ライフサイエンスコーパス: neuronal cell

1 tion and accumulation of protein deposits in neuronal cells.

2 al mechanisms for the effects of caffeine on neuronal cells.

3 ve to differentiated tumor progeny or normal neuronal cells.

4 n results in poor dissemination of VZV among neuronal cells.

5 ever, these cells can be differentiated into neuronal cells.

6 les in microglial cells and their effects on neuronal cells.

7 glia-like meningeal cells differentiating to neuronal cells.

8 nsition Protein 4 (HMGB4L1) are expressed in neuronal cells.

9 r supporting cells, and several types of non-neuronal cells.

10 ation from extracts of radiolabeled islet or neuronal cells.

11 t does not self-assemble, nor is it toxic to neuronal cells.

12 m to potential U incorporation pathways into neuronal cells.

13 e finely-balanced gene control mechanisms in neuronal cells.

14 t of cell migration on ATF4 reduction in non-neuronal cells.

15 subcellular localization in non-neuronal and neuronal cells.

16 nvert mouse embryonic fibroblasts to induced neuronal cells.

17 e and expression of WT and mutant Dcx in non-neuronal cells.

18 from mouse embryonic fibroblasts to induced neuronal cells.

19 supporting SVIL as a cofactor for LSD1+8a in neuronal cells.

20 ) hyperactivates HUSH-mediated repression in neuronal cells.

21 sitol 4-phosphate (PI4P) in the membranes of neuronal cells.

22 E-SIMS) to investigate the lipid profiles of neuronal cells.

23 at serine 181 (Ser181) was described in non-neuronal cells.

24 ansmission of ORF7-deficient virus among the neuronal cells.

25 o accumulate in filopodia in neurons and non-neuronal cells.

26 nd exhibit cytotoxic effects when applied to neuronal cells.

27 alpha2AAR is significantly enhanced in these neuronal cells.

28 oducing a uniform population of mature human neuronal cells.

29 A3B has emerged as a tumor suppressor in non-neuronal cells.

30 otranspose efficiently in mature nondividing neuronal cells.

31 moted expression of neuronal features in non-neuronal cells.

32 e variety of PrP(C) protein interactors, the neuronal cell adhesion molecule (NCAM) has been studied

33 Several novel substrates, including the neuronal cell adhesion protein NrCAM, are involved in br

34 After replication in neuronal cells, all PRV180G progeny exclusively contain

35 of spinal cord motor neurons, with other non-neuronal cells also transduced.

36 ha-syn) accumulation in the CNS may underlie neuronal cell and synaptic dysfunction leading to motor

37 we show that protein fibrils are taken up by neuronal cells and act as prion-like seeds for elongatio

38 ces in the regulome between neuronal and non-neuronal cells and ascribes putative functional roles to

39 ys an important role in the specification of neuronal cells and continues to be expressed in postmito

40 ternalization of pre-formed fibrils into non-neuronal cells and dopaminergic neurons matched the effi

41 eduled accumulation of neuronal mRNAs in non-neuronal cells and ensures coordinated upregulation of t

42 -43 fragment mediated toxicity, in mammalian neuronal cells and flies.

43 uggest that NGB exerts protective effects to neuronal cells and is implicated in reducing the severit

44 h express cellular markers characteristic of neuronal cells and pericytes.

45 lar space from those that reflect changes in neuronal cells and processes.

46 pressed in CNS interstitial cells, including neuronal cells and progeny.

47 activity had slower replication in mammalian neuronal cells and reduced virulence in 2-day-old mice.

48 d EPO-like cytoprotective effects in primary neuronal cells and renal proximal tubular epithelial cel

49 In addition, CQ is nontoxic to neuronal cells and shows significant blood brain barrier

50 nt for deltaR export and surface delivery in neuronal cells and suggest that it could be a key modula

51 es of aSyn species determine their effect in neuronal cells and supports a lack of correlation betwee

52 to study dynamics of Akt phosphorylation in neuronal cells and the developing brain and identify pre

53 t range, swine alpha herpesvirus that enters neuronal cells and utilizes intracellular transport proc

54 Silencing WDR47 in hypothalamic GT1-7 neuronal cells and yeast models independently recapitula

55 esembling neural stem cells in the SVZ), (2) neuronal cells, and (3) a cell type with an intermediate

56 r tolerated by brain microvessel endothelial/neuronal cells, and accumulated less in the liver and sp

57 n induced pluripotent stem (hiPS) cells into neuronal cells, and analyzed expression pattern in zebra

58 ked at agents to modulate MTA1 expression in neuronal cells, and granulocyte colony-stimulating facto

59 nerative disease predominantly occurs in non-neuronal cells, and in the brain, alphaBc is mainly foun

60 cell death in fibroblasts, cardiomyoblasts, neuronal cells, and primary cardiomyocytes.

