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1 ery few (450 in each mouse retina, 0.005% of retinal neurons).
2 (important for the high metabolic demands of retinal neurons).
3 croglia/macrophages associate with apoptotic retinal neurons.
4 ectric current to stimulate the nearby inner retinal neurons.
5 ltiple genes expressed specifically in inner retinal neurons.
6 ssion with the modulation of Src activity in retinal neurons.
7 nin potentiates signaling from rods to inner retinal neurons.
8 tion, which is necessary for the survival of retinal neurons.
9 es and decreasing apoptosis of pericytes and retinal neurons.
10 t not genes characteristic of differentiated retinal neurons.
11 a(v)1.3 L-type Ca(2+) channels in salamander retinal neurons.
12 rentiation when in the vicinity of wild-type retinal neurons.
13 s known about propofol's effects on specific retinal neurons.
14 normal electrophysiology at the level of the retinal neurons.
15 zed in photoreceptor cells and in some inner retinal neurons.
16 l roles in processing the light responses of retinal neurons.
17 leads to chronic but reversible silencing of retinal neurons.
18 important role in promoting the survival of retinal neurons.
19 ginates mainly from activity of second-order retinal neurons.
20 or studying the function of coupling between retinal neurons.
21 and progressive loss of adult cerebellar and retinal neurons.
22 ture and interactions in the spike trains of retinal neurons.
23 the activity of second-order hyperpolarizing retinal neurons.
24 unced expression in photoreceptors and other retinal neurons.
25 c degeneration of cerebellar, brainstem, and retinal neurons.
26 le is known about the responses of the inner retinal neurons.
27 retinal vasculature can result in damage to retinal neurons.
28 (RPG) expression and the differentiation of retinal neurons.
29 n synaptic activity and AMPAR trafficking in retinal neurons.
30 n cAMP levels and PKA activity in developing retinal neurons.
31 + and the actin cytoskeleton organization in retinal neurons.
32 ot solely photoreceptor cells but also inner retinal neurons.
33 metabolism increased insulin sensitivity in retinal neurons.
34 hich are derived from the second-order inner retinal neurons.
35 CoCl(2) upregulated Hsp27 in cultured retinal neurons.
36 ), can block differentiation and function of retinal neurons.
37 vels in the glia, but very low levels in the retinal neurons.
38 stnatal retina, and it is expressed by inner retinal neurons.
39 ts their level of innervation by more distal retinal neurons.
40 tic connections between specific subtypes of retinal neurons.
41 d for coincidence and threshold detection in retinal neurons.
42 lved in the development of multiple types of retinal neurons.
43 and formed a cell layer connected with host retinal neurons.
44 inal homeostasis and support the survival of retinal neurons.
45 cells (MGPCs) with the ability to regenerate retinal neurons.
46 d dopamine-dependent GABA release from other retinal neurons.
47 mprise approximately 1/2 of a percent of all retinal neurons.
48 that are expressed in overlapping subsets of retinal neurons.
49 rriers and thereby access and photosensitize retinal neurons.
50 cell death but spare second- and third-order retinal neurons.
51 ous reservoir may recover function of "sick" retinal neurons.
52 erve to replace or resurrect dead or injured retinal neurons.
53 nd subsequent regeneration of HuC/D(+) inner retinal neurons.
54 faster cone-driven responses in second-order retinal neurones.
55 d precursor cells, whereas loss of any other retinal neurons activates Muller glia proliferation to p
59 ller glia upregulate genes characteristic of retinal neurons after growth factor stimulation in vitro
60 n shown to be effective in transducing inner retinal neurons after intravitreal injection in several
61 and an acute treatment increased survival of retinal neurons after optic nerve crush (ONC) in rodent
63 as a negative feedback mechanism protecting retinal neurons against glutamate-induced excitotoxicity
66 e postsynaptic current (PSC) in second-order retinal neurons and (2) capacitance measurements of vesi
67 ng of spontaneous activity in populations of retinal neurons and by making whole-cell recordings from
69 c sequence of circuit models that represents retinal neurons and connections and fitted them to the e
70 a variety of diseases involving the death of retinal neurons and contributes to neurodegenerative pro
73 cid metabolites differentially gate TRPV4 in retinal neurons and glia, with potentially significant c
79 ty of progenitor cells to differentiate into retinal neurons and is highly expressed by human Muller
80 olecule identified that is produced by dying retinal neurons and is necessary to induce Muller glia t
82 to result from a complex interaction between retinal neurons and Muller glia, which release toxic mol
83 med that MMP activity occurred only in these retinal neurons and not in glial or other retinal cell t
84 ynthase (NOS), modulates the function of all retinal neurons and ocular blood vessels and participate
85 tion that reveals GC somas, axons, and other retinal neurons and permits their quantitative analysis.
