-OHDA lesions of nigrostriatal axons nor the dorsal noradrenergic bundle
16 or parkinsonism with the degree of injury to nigrostriatal axons, as reflected by in vitro fiber leng
17 responsive dystonia, but also predisposes to nigrostriatal cell loss.
18 in severe reduction of dopamine synthesis in nigrostriatal cells and are the most common cause of DOP
19  essential enzyme for dopamine production in nigrostriatal cells.
20 n primates with authentic Lewy pathology and nigrostriatal changes indicative of early Parkinson's di
21 ial striatum (DMS) and midbrain areas of the nigrostriatal circuit are critically associated to strok
22 l and electrophysiological properties of the nigrostriatal circuit in behaviorally asymptomatic 6- to
23 or behavior, but growing data implicate this nigrostriatal circuit in emotion.
24                            It is then in the nigrostriatal circuit that action initiation per se begi
25 d restore functionality of the reconstructed nigrostriatal circuit to mediate improvements in motor f
26 rons, which provide axons to reconstruct the nigrostriatal circuit.
27 rochemical and structural homeostasis in the nigrostriatal circuit.
28 Mfn1 yielded no corresponding defects in the nigrostriatal circuit.
29 e widely used to produce degeneration of the nigrostriatal circuitry.
30 tain an outcome, we found neural activity in nigrostriatal circuits specifically signalling the initi
31 , in parallel with PPN and HB influences, to nigrostriatal circuits.
32 rpose of this study was to determine whether nigrostriatal DA depletion affects measures of insulin r
33 r, these results support the hypothesis that nigrostriatal DA depletion impairs insulin signaling in
34             Here we investigated the role of nigrostriatal DA in fear extinction.
35  abnormality promoting mechanisms leading to nigrostriatal DA neuron death in PD.
36 st that neurons other than or in addition to nigrostriatal DA neurons contributed to protection of fo
37 cteristic electrophysiological properties of nigrostriatal DA neurons, produce high levels of dopamin
38  can contribute to the preferential death of nigrostriatal DA neurons.
39                   These data suggest that in nigrostriatal DA pathway, chronic nicotine enhancement o
40  5-HT upregulation following the loss of the nigrostriatal DA projection and that the upregulated 5-H
41 ve flies and report optogenetically elicited nigrostriatal DA release as well as mesoaccumbens dopami
42                               Interestingly, nigrostriatal DA signaling disruption in Parkinson's dis
43 ely in identified mesolimbic DA VTA, but not nigrostriatal DA SN, neurons.
44                                              Nigrostriatal DA thus represents a novel target to enhan
45 s a mechanism by which DAT and Oct3 modulate nigrostriatal damage induced by PQ(2+)/PQ(+) redox cycli
46  this, we investigated the effect of varying nigrostriatal damage on alpha6beta2* and alpha4beta2* re
47 r is decreased to a much greater extent with nigrostriatal damage than the alpha4beta2* subtype raisi
48 aptic FosB activity, indicative of increased nigrostriatal damage when compared with WT MPTP-treated
49 ecreased to a similar extent with increasing nigrostriatal damage, indicating that both subtypes cont
50  population is more important with increased nigrostriatal damage.
51  release also decreased proportionately with nigrostriatal damage.
52 rbations of mitochondrial dynamics can cause nigrostriatal defects and may be a risk factor for the n
53 esterol-lowering drug, could protect against nigrostriatal degeneration after 1-methyl-4-phenyl-1,2,3
54 T mutant alpha-synuclein induced progressive nigrostriatal degeneration and reduced locomotion.
55 uroregulatory activities affect the tempo of nigrostriatal degeneration during Parkinson's disease (P
56            Symptomatic models of PD based on nigrostriatal degeneration have a high degree of predict
57 his model may provide insight into selective nigrostriatal degeneration in human IBGC and other Parki
58  of RANTES and eotaxin could protect against nigrostriatal degeneration in MPTP-intoxicated mice.
59        This study investigated the extent of nigrostriatal degeneration in patients with Parkinson's
60 mechanism by which loss of PINK1 may lead to nigrostriatal degeneration in PD.
61 itopes that exacerbate neuroinflammation and nigrostriatal degeneration in the 1-methyl-4-phenyl-1,2,
62 cate that IFN-gamma mediates age-progressive nigrostriatal degeneration in the absence of exogenous s
63 s of MEF2 activity, plays a critical role in nigrostriatal degeneration in vivo.