61 ent of VZV capsids, virus transmission among neuronal cells, and probably the neuropathy induced by V

62 ZV cytoplasmic envelopment in differentiated neuronal cells, and the envelopment deficiency caused by

63 These neuronal cells are able to support a productive HSV-1 in

64 induced pluripotent stem (iPS) cell-derived neuronal cells are needed to validate our preliminary fi

65 urofilament light chains (NfL) are unique to neuronal cells, are shed to the cerebrospinal fluid (CSF

66 e same markers of retinal ganglion cells and neuronal cells as seen in 661W cells.

67 rtant role in regulating the excitability of neuronal cells, as highlighted by mutations in Kcnq2 and

68 ized by the mouse neutralization assay and a neuronal cell-based assay.

69 -synuclein (Sncg), and some other markers of neuronal cells (beta-III tubulin, NeuN and MAP2).

70 However, the neuronal cell biology that underlies axon regeneration i

71 t motor along microtubules from axon tips to neuronal cell bodies (retrograde transport) or from cell

72 ystem and is found in recycling endosomes in neuronal cell bodies and axons.

73 nied by deposition of alpha-synuclein within neuronal cell bodies and axons.

74 nal synaptic contacts with auditory efferent neuronal cell bodies and dendrites, as well as unlabeled

75 1W subcellular localization is restricted to neuronal cell bodies and is not detected at axon initial

76 Neuronal cell bodies are captured from perfused mouse br

77 mediaries, the intercalation of post-mitotic neuronal cell bodies during VNC formation.

78 es essential roles for glial ensheathment of neuronal cell bodies in CNS homeostasis as well as Spz3

79 lutamate and muscimol to activate or inhibit neuronal cell bodies in distinct locations along the ros

80 tute the neurofibrillary tangles observed in neuronal cell bodies in individuals with Alzheimer's dis

81 eaches white matter fibres more readily than neuronal cell bodies in STN, which may help explain anat

82 Dynein synthesized in neuronal cell bodies is conveyed into the axon by slow t

83 ic and axonal contacts, but how glia support neuronal cell bodies is unclear.

84 was observed in processes, varicosities, and neuronal cell bodies of the olfactory bulb, granular zon

85 lia (which associate almost exclusively with neuronal cell bodies) to understand glia-soma interactio

86 ossibly CA2, PDE11A4 is expressed throughout neuronal cell bodies, dendrites (stratum radiatum), and

87 ppresses the buildup of synaptic proteins in neuronal cell bodies, hence may play an adaptive role to

88 riatal nerve terminal function compared with neuronal cell bodies, in accordance with the post-mortem

89 In neuronal cell bodies, increased DAcyt was not due to tra

90 mutant gene are expressed at the surface of neuronal cell bodies; however, they do not associate wit

91 l day 30 Snord116p-/m+ mice the reduction in neuronal cell body size was associated with decreased ne

92 ission by transporting mitochondria from the neuronal cell body throughout the bundles of DRG axons.

93 p to 40%) of axonal processes contacting the neuronal cell body.

94 Expression of mutant CCNF in neuronal cells caused abnormal ubiquitination and accumu

95 In non-neuronal cells, CD2AP, like other adaptor proteins, func

96 ectively traces monoamine exocytosis in both neuronal cell culture and brain tissue.

97 ity by using optical nanoscopy directly in a neuronal cell culture model of Parkinson's disease.

98 In a neuronal cell culture model, ACSS2 increases in the nucl

99 ificantly increased human Abeta secretion in neuronal cell culture models.

100 function of sex in juvenile mice or primary neuronal cell cultures is largely unknown even though bo

101 s system (CNS), axonal damage often triggers neuronal cell death and glial activation, with very limi

102 st that birth may be an important trigger of neuronal cell death and identify transient cell groups t

103 ic endogenous mechanism that interferes with neuronal cell death and ischemic brain injury.

