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1 ite of ATP it is present in every neuron and glial cell.
2 igment epithelium and for neighboring Muller glial cells.
3 for interneurons and not for motoneurons or glial cells.
4 stem (ENS), which is composed of neurons and glial cells.
5 a gain-of-function chloride channelopathy of glial cells.
6 lecules, and suppressed nigral activation of glial cells.
7 to hair cell-like cells, but not neurons or glial cells.
8 pendent protein kinase 1 (PKG1) signaling in glial cells.
9 tiate a partial formation of new neurons and glial cells.
10 e human brain, and a range of 40-130 billion glial cells.
11 niques to differentiate between neuronal and glial cells.
12 tatory and inhibitory neurons, as well as in glial cells.
13 switch to distinguish astrocytes from other glial cells.
14 peripheral nervous system (PNS), and enteric glial cells.
15 , where they mediate modulatory roles and in glial cells.
16 proteins, and decreased activation of Muller glial cells.
17 selectively remove C9orf72 from neurons and glial cells.
18 tochondrial function in cultured neurons and glial cells.
19 diated cholesterol synthesis in neuronal and glial cells.
20 inhibit expression of inflammatory genes in glial cells.
21 gulation when its function is manipulated in glial cells.
22 acroautophagy, and in some cases transfer to glial cells.
23 rectifying K(+) channel Kir4.1 in satellite glial cells.
24 onomously assembled by these axon-associated glial cells.
25 ify and measure specific types of neurons or glial cells.
26 and lytic infection by neurotropic JCPyV in glial cells.
27 rectifying K(+) channel Kir4.1 in satellite glial cells.
28 the accumulation of lipid droplets in those glial cells.
29 including pre- and post-synaptic neurons and glial cells; 60 papers were included in this review.
32 studies have suggested that it also inhibits glial cell activation in rodents, and may alter opioid-m
33 enzyme expression, fragmented mitochondria, glial cell activation, muscle atrophy, weight loss, and
34 To enable stable measurement of neuronal and glial cell activity in behaving mice, we have developed
35 ut there has been little study of persistent glial cell activity in brains of athletes with sports-re
42 ccumulation of lipid droplets in neighboring glial cells, an event that may, in turn, contribute to n
43 stricted to two populations of Repo-positive glial cells: an invasive population, characterized by JN
46 tion and premature differentiation of radial glial cells and aberrant positioning of newborn neurons.
47 e at the fovea recovered and the presence of glial cells and cystoid space resolved gradually after s
48 alytes from single iPSC-derived neuronal and glial cells and have molecularly characterized subpopula
49 gest decreased axonal density with increased glial cells and higher myelination in this subpopulation
51 rtical neural progenitor cells (NPCs)-radial glial cells and intermediate progenitor cells-was reduce
52 y results from a pool of infectious virus in glial cells and is regulated by the antiviral RNAi pathw
53 y, we performed time-lapse imaging of radial glial cells and measured filopodial motility in the inta
59 nistically, IL4-10 inhibited the activity of glial cells and reduced spinal cord and dorsal root gang
60 mesenchyme, differentiated into neurons and glial cells and showed neuronal activity, as measured by
64 ctive axons are preferentially myelinated by glial cells, and if so, whether axo-glial synapses are i
65 new link between commensal bacteria, enteric glial cells, and ILC3s that is required for intestinal h
66 ells, their antineuroinflammatory effects on glial cells, and the ability to ameliorate nesting behav
69 se mutation (S140G), neurons accumulate, and glial cells are dispersed along the rostral migratory st
71 the primary immune responders in the brain, glial cells are implicated as key players in the onset a
77 ows that astrocytes, the most numerous brain glial cells, are sensitive to physiological changes in P
78 e a novel function for the Kif13b kinesin in glial cells as a key component of the PI3K/AKT signaling
79 challenge us to consider the contribution of glial cells as drivers of epileptogenesis in acquired ep
82 n of the metabolic activation in neurons and glial cells, as well as of the macroscopic measurements
84 ptor AXL is highly expressed by human radial glial cells, astrocytes, endothelial cells, and microgli
85 and that perisynaptic Schwann cells (PSCs), glial cells at the NMJ, regulate morphological stability
87 tion of surface receptors within neurons and glial cells by affecting their delivery to lysosomes for
88 on of NF-kappaB-dependent gene expression in glial cells by stabilizing nuclear corepressor proteins,
89 We have recently demonstrated that reactive glial cells can be directly reprogrammed into functional
92 ation and shows that calcium originated from glial cells can regulate neuronal intracellular pathways
94 wing perturbations to peripheral myelinating glial cells, centrally derived oligodendrocyte progenito
96 itions colonization of the lamina propria by glial cells commences during early postnatal stages but
97 Following neuronal degeneration, quiescent glial cells converted to an activated state showing a de
102 Inflammasome-mediated IL-1beta secretion in glial cells depends on TLR2 and MyD88 adapter-like/TIRAP
105 em (e.g., neurogenesis, synaptic plasticity, glial cell development) and immune functions (e.g., immu
107 ms of molecular control related to nerve and glial cell differentiation, neuronal excitability, axon
108 whether mechanotransduction plays a role in glial cell differentiation, we cultured Schwann cells (S
109 in, demonstrating that, although perineurial glial cells display plasticity despite myelin perturbati
110 step process in which Pax6-expressing radial glial cells divide in the VZ to produce Tbr2-expressing
111 igation of spindle orientation during radial glial cell division, revealed that NFIX promotes the gen
112 ance and exaggerated release of glutamate by glial cells during immune activation leads to glutamate