64                                  The pace of nigrostriatal degeneration, both with regards to striata
65 ssion diminished or removed the male bias in nigrostriatal degeneration, mitochondrial degradation, D
66 l plasticity, which, in the absence of overt nigrostriatal degeneration, suggest there are age-relate
67 thic basal ganglia calcification (IBGC), and nigrostriatal degeneration.
68 nd natural Tregs reversed N-alpha-syn T cell nigrostriatal degeneration.
69 e substantia nigra pars compacta, leading to nigrostriatal degeneration.
70 hite matter signal hyperintensity burden and nigrostriatal denervation as independent variables demon
71      Acute trkB blockade in rats with stable nigrostriatal denervation attenuated the forelimb akines
72 f significant cerebral amyloid deposition or nigrostriatal denervation was a strong predictor of conv
73 natal LPS exposure, and in vitro analysis of nigrostriatal development in organotypic cultures prepar
74                          Such alterations in nigrostriatal development may demonstrate how adverse pe
75 nization of behaviour, and is compromised in nigrostriatal disorders like Parkinson's and Huntington'
76                                              Nigrostriatal dopamine (DA) is critical to action select
77 f insulin resistance and the degeneration of nigrostriatal dopamine (DA) neurons are both mediated by
78                 The cause of degeneration of nigrostriatal dopamine (DA) neurons in idiopathic Parkin
79                          Progressive loss of nigrostriatal dopamine (DA) neurons is the neuropatholog
80 's disease (PD) involves progressive loss of nigrostriatal dopamine (DA) neurons over an extended per
81 neration of a unique population of cells-the nigrostriatal dopamine (DA) neurons-that occurs in Parki
82          Recent data suggest that lesions of nigrostriatal dopamine axons cause a loss of PF neurons,
83 ng, we found that optogenetic stimulation of nigrostriatal dopamine axons rapidly and persistently el
84                     Here we demonstrate that nigrostriatal dopamine biases ongoing action selection.
85  cell loss in parkinsonism is independent of nigrostriatal dopamine degeneration.
86  is a primary event rather than secondary to nigrostriatal dopamine degeneration.
87                                   Unilateral nigrostriatal dopamine depletion also causes a contralat
88                                   Unilateral nigrostriatal dopamine depletion in animals induces cont
89                                    Sustained nigrostriatal dopamine depletion increases the serine/th
90                      These data confirm that nigrostriatal dopamine depletion is accompanied by profo
91 stantia nigra pars compacta, suggesting that nigrostriatal dopamine dysfunction precedes detectable p
92  in the maintenance and protection of normal nigrostriatal dopamine function by activating UCP2-depen
93       These results unveil a crucial role of nigrostriatal dopamine in integrating diverse informatio
94 aintain intact cognitive performance despite nigrostriatal dopamine loss.
95                                              Nigrostriatal dopamine neuron lesions did not elicit deg
96 ive disorder pathologically characterized by nigrostriatal dopamine neuron loss and the postmortem pr
97                           However, even when nigrostriatal dopamine neuron loss is severe enough to c
98                     We identify two parallel nigrostriatal dopamine neuron subpopulations differing i
99  SNCA-OVX mice display age-dependent loss of nigrostriatal dopamine neurons and motor impairments cha
100 y be related to the initial pathology of the nigrostriatal dopamine neurons and resulting dopamine de
101 t estrogen may elicit a beneficial effect on nigrostriatal dopamine neurons in PD.
102               Recent evidence indicates that nigrostriatal dopamine neurons inhibit striatal projecti
103 ss of the PPTg with bilateral destruction of nigrostriatal dopamine neurons that mimics human pathoph
104 erent time points, changes in firing rate of nigrostriatal dopamine neurons, as well as dopamine sign
105 isease (PD) is mainly due to degeneration of nigrostriatal dopamine neurons.
106 erative disorder that results in the loss of nigrostriatal dopamine neurons.