86 o dedifferentiate, migrate, and generate new retinal neurons and photoreceptor cells by alpha-aminoad
87 kb promoter directed transgene expression to retinal neurons and progenitor cells, the activity of mu
88 xpressed by non-overlapping subsets of chick retinal neurons and promote their lamina-specific arbori
92 at insulin mediates a prosurvival pathway in retinal neurons and that normal retina expresses a highl
93 done to achieve higher yields of functioning retinal neurons and to promote better integration within
98 hyperpolarizing second- and all third-order retinal neurons; and TTX (tetrodotoxin, 6 muM), to block
103 urposes of this study were to identify which retinal neurons are infected and to determine the routes
105 ge-gated sodium channels (Na(v) channels) in retinal neurons are known to contribute to the mammalian
107 Our results indicate that multiple types of retinal neurons are potential circadian clock neurons th
110 clock genes in individual, identified mouse retinal neurons, as well as characterized the clock gene
113 of Casz1 increases production of early-born retinal neurons at the expense of later-born fates, wher
114 portant in shaping responses of second-order retinal neurons at the tonically active photoreceptor sy
115 However, the extent to which regenerated retinal neurons attain appropriate morphologies and circ
116 NAs in terminally differentiated adult human retinal neurons based on their sequence conservation acr
117 ds and cones, after processing by downstream retinal neurons (bipolar, horizontal, amacrine and gangl
120 signaling did not prevent differentiation of retinal neurons, but it did disrupt spatial patterning i
121 ive in hippocampal, dorsal root ganglia, and retinal neurons, but its propermeability, vasodilatatory
122 mediate the initial proliferative arrest of retinal neurons, but may indirectly induce arrest in RPC
124 can signal changes in light levels to inner retinal neurons, but the role of glutamate in communicat
125 multipotent retinal stem cells that generate retinal neurons by homeostatic and regenerative developm
126 layed rectifier potassium (K(V)) channels in retinal neurons by means of a metabotropic receptor path
128 Under these conditions and pathologies, retinal neurons can die via apoptosis that may be due to
130 result in photoreceptor loss, but the inner retinal neurons can survive, making them potentially ame
131 study suggests that changes in the output of retinal neurons caused by disturbances in outer retinal
132 precise synaptic connections among distinct retinal neuron cell types is critical for processing vis
133 s have neurogenic potential and can generate retinal neurons, confirming a hypothesis, first proposed
134 esults provide a better understanding of how retinal neurons connect to the central circadian pacemak
135 hes: 1) hydrogen peroxide (H(2)O(2))-induced retinal neuron degeneration in vitro, and 2) light-induc
137 We found that in the absence of microglia, retinal neurons did not undergo overt cell death or beco
139 otein, activates Atonal (Ato) expression and retinal neuron differentiation synergistically with the
140 clude that Isl1 has an indispensable role in retinal neuron differentiation within restricted cell po
141 gnificantly increased the apoptotic death of retinal neurons during embryonic and postnatal developme
148 nds were also present in certain other adult retinal neurons, for example, horizontal cells and amacr
149 he absence of beta1-Integrin or Cas function retinal neurons form ectopic cell clusters beyond the in
150 ecific structure, in which specific types of retinal neurons form highly selective synapses to transf
152 show a simultaneous requirement for Math5 in retinal neuron formation and cell cycle progression.