113 in tissue pathology, including inflammation, glial cell dysfunction, and angiogenesis, its role in th
114 netrin-1 signaling is involved in the NG2(+) glial cell early proliferative, late repopulation, and d
117 dy how an essential subpopulation of enteric glial cells (EGCs) residing within the intestinal mucosa
122 bleaching and photoconversion experiments in glial cells expressing vimentin, glial fibrillary acidic
124 that in Crohn's disease, enteric neurons and glial cells form a functional unit reacting to inflammat
128 , we examined the effects of BNN27 on neural/glial cell function, apoptosis, and inflammation in the
129 protein, and we demonstrate that myelinating glial cells function normally in the presence of high CH
130 fluorescence stainings using markers against glial cells (GFAP), endothelial cells (CD34) and macroph
134 t endogenous netrin-1 plays a role in NG2(+) glial cell homeostasis that is distinct from its role in
137 neuron cultures is possible, the removal of glial cells ignores physiologically relevant cell-cell i
139 s was increased by CS from Brucella-infected glial cells in an IL-1beta-dependent fashion, and the in
140 us consensus about the relative abundance of glial cells in human brains that persisted for half a ce
141 ersistent pain in animal models, the role of glial cells in human pain disorders remains unknown.
144 g-standing controversy regarding the role of glial cells in regulating blood flow, demonstrating that
146 These results demonstrate that a subset of glial cells in the adult auditory nerve exhibit several
149 expressed by primary sensory neurons and by glial cells in the central nervous system, but their exp
153 and it causes cell-cycle deficits of radial glial cells in the embryonic mouse cortex and human fore
155 ces of the new insights into true numbers of glial cells in the human brain, and the promise and pote
157 the initial colonization and homeostasis of glial cells in the intestinal mucosa are regulated by th
159 examined the repopulation dynamics of NG2(+) glial cells in the mature and aged mice gray matter.
161 ation and characterized, for the first time, glial cells in the planarian CNS that respond to injury
163 in neuronal development, and the function of glial cells in this process is not fully understood.
165 roadblock for mammalian spinal cord repair, glial cells in zebrafish form a bridge across severed sp
166 roduction by brain-resident cells, including glial cells, in resistance against cerebral infections r
167 t brain cell types, especially in non-neuron glial cells, induces fragile X syndrome (FXS) phenotypes
168 haII-spectrin breakdown products, SBDPs) and glial cell injury biomarker, glial fibrillary acidic pro
171 ity, but it has remained unclear whether NG2 glial cells integrate and respond to synaptic input.
173 mation in which overmigration of neurons and glial cells into the arachnoid space results in the form
176 These extracts were used to treat primary glial cells isolated from human APOE-targeted-replacemen
177 hat non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells
182 rted to be necessary for the function of the Glial cell line-derived neurotrophic factor (GDNF) famil
183 rophic effects, the therapeutic potential of glial cell line-derived neurotrophic factor (GDNF) has b
184 , we describe a novel, biphasic function for glial cell line-derived neurotrophic factor (GDNF) in th
186 brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) may b
187 m.SIGNIFICANCE STATEMENT Delivery of ectopic glial cell line-derived neurotrophic factor (GDNF) promo
190 we evaluate the differential potency of NGF, glial cell line-derived neurotrophic factor (GDNF), brai
191 We also found that intraspinally expressed glial cell line-derived neurotrophic factor (GDNF), but
192 tor tyrosine kinase that is activated by the glial cell line-derived neurotrophic factor family ligan
193 receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor family of ex
194 ice lacking the neurotrophic factor receptor glial cell line-derived neurotrophic factor family of re
195 ly if vanishingly small amounts (1 pg/ml) of glial cell line-derived neurotrophic factor were include
196 The ability of the HS-binding neuropeptide glial-cell-line-derived neurotrophic factor (GDNF) to in
198 bout the effects of ALS on motor neurons and glial cells, little is known about its effect on proprio
199 astrocytes, which are the major non-neuronal glial cells, may play an important role in AD pathogenes
202 ons only, with the prevailing view assigning glial cells mere specify supportive functions for synapt
205 servations indicate that therapies targeting glial cells might provide benefit for those afflicted by
206 anscription factors Distal-less 3 (DLX3) and Glial cell missing-1 (GCM1) have been shown to coordinat
207 ntiation, including hCYP19A1/aromatase P450, glial cells missing 1 (GCM1), frizzled 5 (FZD5), WNT2, S
208 on of H3R17 methylation results in defective glial cell morphology and a sensory defect in a subpopul
210 r disorder or animal models, such as reduced glial cell number in the prefrontal cortex of patients,
212 We expressed this EAAT1(P>R) mutation in glial cells of Drosophila larvae and found that these la
213 overexpression of sEH in the retinal Muller glial cells of non-diabetic mice resulted in similar ves
214 quaporin 4 (AQP4) is highly expressed in the glial cells of the central nervous system and facilitate
216 nce, viral infection, and replication in the glial cells of the CNS and escape from immunosurveillanc
217 porin-4 (AQP4), the primary water channel in glial cells of the mammalian brain, plays a critical rol
218 ly was found in the cytoplasm of neurons and glial cells of the prefrontal cortex at 4 and 24 hours p
220 ion occurring between different neuronal and glial cells or between neurons and other peripheral tiss
221 ested if CRB expression restricted to Muller glial cells or photoreceptors or co-expression in both i
223 sal EGCs is continuously renewed by incoming glial cells originating in the plexi of the gut wall.
