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1 Bergmann glia and retinal Muller cells, nonforebrain ast
2 Bergmann glia-specific expression of mutant ataxin-7 was
3 Bergmann glial cells (BGs), astrocytes of the cerebellar
4 Bergmann glial processes are abnormal and GFAP-positive
5 rya of radial cells in the telencephalon; 2) Bergmann glia in the cerebellum; 3) astrocytes; 4) tanic
8 ted with the breaches in the BM and abnormal Bergmann glial networks during postnatal cerebellar deve
12 process, granule neurons (GNs) migrate along Bergmann glia (BG), which are specialized astroglial cel
13 O mice, possibly as a consequence of altered Bergmann glia orientation or reduced granule cell number
14 pressed in both Purkinje cells (GluR2/3) and Bergmann glia (GluR4) throughout postnatal development.
15 The results demonstrate that astrocytes and Bergmann glia cells are the first cells of the brain par
17 PA receptors expressed by Purkinje cells and Bergmann glia cells are activated predominantly by synap
19 ved in cerebellar cortex: Purkinje cells and Bergmann glia were positive for both subunits, whereas g
23 important counterexamples to both James' and Bergmann's temperature-size rules, respectively, undermi
24 vivo results in deficient granule neuron and Bergmann glia differentiation as well as in abnormal Pur
25 ings were obtained from Purkinje neurons and Bergmann glia in mouse cerebellar slices to determine th
34 and/or cytoplasmic inclusions in astrocytes, Bergmann glia, and neurons, as well as relationships bet
36 es indicates that the glutamate transient at Bergmann glial membranes reaches a lower concentration t
37 s high-concentration glutamate transients at Bergmann glia cell membranes that are necessary to activ
38 is expressed by virtually all astrocytes, by Bergmann glial cells in cerebellum, by Muller cells in r
40 cytosolic Ca(2+) regulates uptake of K(+) by Bergmann glia, thus providing a powerful mechanism for c
44 e neuronal GABA(A) receptors were wrapped by Bergmann glia processes containing glial GABA(A) recepto
45 stence of radial glia (RG)-like cells called Bergmann glia (BG) are hallmarks of the mammalian cerebe
46 two patients showed loss of Purkinje cells, Bergmann gliosis and deep cerebellar white matter inflam
49 tical basal radial glia (bRG) and cerebellar Bergmann glia (BG) are basal progenitors derived from ve
51 utamate transporters expressed by cerebellar Bergmann glial cells are activated by neurotransmitter r
52 amate to outside-out patches from cerebellar Bergmann glia activates anion-potentiated glutamate tran
54 prenatally but became enriched in cerebellar Bergmann glia early postnatally and then was also presen
55 ocytes, microglia, and subsets of cerebellar Bergmann glia, spinal motor neurons, macrophages, and de
57 r, quantal events recorded in rat cerebellar Bergmann glial cells (BGs) have fast kinetics, comparabl
58 Recent studies have shown that cerebellar Bergmann glia display coordinated Ca(2+) transients in l
62 ith impaired glutamate transport in cultured Bergmann glia, cerebellar slices and cerebellar synaptos
64 as well as the importance of time-dependent Bergmann glia differentiation during cerebellar developm
65 nted folia, profound granule cell depletion, Bergmann gliosis, and signs of Purkinje cell deafferenta
66 n marker, but was present in differentiating Bergmann glia that expressed brain lipid binding protein
67 and decreased the number of differentiating Bergmann glia, without significantly altering the non-gl
68 -8a mutation in mice results in disorganized Bergmann glial scaffolding, defective granule cell migra
69 owed severe ataxia associated with disrupted Bergmann fiber scaffold formation, impaired granule neur
70 ts that Ric-8a is essential for the enhanced Bergmann glia-basement membrane adhesion required for fi
71 change because modern coyotes do not follow Bergmann's rule, which states body size increases with d
72 times on the Rotarod, suggesting a role for Bergmann glia-expressed Punc in the cerebellar control o
74 ic neurons and defects in fissure formation, Bergmann glia organization and basement membrane integri
76 ll patch-clamp recordings were obtained from Bergmann glia in mice cerebellar slices to determine whe
77 NBC mRNA was present in glial cells (e.g., Bergmann glia of cerebellum and hippocampal astrocytes)
78 ease may provide a geographical cue to guide Bergmann glia cell membranes to surround active synapses
79 lar K(+) evoked by agonist-induced Ca(2+) in Bergmann glia transiently increased spike activity of Pu
80 study addresses the function of caspase-3 in Bergmann glia development by utilizing a Bergmann glial
81 hat directed expression of polyQ-ataxin-7 in Bergmann glia (BG) in transgenic mice leads to ataxia an
82 and generated mice that express ataxin-7 in Bergmann glia of the cerebellum with the Gfa2 promoter.
84 y glutamate transporter-mediated currents in Bergmann glia cells follow the rules of synaptic release
85 ceptor and glutamate transporter currents in Bergmann glia that have a rapid onset, suggesting that g
86 abnormalities result from primary defects in Bergmann glia since mutations in granule cells do not sh
87 e transporter currents were also elicited in Bergmann glial cells and Purkinje neurons of the cerebel
89 rotein gamma-5, which is highly expressed in Bergmann glia, a cell type possessing only CP-AMPARs.