154 tivation of the receptor by G1 protected the retinal neuron from insult, whereas G15, an antagonist o
155 demonstrate that EGCG provides protection to retinal neurones from oxidative stress and ischemia/repe
156 ave developed efficient methods for deriving retinal neurons from human embryonic stem (hES) cells.
158 have a robust ability to regenerate injured retinal neurons from Muller glia (MG) that activate the
161 ogenitors differentiate primarily into inner retinal neurons (ganglion and amacrine cells), with func
162 lacking TGF-beta receptor II (TGFbetaRII) in retinal neurons had reduced C1q expression in RGCs and r
164 cted time to develop blindness suggests that retinal neurons have an endogenous mechanism for protect
167 ansmission, dopamine modulates all layers of retinal neurons; however, it is not well understood how
168 markers and by the expression of markers of retinal neurons (HuD, betaIII tubulin, rhodopsin, BRN3B,
170 lamin B2 prevents proper lamination of adult retinal neurons, impairs synaptogenesis, and reduces con
171 of S1R in the nuclear envelope in all three retinal neurons implicates a potential role of S1R in mo
173 hich have biases toward producing subsets of retinal neurons in a terminal division, with the types o
175 ng provides a trophic signal for transformed retinal neurons in culture, but the in vivo role of Akt
176 ng provides a trophic signal for transformed retinal neurons in culture, but the role of IR activity
182 f ptc+/- mice could be induced to regenerate retinal neurons in response to damage, we bred ptc+/- mi
183 GFP) (Chop2-GFP) were evaluated in the inner retinal neurons in the common marmoset Callithrix jacchu
185 Subsequently, the number of fluorescent retinal neurons in the group that received one treatment
187 expression of ChR2 was observed in the inner retinal neurons in the marmoset retina through intravitr
188 report that HDAC4 regulates the survival of retinal neurons in the mouse in normal and pathological
190 rce of stem cells is important for producing retinal neurons in three-dimensional (3D) organ cultures
195 oping mice studied, we detected infection of retinal neurons; in many mice, this was also associated
196 op2-GFP was observed in all major classes of retinal neurons, including all major types of ganglion c
197 d by the upregulation of specific markers of retinal neurons, including betaIII tubulin, rhodopsin, B
198 an extensive gap junction network with other retinal neurons, including other ipRGCs, which shapes th
199 ) channels play important roles in mammalian retinal neurons, including photoreceptors, bipolar cells
200 rhodopsins, such as ChR2, in surviving inner retinal neurons is a potential strategy for the restorat
202 Therefore, although the Sema3E secreted by retinal neurons is evenly distributed throughout the ret
203 hows that extrinsic feedback from developing retinal neurons is important for the temporal expression
204 ulated crosstalk between the vasculature and retinal neurons is increasingly recognized as a major fa
205 ission at ribbon synapses of cones and other retinal neurons, it is unknown whether Gbetagamma contri
206 their ability to up-regulate genes found in retinal neurons, it was concluded that these sphere-form
207 This protocol can also be applied to study retinal neurons labeled with other two photon-excitable
209 x36) subunits, which are highly expressed by retinal neurons, markedly reduced loss of neurons and op
210 constitutive expression of SOCS6 protein in retinal neurons may improve glucose metabolism, while el
211 nal progenitor cells that differentiate into retinal neurons, mimicking the responses observed in the
212 By use of protocols that preserve proximal retinal neuron morphology, we have examined the shape, d
215 n preparing the eye for vision by regulating retinal neuron number and initiating a series of events
216 by a light-response pathway that suppresses retinal neuron number, limits hypoxia and, as a conseque
218 e that expression of ChR2 in surviving inner retinal neurons of a mouse with photoreceptor degenerati
219 f cell apoptosis and caspase-3 activation in retinal neurons of C57Bl/6 mice within days of diabetes
222 inst loss of fluorescence within fluorescent retinal neurons of Thy1-CFP mice after optic nerve crush
223 operational range of rod bipolar cells, the retinal neurons operating immediately downstream of rod
225 adult retinal architecture, the survival of retinal neurons, or the laminar organization of their de
226 ferred expression of this isotype in certain retinal neurons plays a cell specific role, or whether i
