ライフサイエンスコーパス: Bergmann glia

1 nd was particularly strong in the cerebellar Bergmann glia.

2 ncephalic radial glia, as well as cerebellar Bergmann glia.

3 as also detected in both granule neurons and Bergmann glia.

4 ursors and it induces the differentiation of Bergmann glia.

5 an alteration of glutamate uptake played by Bergmann glia.

6 mma-5 acts as a TARP and serves this role in Bergmann glia.

7 ell dendritic growth and their enwrapping by Bergmann glia.

8 ensheathment of CF/Purkinje cell synapses by Bergmann glia.

9 , suggested a role in the differentiation of Bergmann glia.

10 this enzyme in promoting differentiation of Bergmann glia.

11 tion of ventricular zone-derived neurons and Bergmann glia.

12 he SoxB1 subgroup), is also expressed in the Bergmann glia.

13 ht link between copper homeostasis in PN and Bergmann glia.

14 elopmental interaction of Purkinje cells and Bergmann glia.

15 protein, expressed in astrocytes as well as Bergmann glia.

16 but is restricted to proliferating GCPs and Bergmann glia.

17 plitude of the AMPA receptor response in the Bergmann glia (840 +/- 240%; n = 8) with the shift in th

18 rotein gamma-5, which is highly expressed in Bergmann glia, a cell type possessing only CP-AMPARs.

19 t cerebellum, Sox 1 is only expressed in the Bergmann glia, a population of radial glia present in th

20 amate to outside-out patches from cerebellar Bergmann glia activates anion-potentiated glutamate tran

21 of Purkinje cells (PC) in regions of robust Bergmann glia activation in Cln3(-/-) mice and human JNC

22 We used the change in the EC50 of the Bergmann glia AMPA receptors produced by cyclothiazide (

23 ) channels inhibited ectopic transmission to Bergmann glia and decreased EPSC decay time.

24 d developmental failure of Purkinje neurons, Bergmann glia and granule neurons.

25 we observe parallel ontogeny of D-serine in Bergmann glia and NR2A/B in Purkinje cells, suggesting a

26 lar distribution of GABA(A) receptors in the Bergmann glia and Purkinje cells in the molecular layer

27 uron precursors and precocious maturation of Bergmann glia and Purkinje neurons.

28 Bergmann glia and retinal Muller cells, nonforebrain ast

29 In addition, the protein was induced in Bergmann glia and scattered microglia/macrophages in the

30 ter granule cells detach from the surface of Bergmann glia and the somata become transiently round, w

31 ty, Purkinje cells (Pcs), an early cohort of Bergmann glia, and four classes of GABAergic interneuron

32 in-1 is found in perivascular astrocytes and Bergmann glia, and is not PSD-enriched.

33 and/or cytoplasmic inclusions in astrocytes, Bergmann glia, and neurons, as well as relationships bet

34 granule and Purkinje cells, the alignment of Bergmann glia, and the integrity of the basement membran

35 long the Purkinje cell layer (PCL), in which Bergmann glia are generated up to first the postnatal we

36 Cerebellar Bergmann glia are radial astrocytes that are implicated

37 beta2 and beta3, are expressed in cerebellar Bergmann glia as well as granule neurons.

38 is expressed in newborn and adult cerebellar Bergmann glia astrocytes.

39 The first morphologically definable Bergmann glia, astrocytes, and oligodendrocytes were als

40 lgi cells, and molecular layer interneurons; Bergmann glia, astrocytes, and resting microglia also ex

41 0 dpi, most labeled cells had developed into Bergmann glia, astrocytes, oligodendrocytes, and interne

42 reveal a novel role of Ric-8a in modulating Bergmann glia-basement membrane adhesion during foliatio

43 ts that Ric-8a is essential for the enhanced Bergmann glia-basement membrane adhesion required for fi

44 We also find that weakening Bergmann glia-basement membrane interaction by beta1 int

45 tical basal radial glia (bRG) and cerebellar Bergmann glia (BG) are basal progenitors derived from ve

46 stence of radial glia (RG)-like cells called Bergmann glia (BG) are hallmarks of the mammalian cerebe

47 Focusing on cerebellar Bergmann glia (BG) cells, which exhibit the highest rate

48 hat directed expression of polyQ-ataxin-7 in Bergmann glia (BG) in transgenic mice leads to ataxia an

49 ion of glia and subsequent disruption of the Bergmann glia (BG) scaffold.