227 lls or polydendrocytes, which are a resident glial cell population in the mature mammalian central ne
229 recursor cells, represent a new entity among glial cell populations in the central nervous system.
232 duces a local rise in cytoplasmic calcium in glial cell processes at these nonsynaptic functional jun
233 c spectrin structures in a small fraction of glial-cell processes in four types of glial cells cultur
234 ZIKA-NS2A, but not DENV-NS2A, reduces radial glial cell proliferation and causes AJ deficits in human
235 Dystroglycan also regulates perinatal radial glial cell proliferation and transition into intermediat
238 udies provide evidence of a novel pathway in glial cells regulated by swip-10 that limits DA neuron e
239 onal alterations, and loss of retinal Muller glial cells resembling human macular telangiectasia type
240 For instance, enteric glia, a collection of glial cells residing within the walls of the intestinal
242 protein 18 kDa (TSPO), a marker of activated glial cell response, in a cohort of National Football Le
244 ated in a temporal sequence, with all radial glial cells (RGCs) contributing to both lower and upper
246 rtical ventricular zone (VZ) contains radial glial cells (RGCs) with restricted fate potentials.
247 sitions from neuroepithelial cells to radial glial cells (RGCs), and later, a subpopulation of slowly
248 The polarity and organization of radial glial cells (RGCs), which serve as both stem cells and s
250 t their expression and function in satellite glial cells (SGCs) of sensory ganglia have not been expl
252 tina may contain nonastrocytic inner retinal glial cells, similar to those described in the avian ret
253 he proper number of the diverse neuronal and glial cell subtypes that constitute the functional retin
255 al mediated by gliotrophic FGF signaling.How glial cells, such as astrocytes, acquire their character
259 nervous system (ENS) consists of neurons and glial cells that differentiate from neural crest progeni
260 that MsContactin is selectively expressed by glial cells that ensheath the migratory neurons (express
262 CNS myelin is produced by oligodendrocytes, glial cells that extend multiple membrane processes to w
264 sterol also is required by oligodendrocytes, glial cells that make myelin, to express myelin genes an
265 th factor a (ctgfa) is induced in and around glial cells that participate in initial bridging events.
268 ic homeodomain CsREPO were both expressed in glial cells that surround sensory neurons and also in mu
269 n two processes that require phagocytosis by glial cells, the immune cells in the brain: neuronal cle
271 p in the submucosa, might arise from enteric glial cells through hormone-dependent PKA signaling.
272 They communicate with neurones and other glial cells through the release of signalling molecules.
273 Zac1 delayed the transition of apical radial glial cells to basal intermediate neuronal progenitors a
278 therapeutic approaches to reprogram resident glial cells to replace retinal neurons have been propose
279 nce for a defined, intrinsic contribution of glial cells to SMA disease pathogenesis and suggests tha
280 active neurons stimulate Ca(2+) increases in glial cells, triggering glial release of vasodilating ag
281 Despite the importance of this heterogeneous glial cell type for brain development and function, the
287 ive tissue comprised of six neuronal and one glial cell types, each of which develops in prescribed p
290 N1 is mostly expressed by neurons and not by glial cells under normal conditions, similar to the expr
292 is, meningitis, and meningoencephalitis, and glial cells were identified as principal targets of infe
295 rt by suppressing Notch activation in radial glial cells, which leads to the increased expression of
296 rescued by restoring chloride homeostasis to glial cells with a Na(+)-K(+)-2Cl(-) cotransporter.
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