104 e regulatory networks in nerve regeneration, neuronal cell death and neuropathy in different populati

105 gonists block c-Jun upregulation and prevent neuronal cell death following excitotoxic insults.

106 ivation prior to alpha-synuclein-independent neuronal cell death in GBA1 deficiency and suggests upre

107 aminobutyric acid modulator propofol induces neuronal cell death in healthy immature brains by unbala

108 ) activated apoptotic pathways and increased neuronal cell death in IL-21 receptor-deficient (IL-21R-

109 s, reduced brain infarction, and ameliorated neuronal cell death in MCAO rats.

110 Neuronal cell death in neurodegenerative diseases is not

111 hways play an important role in dopaminergic neuronal cell death in Parkinson's disease (PD).

112 GSK3beta by Ser(389) phosphorylation causes neuronal cell death in subregions of the hippocampus and

113 and 30 mum) acted synergistically to induce neuronal cell death in vitro, which was prevented by the

114 ve mutant of MEK5 is sufficient to attenuate neuronal cell death induced by selective inhibition of R

115 after axotomy, implicating their actions in neuronal cell death upon nerve injury.

116 As a result of SCH treatment, neuronal cell death via up-regulation of Akt-mediated pa

117 nsheathment of neuron cell bodies, increased neuronal cell death, and defects in animal behavior.

118 ensory neurons including physiological pain, neuronal cell death, and nerve regeneration.

119 ggests that synapse alterations, rather than neuronal cell death, are the causes of neuronal dysfunct

120 otentials, Muller cell reactive gliosis, and neuronal cell death, as assayed by TUNEL staining and re

121 Acute secondary neuronal cell death, as seen in neurodegenerative diseas

122 We focus on the hippocampus neuronal cell death, as well as the potential link betwe

123 siology, astrocyte and microglia activation, neuronal cell death, axonal retraction, and development

124 HK2 and LDHA during differentiation leads to neuronal cell death, indicating that the shut-off aerobi

125 sive neurodegeneration, including widespread neuronal cell death, neuroinflammation, increased produc

126 kade of TIM-3 markedly reduces infarct size, neuronal cell death, oedema formation and neutrophil inf

127 ng c.1999G>A leads to dendritic swelling and neuronal cell death, suggestive of excitotoxicity mediat

128 mox1) in microglia is necessary to attenuate neuronal cell death, vasospasm, impaired cognitive funct

129 Neuronal cell death-specific treatment approaches, such

130 s are the main toxic species contributing to neuronal cell death.

131 , synaptic loss, and eventually irreversible neuronal cell death.

132 uli leads to synaptic loss, dysfunction, and neuronal cell death.

133 ted VCP elicits excessive mitophagy, causing neuronal cell death.

134 al ER stress signaling, thus contributing to neuronal cell death.

135 cantly attenuated oxidation-induced striatal neuronal cell death.

136 aspase pathway, ultimately inducing striatal neuronal cell death.

137 e release of glutamate, which contributes to neuronal cell death.

138 he first to find that loss of OGT results in neuronal cell death.

139 xcitotoxic levels of glutamate contribute to neuronal cell death.

140 ed with neurogenesis, synapse formation, and neuronal cell death.

141 ressive mechanism for the terminal phases of neuronal cell degeneration and death in human neurodegen

142 critical for oxidative stress resistance in neuronal cells; deletion of this gene causes neurodegene

143 h deficiency of the Gclc in their entire CNS neuronal cells develop at 4 weeks: progressive motor neu

144 on of Numb to generate isoforms that promote neuronal cell differentiation and neurite outgrowth.

145 Neuronal cells dissociated from SNE-injured and contrala

146 altered current across the GABAA receptor in neuronal cells due to changes in ion gradients (HCO3(-)

147 mple, nervous fibers, or guide the growth of neuronal cells during regeneration.

148 Neuronal cells express considerable plasticity respondin

149 The induced neuronal cells expressed various neuron-specific protein

150 e structure that contains distinct layers of neuronal cells expressing characteristic markers of huma

151 phagy markers and reduced autophagic flux in neuronal cells expressing P301L-Tau.