50 process, granule neurons (GNs) migrate along Bergmann glia (BG), which are specialized astroglial cel

51 rasynaptic transmission from PFs to adjacent Bergmann glia (BG).

52 involves the generation of granule cells and Bergmann glias (BGs).

53 Thus, large networks of Bergmann glia can be activated by specific animal behavi

54 s high-concentration glutamate transients at Bergmann glia cell membranes that are necessary to activ

55 ease may provide a geographical cue to guide Bergmann glia cell membranes to surround active synapses

56 In the cerebellum, Bergmann glia cells (BGs) are intimately associated with

57 PA receptors expressed by Purkinje cells and Bergmann glia cells are activated predominantly by synap

58 The results demonstrate that astrocytes and Bergmann glia cells are the first cells of the brain par

59 In the cerebellar cortex the processes of Bergmann glia cells encase synapses between presynaptic

60 y glutamate transporter-mediated currents in Bergmann glia cells follow the rules of synaptic release

61 Specific assays show that in Bergmann glia cells Gpr37l1 is associated with primary c

62 ith impaired glutamate transport in cultured Bergmann glia, cerebellar slices and cerebellar synaptos

63 ebellar molecular layer thickness or prevent Bergmann glia degeneration.

64 study addresses the function of caspase-3 in Bergmann glia development by utilizing a Bergmann glial

65 vivo results in deficient granule neuron and Bergmann glia differentiation as well as in abnormal Pur

66 as well as the importance of time-dependent Bergmann glia differentiation during cerebellar developm

67 er an unexpected role for PTEN in regulating Bergmann glia differentiation, as well as the importance

68 Recent studies have shown that cerebellar Bergmann glia display coordinated Ca(2+) transients in l

69 eceptor pathway, is specifically required in Bergmann glia during cerebellar foliation.

70 prenatally but became enriched in cerebellar Bergmann glia early postnatally and then was also presen

71 rters (homologous to the transporters in the Bergmann glia ensheathing the Purkinje cells), nor did i

72 Using two-photon microscopy we found that Bergmann glia exhibit three forms of Ca(2+) excitation i

73 results demonstrate for the first time that Bergmann glia express functional GlyT1 that can work in

74 To determine whether Bergmann glia express functional transporters that can m

75 times on the Rotarod, suggesting a role for Bergmann glia-expressed Punc in the cerebellar control o

76 n arises in networks of at least hundreds of Bergmann glia extending across several hundred microns o

77 t the onset of foliation, when ric-8a mutant Bergmann glia fail to maintain adhesion to the basement

78 ity traces for up to >100 Purkinje cells and Bergmann glia from single recordings.

79 Moreover, the Bergmann glia GABA(A) receptors were often located in cl

80 pressed in both Purkinje cells (GluR2/3) and Bergmann glia (GluR4) throughout postnatal development.

81 ll patch-clamp recordings were obtained from Bergmann glia in mice cerebellar slices to determine whe

82 ings were obtained from Purkinje neurons and Bergmann glia in mouse cerebellar slices to determine th

83 nd Na+/Cl--dependent taurine transporters in Bergmann glia in slices.

84 receptor subunit is expressed exclusively in Bergmann glia in the adult rodent.

85 e glomerular layer of olfactory bulbs and in Bergmann glia in the cerebellum.

86 resent in protoplasmic astrocytes, including Bergmann glia in the cerebellum.