107 ciated not only with the degeneration of the nigrostriatal dopamine neurotransmission, but also with
108                Our findings suggest that the nigrostriatal dopamine pathway is involved to some exten
109 ia since their activation reduces mesolimbic nigrostriatal dopamine release (which conveys antipsycho
110                           Lesions of the rat nigrostriatal dopamine system by injection of 6-hydroxyd
111 tudents of Parkinson's disease who study the nigrostriatal dopamine system that originates in the sub
112 food addiction indicates that mesolimbic and nigrostriatal dopamine systems often are cited as mechan
113              This article gives an update on nigrostriatal dopamine terminal imaging, with emphasis o
114 G) structures also revealed a major role for nigrostriatal dopamine, the striatum, and the external g
115 -stage Parkinson's disease (PD) with reduced nigrostriatal dopamine, whereas, asymptomatic carriers h
116 ine on functional alpha4beta2* nAChRs in the nigrostriatal dopaminergic (DA) pathway.
117 signaling in MPTP-induced loss and repair of nigrostriatal dopaminergic (DAergic) neurons prompted us
118 A) synthase, is selectively expressed by the nigrostriatal dopaminergic (nDA) neurons that preferenti
119         We conclude that 5-HT(2C)Rs regulate nigrostriatal dopaminergic activity and function both at
120 ion regulates PKCdelta expression to augment nigrostriatal dopaminergic cell death, which could contr
121  stress responses to better understand how a nigrostriatal dopaminergic deficit increases the prevale
122      Three weeks later, after behavioral and nigrostriatal dopaminergic deficits had developed, rats
123 pamine toxic lesion and a genetic model with nigrostriatal dopaminergic deficits, we found that acute
124 four patients referred for the assessment of nigrostriatal dopaminergic degeneration were scanned usi
125 tor performance independent of the degree of nigrostriatal dopaminergic denervation in Parkinson's di
126 otor impairment independent of the degree of nigrostriatal dopaminergic denervation in Parkinson's di
127 s a more robust determinant of hyposmia than nigrostriatal dopaminergic denervation in subjects with
128 ects of both leucoaraiosis and the degree of nigrostriatal dopaminergic denervation on motor features
129 ic terminal loss in thalamus and cortex, and nigrostriatal dopaminergic denervation, on postural sens
130 atients, indicating Parkinson's disease-like nigrostriatal dopaminergic denervation.
131 ough not with differential serotoninergic or nigrostriatal dopaminergic denervation.
132 r determinant of axial motor impairment than nigrostriatal dopaminergic denervation.
133 atients with PD are associated with impaired nigrostriatal dopaminergic function resulting in abnorma
134            We describe clinical, genetic and nigrostriatal dopaminergic imaging ([(123)I]N-omega-fluo
135 -tetrahydropyridine (MPTP)-induced bilateral nigrostriatal dopaminergic lesions after unilateral puta
136 hyperactivation in vivo and in vitro rescues nigrostriatal dopaminergic neurodegeneration induced by
137  Pit3x-deficient mice, a model for selective nigrostriatal dopaminergic neurodegeneration, we tested
138  potential beneficial effects of estrogen on nigrostriatal dopaminergic neuron degeneration in postme
139 DLS infarction evoked abnormal plasticity in nigrostriatal dopaminergic neurons and DMS D1-neurons, c
140            Although the gross anatomy of the nigrostriatal dopaminergic neurons was normal in DRD mic
141 D) is characterized by a progressive loss of nigrostriatal dopaminergic neurons.
142 order characterized by a progressive loss of nigrostriatal dopaminergic neurons.
143 interact together to influence the number of nigrostriatal dopaminergic neurons.
144                                   Diminished nigrostriatal dopaminergic neurotransmission is a bioche
145 es a reliable and reproducible lesion of the nigrostriatal dopaminergic pathway and neurodegeneration
146 rized by the progressive degeneration of the nigrostriatal dopaminergic pathway and the emergence of
147 ) without FUS, ameliorates the damage to the nigrostriatal dopaminergic pathway in the sub-acute MPTP
148 eceptor subtype on functions mediated by the nigrostriatal dopaminergic pathway is less clear.
149  gene) delivery attenuates the damage to the nigrostriatal dopaminergic pathway, by allowing the entr
150 ghout the rodent brain, including within the nigrostriatal dopaminergic pathway.
151 n inclusions precedes the involvement of the nigrostriatal dopaminergic pathway.
152             Toxic organic cations can damage nigrostriatal dopaminergic pathways as seen in most park
153 long the trajectory of mesocorticolimbic and nigrostriatal dopaminergic pathways.
154 viorally to determine the integrity of their nigrostriatal dopaminergic pathways.