90 ar glutamate transporter GLAST, expressed in Bergmann glia, only fall progressively from 3 months onw
91 nt with positive immunostaining for GlyT1 in Bergmann glia while inhibitors of glycine transport thro
95 nd gamma1 immunoreactivity were localized in Bergmann glia processes that wrapped Purkinje cell somat
97 erebellar cortex, APOE mRNA was seen only in Bergmann glial cells and scattered astrocytes but not in
98 We provide evidence that loss of PTEN in Bergmann glia leads to premature differentiation of this
101 we observe parallel ontogeny of D-serine in Bergmann glia and NR2A/B in Purkinje cells, suggesting a
105 n of glutamate transporters in an individual Bergmann glial cell enhanced mIPSC frequency recorded in
106 lgi cells, and molecular layer interneurons; Bergmann glia, astrocytes, and resting microglia also ex
107 0 dpi, most labeled cells had developed into Bergmann glia, astrocytes, oligodendrocytes, and interne
109 reveal a novel role of Ric-8a in modulating Bergmann glia-basement membrane adhesion during foliatio
110 t the onset of foliation, when ric-8a mutant Bergmann glia fail to maintain adhesion to the basement
112 luding astrocytes, large projection neurons, Bergmann glia, Schwann cells, and ganglionic satellite c
114 mate concentrations or by using nonsaturated Bergmann glial AMPA receptors to monitor presynaptic rel
115 granule and Purkinje cells, the alignment of Bergmann glia, and the integrity of the basement membran
116 ty, Purkinje cells (Pcs), an early cohort of Bergmann glia, and four classes of GABAergic interneuron
117 -out modes, respectively, depolarizations of Bergmann glia to +20 mV induced a 73% increase in the op
121 ll migration secondary to disorganization of Bergmann glial cell fibers cause cerebellar developmenta
123 n arises in networks of at least hundreds of Bergmann glia extending across several hundred microns o
128 In the cerebellar cortex the processes of Bergmann glia cells encase synapses between presynaptic
130 However, the functional significance of Bergmann glial Ca(2+) signaling remains poorly understoo
131 transformation in the developmental state of Bergmann glia occurring after suppression of caspase-3 a
132 ter granule cells detach from the surface of Bergmann glia and the somata become transiently round, w
134 hat the formation of this Sox2/Sox9 positive Bergmann glia population does not require the presence o
136 er an unexpected role for PTEN in regulating Bergmann glia differentiation, as well as the importance
137 of Purkinje cells (PC) in regions of robust Bergmann glia activation in Cln3(-/-) mice and human JNC
138 expressed glutamate transporters can shield Bergmann glial AMPA receptors and presynaptic metabotrop
139 estingly, despite the apparent death of some Bergmann glia, there was up-regulation of glial fibrilla
140 in neuronal migration, glutamate stimulates Bergmann glia to form and release D-serine, which, toget
141 Using two-photon microscopy we found that Bergmann glia exhibit three forms of Ca(2+) excitation i
142 results demonstrate for the first time that Bergmann glia express functional GlyT1 that can work in
143 e vermis, the densities of microglia and the Bergmann glial expression of metallothionein I/II and th
144 gration of immature granule neurons down the Bergmann glial fibers into the internal granule cell lay
145 f MMP-2 was mainly localized in the EGL, the Bergmann glial fibers, and the Purkinje cell layer (PCL)
146 se Bergmann glia processes as well as in the Bergmann fibers, it was more pronounced in the Purkinje
147 plitude of the AMPA receptor response in the Bergmann glia (840 +/- 240%; n = 8) with the shift in th
148 lar distribution of GABA(A) receptors in the Bergmann glia and Purkinje cells in the molecular layer
149 rters (homologous to the transporters in the Bergmann glia ensheathing the Purkinje cells), nor did i
151 t cerebellum, Sox 1 is only expressed in the Bergmann glia, a population of radial glia present in th
154 ons secrete FGF9 to control formation of the Bergmann fiber scaffold, which in turn, guides their own
157 entrated principally in the processes of the Bergmann glia located in the vicinity of the Purkinje ce
159 release may account for the majority of the Bergmann glial AMPA response evoked by climbing fiber st
160 se results are consistent with a role of the Bergmann glial GABA(A) receptors in sensing GABAergic sy
161 transmission activates AMPA receptors on the Bergmann glial cell processes that envelop parallel fibr
162 ell population that is intermingled with the Bergmann glia of the adult murine cerebellar cortex, exp
163 luR2/3 immunolabeling also occurred in these Bergmann glia processes as well as in the Bergmann fiber
165 ny neuronal population, but was localized to Bergmann glial in the cerebellum and a subset of the oli
166 ever, its expression changed from neurons to Bergmann glia once these glial cells had completed their
167 ATP7A switches during development from PN to Bergmann glia, the cells supporting PN function in adult
168 7B target protein, ceruloplasmin, from PN to Bergmann glia, where ATP7A (Menkes disease protein) is p
172 long the Purkinje cell layer (PCL), in which Bergmann glia are generated up to first the postnatal we
173 osphacan immunoreactivity is associated with Bergmann glial fibers in the molecular layer and their c
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