152 were abolished in TLR4 knockout mice and in neuronal cells expressing TLR4 siRNAs.

153 ppression of a Notch repressor to assign non-neuronal cell fate.

154 to begin when pioneer axons extend over non-neuronal cells, forming tracts guiding follower axons.

155 s platform to identify strategies to protect neuronal cells from mutant huntingtin induced death.

156 Compound 23 protected hippocampal neuronal cells from the excitotoxic insult, while efavir

157 tivity and/or gradual loss of the identified neuronal cell group provides a neurophysiological basis

158 ression appears to be specific to individual neuronal cell groups instead of being associated with al

159 malian brain at the resolution of individual neuronal cell groups is not known.

160 rons during development, but its role in non-neuronal cells has been less studied.

161 broaden the concept of homeosis to the many neuronal cell identity transformations that have been un

162 roniotaalpha meaning 'glue') pertains to non-neuronal cells in the central (CNS) and peripheral nervo

163 found that cobalamin scavenged superoxide in neuronal cells in vitro treated with the reduction-oxida

164 estigation of phenotypes of FTLD-Tau patient neuronal cells in vitro, it remains unclear how FTLD-Tau

165 red human cells and in Drosophila muscle and neuronal cells in vivo.

166 of previously inaccessible neuronal and non-neuronal cells in vivoSIGNIFICANCE STATEMENT Instruction

167 Conversely, overexpression of POX in neuronal cells increased ROS levels and activated ROS-de

168 Studies in non-neuronal cells indicate that actin cytoskeletal regulato

169 rologous expression of APLP1 or APLP2 in non-neuronal cells induces presynaptic differentiation in co

170 We review how non-neuronal cells interact with nociceptive neurons by secr

171 In GD iPSC-derived neuronal cells (iPSC-NCs), GBA1 mutations caused widespr

172 ient because damage to other neurons and non-neuronal cells is common in retinal and optic nerve dise

173 educed proliferation, resulting in decreased neuronal cell-layer volume resembling microcephaly.

174 ified the impact of microglial activation on neuronal cells, leading to suppression of neurotoxicity.

175 Galpha14 expression in cultured hypothalamic neuronal cells, leptin caused a transient down-regulatio

176 In neuronal cell line (NG108-15) in vitro, hypoxia caused a

177 The neuronal cell line along with fibroblasts isolated from

178 al fingerprints that were also observed in a neuronal cell line and in lateral perforant path termina

179 otoxicity of cisplatin in vitro in a sensory neuronal cell line and primary rat dorsal root ganglion

180 ring a TDP-43M337V mutation and NSC-34 motor neuronal cell line expressing TDP-43Q331K mutation, we s

181 Treatment of the human neuronal cell line KELLY and acute 1-methyl-4-phenyl-1,2

182 ates Mef2 activity through PDK1 in mammalian neuronal cell line suggesting that the mechanisms are ev

183 on of GnIH in GnRH neurons by using the GnRH neuronal cell line, GT1-7.

184 nd vasoactive intestinal polypeptide in GnRH neuronal cell line, GT1-7.

185 leads to axonal degeneration in the in vitro neuronal cell line.

186 PrP(Sc) formation in two prion-infected neuronal cell lines (ScGT1 and ScN2a cells) and in scrap

187 By use of human and rat neuronal cell lines (SK-N-SH and PC12), we show that ove

188 uced and showed nuclear translocation in two neuronal cell lines - mouse Neuro-2a and human SH-SY5Y -

189 se-protected cytoplasmic particles in rodent neuronal cell lines and brain.

190 ma of primary mouse cortical neurons and two neuronal cell lines and found that alternative last exon

191 rowth and led to neurite degeneration in the neuronal cell lines and rat motor neurons.

192 ion required R7BP, we analyzed phenotypes of neuronal cell lines expressing RGS7 and Gbeta5 with or w

193 Neuronal cell lines expressing the ANG-ALS variants also

194 sly that COPS5 regulates Abeta generation in neuronal cell lines in a RanBP9-dependent manner.

195 and the ability to induce stress granules in neuronal cell lines.

196 ted AR-12 in prion infected neuronal and non-neuronal cell lines.

197 Here, we found that, in neuronal cells, lipid stress by exposure to elevated pal

198 Here, we confirm that despite ongoing neuronal cell loss because of apoptosis in the myenteric

199 ve condition characterised pathologically by neuronal cell loss due to abnormal tau deposits.