155 f mDAs and the segregation of mesolimbic and nigrostriatal dopaminergic pathways.
156                                      Loss of nigrostriatal dopaminergic projection neurons is a key p
157 hed dopamine release and axonal pathology of nigrostriatal dopaminergic projection.
158 alpha-synuclein conversion and deposition at nigrostriatal dopaminergic synapses in transgenic mice,
159  PD and has a pathophysiological role in the nigrostriatal dopaminergic system and suggest that modul
160                  We attempted to monitor the nigrostriatal dopaminergic system in rats with positron
161 rly PD nonmotor symptoms with imaging of the nigrostriatal dopaminergic system offers a promising pat
162 xplained by a compensatory adaptation of the nigrostriatal dopaminergic system possibly due to decrea
163 sociated with neuroprotective effects in the nigrostriatal dopaminergic system.
164 ts operate in modulating the function of the nigrostriatal dopaminergic system.media-1vid110.1093/bra
165 on of the mesolimbic (nucleus accumbens) and nigrostriatal (dorsal striatum) dopamine pathways using
166 and occipital cortical synaptic activity and nigrostriatal function than PD noncarriers.
167              This study demonstrates altered nigrostriatal function that precedes behavioral parkinso
168 e SN PET measures are relevant biomarkers of nigrostriatal function.
169                   Additionally, the level of nigrostriatal functional connectivity predicted the leve
170 r GABA brake for nigral dopamine systems and nigrostriatal functions, and they raise important questi
171 rgic inhibition of DA release augmented, and nigrostriatal GABA co-release attenuated.
172 -serine levels and consequent improvement of nigrostriatal hypoglutamatergic transmission at glycine
173   Our results reveal independently operating nigrostriatal information streams, with implications for
174 mine transporter (CFT) within 2 months after nigrostriatal injury.
175 ase, we found that behaviorally undetectable nigrostriatal lesions induced a significant disconnectio
176 tical drive to dMSNs decreases after partial nigrostriatal lesions producing no behavioral impairment
177 tic of rodents with lateral hypothalamic and nigrostriatal lesions.
178 ol consumption and to uncover the underlying nigrostriatal mechanism.
179  differentially regulates mesolimbic- versus nigrostriatal-mediated functions.
180 d the ventral tegmental area, which form the nigrostriatal, mesolimbic, and mesocortical pathways.
181 Topographically organized catecholaminergic "nigrostriatal," "mesolimbic," "mesocortical," and spinal
182   In vertebrates, dopamine is central to the nigrostriatal motor and mesolimbic reward systems.
183 plain the selective neurodegeneration of the nigrostriatal motor projection in PD.
184 gest that impaired integrity of dopaminergic nigrostriatal nerve terminals is associated with nigrost
185 de important insights into the topography of nigrostriatal neurodegeneration in Parkinson's disease,
186 -derived LB extracts resulted in progressive nigrostriatal neurodegeneration starting at striatal dop
187 ports diagnosis of a condition not involving nigrostriatal neurodegeneration such as Alzheimer's dise
188        Abnormal imaging indicates underlying nigrostriatal neurodegeneration, supportive of a diagnos
189 owly progressive axon-initiated dopaminergic nigrostriatal neurodegeneration.
190 tion of Lewy body pathology with significant nigrostriatal neurodegeneration.
191 ontrols) with similar degree of MPTP-induced nigrostriatal neurodegeneration; and (4) DA efflux studi
192 cacy of the potent antioxidant C3 to salvage nigrostriatal neuronal function after 1-methyl-4-phenyl-
193 y required for survival of dopaminergic (DA) nigrostriatal neurons and protect them from toxic insult
194 at dopamine is critical for SVZ function and nigrostriatal neurons are the main suppliers of SVZ dopa
195 se durations, we found that mesoaccumbal and nigrostriatal neurons differ substantially in rebound pr
196 re, these results show that mesoaccumbal and nigrostriatal neurons display differential responses to
197  (PPE), and on the integrity of dopaminergic nigrostriatal neurons in hemiparkinsonian mice.
198                                      Loss of nigrostriatal neurons leading to dopamine depletion in t
199                              Degeneration of nigrostriatal neurons of substantia nigra pars compacta
200 reviously reported targeted gene transfer to nigrostriatal neurons using chimeric gC-glial cell line-
201 iata but not from contralateral striata when nigrostriatal neurons were transduced.