230 ities is affected by the spiking activity of retinal neurons, possibly including that of the DA neuro
231 pressing channel rhodopsin-2 (ChR2) in inner retinal neurons, previous studies have demonstrated rest
234 ows that after selective ablation, zebrafish retinal neurons regenerate and reconstruct some, althoug
235 , after a chemical lesion that ablates inner retinal neurons, regenerated retinal bipolar neurons (BP
238 ontrast, the mean proportions of fluorescent retinal neurons remaining in the group treated with MS-2
240 Milner and Do describe how the population of retinal neurons responsible for entrainment of the brain
242 onged light sensitivity on multiple types of retinal neurons, resulting in synaptically amplified res
244 c nerve crush, the proportion of fluorescent retinal neurons retaining fluorescence was 44+/-7% of ba
245 rafish line, in which all different types of retinal neurons show distinct fluorescent spectra, we fo
246 nal deletion of TGF-beta-inhibiting Smad7 in retinal neurons significantly enhanced Smad3 phosphoryla
247 nes associated with neurogenesis, as well as retinal neuron-specific genes, are differentially expres
248 and Sema5B constrain neurites from multiple retinal neuron subtypes within the inner plexiform layer
249 , but rather to the cell lineage (early born retinal neurons) suggesting that the expression of class
250 ersistence of transcripts expressed by inner retinal neurons suggests that despite significant plasti
251 postmitotic, terminally differentiated adult retinal neurons suggests that EGFR has pleiotropic funct
252 and G9a-mediated HKM plays crucial roles in retinal neuron survival and may represent novel epigenet
254 MG-derived neurons express markers of inner retinal neurons, synapse with host retinal neurons, and
255 r for VEGF, was more abundantly expressed in retinal neurons than in endothelial cells, including end
256 rabbit AII amacrine cell, a multifunctional retinal neuron that forms an electrically coupled networ
257 glaucoma are disorders that target specific retinal neurons that can ultimately lead to vision loss.
258 sh (Danio rerio) are capable of regenerating retinal neurons that have been lost due to mechanical, c
259 mine activates a receptor in adult mammalian retinal neurons that is distinct from classical D1 and D
260 genesis is indicated by increased early-born retinal neurons that result from accelerated cell cycle
261 i-bullwhip cells are unconventional types of retinal neurons that utilize the neuropeptides glucagon,
262 s of Sfrs1 function resulted in the death of retinal neurons that were born during early to mid-embry
266 own to modulate the number of other types of retinal neuron-the proapoptotic gene, Bax, and tyrosinas
268 ntenance of retinal polarity and survival of retinal neurons, thus providing the basis for the pathol
269 d unprecedented cellular regulation of VEGF: retinal neurons titrate VEGF to limit neuronal vasculari
270 erently rely on the ability of the remaining retinal neurons to correctly synapse with new photorecep
273 this enhances signal transmission from inner retinal neurons to ganglion cells, potentially allowing
274 etic retina, increases the susceptibility of retinal neurons to injury in the presence of increased c
275 ation and fractionation METHODS: Survival of retinal neurons to metabolic stress after overexpression
276 explore the feasibility of converting inner retinal neurons to photosensitive cells as a possible st
278 uthors have genetically engineered surviving retinal neurons to take on the lost photoreceptive funct
286 ncrease in glucosylceramide composition, R28 retinal neurons were treated with glucosylceramide synth
288 ated whether trafficking of AMPARs occurs in retinal neurons, which are subject to tonic glutamate re
289 ll type that is distinct from other types of retinal neurons, which we termed large glucagon-expressi
292 itric oxide, GABAergic and glycinergic inner retinal neurons with expression of a reporter for the ci
293 ion cells (RGCs) are the best studied of the retinal neurons with respect to the effect of diabetes.
294 during the critical period in development of retinal neurons with small, foveal receptive fields.
296 ted alternative splicing for the survival of retinal neurons, with sensitivity defined by the window
299 ification of the size of every population of retinal neuron, yet genetic variants work largely indepe
300 he formation of the antagonistic surround of retinal neurons, yet the mechanism by which horizontal c
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