200 c overexpression was neuroprotective against neuronal cell loss in BACHD brains, suggesting alphaBc m

201 roglial and astroglial activation as well as neuronal cell loss in epileptogenesis-associated brain r

202 Prior to motor symptom onset or neuronal cell loss in HD, levels of the type 1 cannabino

203 itochondrial dysfunction are responsible for neuronal cell loss.

204 horins play an important role in guidance of neuronal cell migration and were lately linked to regula

205 muli results in the aggregation of aSyn in a neuronal cell model of PD.

206 y in combination with three-dimensional (3D) neuronal cell models derived from human embryonic stem c

207 ote aggregation of alpha-syn in vitro and in neuronal cell models of alpha-syn toxicity.

208 optosis and may induce myelin degradation in neuronal cell models.

209 y in Drosophila, patient-derived neurons and neuronal cell models.

210 assembly might be particularly important for neuronal cell motility in a soft or poorly adhesive matr

211 PA1 channels heterologously expressed in non-neuronal cells, mouse neurons and zebrafish neurons in v

212 In motile non-neuronal cells, myosin-II binds and exerts force upon ac

213 expressing BDNF generated increased daughter neuronal cell numbers post-differentiation, with acceler

214 iven human Hsp110 protein, HspA4L (Apg1), in neuronal cells of a transgenic G85R SOD1YFP ALS mouse st

215 elationship between the degree of binding to neuronal cells of different types of oligomers formed fr

216 The defect was more severe in differentiated neuronal cells of dNPCs and dSY5Y.

217 ected retrograde (dynein based) transport in neuronal cells or mouse nerves.

218 nal bundles in neurite-like processes in non-neuronal cells overexpressing Tau, cell-free reconstitut

219 alpha7 is also expressed in non-neuronal cells, particularly immune cells, where it play

220 y required in the gut endoderm tissue, a non-neuronal cell population, where it mediates adhesion to

221 maturation of a variety of neuronal and non-neuronal cell populations, including those involved in p

222 that soluble Abeta from APP/PS1 mice impairs neuronal cell proliferation using neurosphere cultures.

223 system signaling, AChE can also modulate non-neuronal cell properties, although it remains controvers

224 nonical modes-of-action to infer pathways of neuronal cell protection connected to drug mechanism.

225 Over-expressing pUL37 x 1 in neuronal cells protects against staurosporin and 6-hydro

226 Infected non-neuronal cells release neurotoxic factors such as the vi

227 morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varyin

228 Overexpression of functional NMDAR in non-neuronal cells results in cell death by excitotoxicity,

229 Non-neuronal cells showed clear transcriptional responses th

230 isplayed differential promoter activities in neuronal cells; specifically, haplotype 2 (containing va

231 Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, kerati

232 act to modulate purine receptor activity in neuronal cells, suggesting a molecular mode for in vivo

233 Moreover, miR-133a overexpression in CATH.a neuronal cells suppressed TAT with concomitant upregulat

234 serum antibodies against one or more of the neuronal cell surface antibodies compared with four (4%)

235 based on small case series before the era of neuronal cell surface antibody discovery.

236 beta1-C121W subunits are expressed at the neuronal cell surface in vivo However, despite this, bet

237 ween Wnt-5a and its Frizzled receptor at the neuronal cell surface.

238 3%; P < .001), and had more often coexisting neuronal cell-surface antibodies, mainly against gamma-a

239 igh-affinity association to two receptors on neuronal cell surfaces as the first step of invasion.

240 a central role in dorsal root ganglion (DRG) neuronal cell survival and neurotransmission by transpor

241 growth morphodynamic behaviors in a cultured neuronal cell system.

242 r aim was to develop a protocol for freezing neuronal cells that is compatible with ATAC-Seq; we focu

243 ectrometry to identify proteins expressed in neuronal cells the abundance of which was altered after

244 findings indicate that the susceptibility of neuronal cells to different types of misfolded oligomeri

245 by the Akt/GSK3beta signaling cascade in non-neuronal cells to trigger rapid, dysregulated CME.

246 No evidence of neuronal cell toxicity or induction of inflammatory cell

247 PD mutations leading to energy depletion and neuronal cell toxicity.

248 ular code provides a basis for understanding neuronal cell type specification in RGCs.