202 have emphasized degeneration of dopaminergic nigrostriatal neurons with consequent dysfunction of cor
203 g exposure to toxins that selectively remove nigrostriatal neurons, suggesting that dopamine is criti
204 ned the aphakia mouse, which is deficient in nigrostriatal neurons, we found no detrimental effect to
205 er for presynaptic terminals in dopaminergic nigrostriatal neurons.
206 zation-induced delays in spiking relative to nigrostriatal neurons.
207 ts receptors are constitutively expressed on nigrostriatal neurons.
208                             They also showed nigrostriatal neurotransmission deficits that were manif
209 minergic tracer binding and the diagnosis of nigrostriatal parkinsonism, particularly PD.
210 r Parkinson's disease (PD), it is known that nigrostriatal pathologies do not persist in the acute MP
211                                  Reversal of nigrostriatal pathologies in castrated male mice by subc
212 in could hold the key for driving persistent nigrostriatal pathologies in the MPTP mouse model, and t
213  our results suggest that castration induces nigrostriatal pathologies via iNOS-mediated decrease in
214 ntransgenic animal model to study PD-related nigrostriatal pathologies, paving the way for easy drug
215 le of male sex hormone in castration-induced nigrostriatal pathology.
216 TP), producing bilateral degeneration of the nigrostriatal pathway consistent with early-stage PD.
217 ges as a novel drug target for prevention of nigrostriatal pathway degeneration, the neuropathologica
218 indicated by the progressive degeneration of nigrostriatal pathway dopaminergic neurons and widesprea
219  neurons that project to the striatum in the nigrostriatal pathway express GDNF receptors, GFR alpha1
220 ved FGF signaling, which assures an adequate nigrostriatal pathway formation and target innervation.
221                         In TH-Cre mice whose nigrostriatal pathway had been eliminated unilaterally w
222 mals also exhibited neurodegeneration in the nigrostriatal pathway in a time-dependent manner.
223  in the restoration of the components of the nigrostriatal pathway in MPTP-lesioned mice by measuring
224 y of (18)F-FE-PE2I as a tool for imaging the nigrostriatal pathway in Parkinson disease (PD) with PET
225 l impairment and loss of connectivity of the nigrostriatal pathway in Parkinson disease (PD).
226 nd for DAT quantification and imaging of the nigrostriatal pathway in PD.
227 with the well-established dysfunction of the nigrostriatal pathway in psychosis.
228 into non-human primates causes injury to the nigrostriatal pathway including nigral cell bodies, axon
229                  The progressive loss of the nigrostriatal pathway is a distinguishing feature of Par
230  dopaminergic substantia nigra (SNc)-related nigrostriatal pathway is structurally and functionally c
231 placement of fetal striatal co-grafts in the nigrostriatal pathway might elicit neuritic outgrowth to
232  isolated from the striatum, the location of nigrostriatal pathway nerve terminals, of 3-month-old DJ
233 idbrain dopaminergic neurons project via the nigrostriatal pathway to the striatum to regulate volunt
234  the SMN (hypothetically via the SNc-related nigrostriatal pathway) and SN (hypothetically via the VT
235 biting a decrease in dopamine release in the nigrostriatal pathway, as measured with fast-scan cyclic
236    However, the influence of the tVTA on the nigrostriatal pathway, from the substantia nigra pars co
237  general and how it affects the dopaminergic nigrostriatal pathway, in particular.
238 n nucleus, and it innervates, apart from the nigrostriatal pathway, several motor-related areas.
239 al dopaminergic neurons and consequently the nigrostriatal pathway, which has been found to innervate
240 lpha- synuclein (hA53T-alpha-syn) in the rat nigrostriatal pathway, with or without treatment using t
241 y of (18)F-FE-PE2I as an imaging tool of the nigrostriatal pathway.
242 res of PD is loss of dopamine neurons in the nigrostriatal pathway.
243 th animals treated only with 6-OHDA into the nigrostriatal pathway.
244 , and functional lesions of the dopaminergic nigrostriatal pathway.
245  response to dopaminergic dysfunction of the nigrostriatal pathway.
246 s disease process, not just the dopaminergic nigrostriatal pathway.
247 rkinson's disease, suggesting defects in the nigrostriatal pathway.
248 ting a neuroprotective role for RGS10 in the nigrostriatal pathway.