87 rya of radial cells in the telencephalon; 2) Bergmann glia in the cerebellum; 3) astrocytes; 4) tanic

88 HO-1 was induced in Bergmann glia in the vermis of cerebellum.

89 D-Serine in the radial processes of Bergmann glia is also well positioned to regulate NMDA r

90 Furthermore, loss of Huwe1 in Bergmann glia leads to extensive disorganization of this

91 We provide evidence that loss of PTEN in Bergmann glia leads to premature differentiation of this

92 entrated principally in the processes of the Bergmann glia located in the vicinity of the Purkinje ce

93 The second is to establish the correct Bergmann glia morphology, which is crucial for granule c

94 transformation in the developmental state of Bergmann glia occurring after suppression of caspase-3 a

95 NBC mRNA was present in glial cells (e.g., Bergmann glia of cerebellum and hippocampal astrocytes)

96 ell population that is intermingled with the Bergmann glia of the adult murine cerebellar cortex, exp

97 and generated mice that express ataxin-7 in Bergmann glia of the cerebellum with the Gfa2 promoter.

98 o neuronal cells but also was located in the Bergmann glia of the postnatal cerebellum.

99 ever, its expression changed from neurons to Bergmann glia once these glial cells had completed their

100 ar glutamate transporter GLAST, expressed in Bergmann glia, only fall progressively from 3 months onw

101 ic neurons and defects in fissure formation, Bergmann glia organization and basement membrane integri

102 O mice, possibly as a consequence of altered Bergmann glia orientation or reduced granule cell number

103 kinje cell synapses during early ages and at Bergmann glia plasma membrane in the adult.

104 Thus, Bergmann glia play a previously unappreciated role in co

105 hat the formation of this Sox2/Sox9 positive Bergmann glia population does not require the presence o

106 luR2/3 immunolabeling also occurred in these Bergmann glia processes as well as in the Bergmann fiber

107 e neuronal GABA(A) receptors were wrapped by Bergmann glia processes containing glial GABA(A) recepto

108 nd gamma1 immunoreactivity were localized in Bergmann glia processes that wrapped Purkinje cell somat

109 filled approximately ellipsoidal domains of Bergmann glia processes.

110 luding astrocytes, large projection neurons, Bergmann glia, Schwann cells, and ganglionic satellite c

111 abnormalities result from primary defects in Bergmann glia since mutations in granule cells do not sh

112 Bergmann glia-specific expression of mutant ataxin-7 was

113 Expression of the Bergmann glia-specific glutamate transporter GLAST was r

114 ocytes, microglia, and subsets of cerebellar Bergmann glia, spinal motor neurons, macrophages, and de

115 n marker, but was present in differentiating Bergmann glia that expressed brain lipid binding protein

116 ceptor and glutamate transporter currents in Bergmann glia that have a rapid onset, suggesting that g

117 ATP7A switches during development from PN to Bergmann glia, the cells supporting PN function in adult

118 estingly, despite the apparent death of some Bergmann glia, there was up-regulation of glial fibrilla

119 cytosolic Ca(2+) regulates uptake of K(+) by Bergmann glia, thus providing a powerful mechanism for c

120 -out modes, respectively, depolarizations of Bergmann glia to +20 mV induced a 73% increase in the op

121 in neuronal migration, glutamate stimulates Bergmann glia to form and release D-serine, which, toget

122 lar K(+) evoked by agonist-induced Ca(2+) in Bergmann glia transiently increased spike activity of Pu

123 n addition, the differentiation of RGCs into Bergmann glias was suppressed in KO mice.

124 ved in cerebellar cortex: Purkinje cells and Bergmann glia were positive for both subunits, whereas g

125 In addition, Bergmann glia were TUNEL positive at P21, and they expre

126 7B target protein, ceruloplasmin, from PN to Bergmann glia, where ATP7A (Menkes disease protein) is p

127 nt with positive immunostaining for GlyT1 in Bergmann glia while inhibitors of glycine transport thro

128 and decreased the number of differentiating Bergmann glia, without significantly altering the non-gl