249 deployment of shared presynaptic proteins in neuronal cell type-specific functions.

250 supports the biosynthetic needs of a normal neuronal cell type.

251 ding the structure-function relationship and neuronal cell-type classification.

252 tion factors directly involved in cerebellar neuronal cell-type specification and differentiation.

253 e "second brain" because of the diversity of neuronal cell types and complex, integrated circuits tha

254 To improve the classification of neuronal cell types and the functional characterization

255 ologies for creating a complete inventory of neuronal cell types and their connections in multiple sp

256 future radiotracers that can identify other neuronal cell types and would allow visualization and in

257 It is possible that individual neuronal cell types are not specified by unique transcri

258 rcuits with particular attention to defining neuronal cell types by input and output information stre

259 l neurons show that selective dysfunction of neuronal cell types cannot account for the specific vuln

260 rofiles for 27 cell types and recovered rare neuronal cell types corresponding to as few as one or tw

261 Although the development of different neuronal cell types during early zebrafish (Danio rerio)

262 Three distinct neuronal cell types have been previously defined in the

263 e toxic accumulation of PAP in yeast and non-neuronal cell types in mice [4, 5].

264 Enteric glia also interact with various non-neuronal cell types in the gut wall such as enterocytes,

265 We revisit the classification of neuronal cell types in the nervous system of the nematod

266 2/Nsg1 and P19/Nsg2 are not expressed in all neuronal cell types in vitro.

267 Individual neuronal cell types predominantly express a single FXG t

268 otypic slices, which retain the diversity of neuronal cell types present at postnatal ages, including

269 Moreover, although all neuronal cell types tested exhibited abnormal functional

270 The spinal cord consists of multiple neuronal cell types that are critical to motor control a

271 stereotyped proportions of one glial and six neuronal cell types that are generated in overlapping wa

272 contributions of different neuronal and non-neuronal cell types to hypothalamic inflammatory process

273 ew aims to compare cortical cell numbers and neuronal cell types to the elaboration of progenitor pop

274 A few non-neuronal cell types were detected, including microglia.

275 ptic vesicle release properties vary between neuronal cell types, but in most cases the molecular bas

276 A comprehensive characterization of neuronal cell types, their distributions, and patterns o

277 sociations, were unexpectedly present in non-neuronal cell types.

278 cytes, adipocytes, osteoblasts, and multiple neuronal cell types.

279 back circuits and the diversity of mammalian neuronal cell types.

280 e--and the challenges--of defining mammalian neuronal cell types.

281 embryonically to give rise to differentiated neuronal cell types.

282 ograms has implications for the evolution of neuronal cell types.

283 t from self-renewal and differentiation into neuronal cell types.

284 ar hierarchies and improperly classify major neuronal cell types.

285 es have fomented interest in identifying all neuronal cell types.

286 we express Caspase-LOV specifically in three neuronal cell types: retinal, sensory, and motor neurons

287 mRNA and precursor protein expression in non-neuronal cells varies to a great degree as to the extent

288 genetic variation in murine Il21r influences neuronal cell viability after ischemia by modulating rec

289 restoration of cellular iron homeostasis and neuronal cell viability elicited by inhibition of PHD2 u

290 y experiment, a primary rat subpopulation of neuronal cells was selected for based on high, intracell

291 RNA (shRNA), which was validated in cultured neuronal cells, we found that SRC-1 gene knockdown speci

292 In contrast to non-neuronal cells, we show here that the ICP4 locus cassett

293 patients, transgenic mouse models of AD, and neuronal cells were used to investigate the molecular me

294 ograde transport velocity of mitochondria in neuronal cells, whereas eribulin and vincristine inhibit

295 ast studies did not consider the role of non-neuronal cells, which are now known to play an important

296 lication, we studied AP-7 rat olfactory bulb neuronal cells, which can differentiate in vitro.

297 gh, persistent reporter gene activity in non-neuronal cells while an independent expression cassette

298 e role of SOCE has been poorly documented in neuronal cells with more complicated calcium dynamics.

299 JNKs among MAP2Ks and MAPKs respectively in neuronal cells, with JNK activity positively regulating

300 ing the migration and differentiation of the neuronal cells within the retina.