249 nked to death of dopaminergic neurons in the nigrostriatal pathway.
250  striatal grafts (STR) 2.5 mm rostral in the nigrostriatal pathway.
251 or delay the progressive degeneration of the nigrostriatal pathway.
252 roxy for function of dopamine neurons in the nigrostriatal pathway.
253 ntenance of dopaminergic neurones within the nigrostriatal pathway.
254 oject to the striatum as part of the classic nigrostriatal pathway.
255 lease from the terminals of the dopaminergic nigrostriatal pathway.
256  hippocampus and basal ganglia (specifically nigrostriatal pathways).
257 function in schizophrenia is greatest within nigrostriatal pathways, implicating the dorsal striatum
258 sporter PET ligand that allows assessment of nigrostriatal presynaptic dopaminergic terminal integrit
259                                   Effects on nigrostriatal-projecting neurons were examined using a r
260  living animal models of degeneration in the nigrostriatal projection that a constitutively active fo
261 lude that regrowth of axons within the adult nigrostriatal projection, a system that is prominently a
262                             Mesoaccumbal and nigrostriatal projections are sensitive to stress, and h
263 issural striatal subregions known to receive nigrostriatal projections from this tier, while the dors
264 ial inflammatory responses and led to robust nigrostriatal protection.
265 ) treatment in vivo, Nur77 expression in the nigrostriatal region is dramatically reduced.
266 rons and defective dopamine signaling in the nigrostriatal region.
267     The distribution volume reduction across nigrostriatal regions at 8 weeks ranged from 13-16%, wit
268  abundantly expressed in non-DA cells in the nigrostriatal regions.
269 ical benefit mediated by graft survival with nigrostriatal reinnervation.
270 emonstrate that STN DBS does not protect the nigrostriatal system against alpha-syn overexpression-me
271             Degeneration of the dopaminergic nigrostriatal system and of noradrenergic neurons in the
272 ) dopamine neurons and increases BDNF in the nigrostriatal system and primary motor cortex.
273 that prediction error signals in the brain's nigrostriatal system guide learning for trial-and-error
274 reflected the functional organization of the nigrostriatal system observed in histological and electr
275  neurons induces remarkable adaptions in the nigrostriatal system where limited amounts of dopamine i
276                                       In the nigrostriatal system, BDNF expression was upregulated in
277 e played by the tVTA as a GABA brake for the nigrostriatal system, demonstrating a critical influence
278 he result of dopaminergic dysfunction of the nigrostriatal system, the clinical manifestations of Par
279  function of TGF-beta signaling in the adult nigrostriatal system, we generated transgenic mice with
280 ntially regulates trophic factors within the nigrostriatal system.
281 ophic factors in the intact and degenerating nigrostriatal system.
282 rescued with ectopic Nur77 expression in the nigrostriatal system.
283 he loss of dopamine-producing neurons in the nigrostriatal system.
284 nigra (SN) and affected the integrity of the nigrostriatal system.
285 lated motor deficits and degeneration of the nigrostriatal system.
286 on and separate parsing of inputs within the nigrostriatal system.SIGNIFICANCE STATEMENT Prior studie
287 of rates of metabolism in the mesolimbic and nigrostriatal systems with the amount of MPD-induced beh
288 ls in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients w
289 ut only correlates with in vitro measures of nigrostriatal terminal fields when nigral cell loss does
290 urons in substantia nigra or degeneration of nigrostriatal terminals at 12 months.
291 OPA and NET-mediated DA reuptake in lesioned nigrostriatal terminals may have a role in LID severity
292 vation of presynaptic nicotinic receptors on nigrostriatal terminals that evoke GABA release from the
293 ivo association between the integrity of the nigrostriatal tract (defined by correlational tractograp
294                                Assessment of nigrostriatal tract integrity may be suitable as a bioma
295 acerebral infusion of FGF20 protects against nigrostriatal tract loss in the 6-hydroxydopamine lesion
296 anine (S129A) or to aspartate (S129D) in the nigrostriatal tract of the rat to investigate the effect
297 mmunoreactive neurons and total cells in the nigrostriatal tract, improves the motor performance in M
298 , significantly elevated FGF20 levels in the nigrostriatal tract.
299                                     Results: Nigrostriatal tracts were identified in both hemispheres
300 s, proving a regulatory role of FGF-2 during nigrostriatal wiring.

 
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