ライフサイエンスコーパス: glomus cell

1 of [Ca(2+)](i) and intercellular coupling in glomus cells.

2 by ratio fluorometry in isolated cat and rat glomus cells.

3 ings enveloped tyrosine hydroxylase-positive glomus cells.

4 g of the suppressant effect on K+ current of glomus cells.

5 tors modulate junctional conductance between glomus cells.

6 d variations in the response pattern between glomus cells.

7 ous response pattern similar to that seen in glomus cells.

8 for identifying highly expressed genes in CB glomus cells.

9 nt G protein-coupled receptor (Olfr78) in CB glomus cells.

10 s an approximately 20 pS channel in isolated glomus cells.

11 ld by an inhibitor of Kv2, a major Kv in rat glomus cells.

12 tion of hypoxia and acidosis at the level of glomus cells.

13 sensitivity to acidosis and hypoxia in most glomus cells.

14 3 (ASIC3) which we had identified earlier in glomus cells.

15 a did not change the Em of nerve endings and glomus cells.

16 d by hypoxia were greater in CHF versus sham glomus cells.

17 sensitivity of IK and RMP to hypoxia in sham glomus cells.

18 ssion of Kv3.4 but not Kv4.3 channels in CHF glomus cells.

19 transmembrane Ca2+ influx into carotid body glomus cells.

20 geted to the plasma membrane in carotid body glomus cells.

21 TRPC proteins studied were present in type I glomus cells.

22 ent nerve terminals that encircle individual glomus cells.

23 Release of transmitter from glomus cells activates the sensory afferent fibers to tr

24 In carotid body chemosensitive glomus cells, activation of toll-like receptors increase

25 ntified acetate (which is known to affect CB glomus cell activity) as an agonist for the most highly

26 Carotid body glomus cells also expressed IL-1 receptor and responded

27 Isolated carotid body glomus cells also sense glucose, and animal studies have

28 In carotid body glomus cells, AMPK is thought to link changes in arteria

29 In CHF glomus cells, an AT1 receptor (AT1R) antagonist, L-158 8

30 taneous stimulation and recording of coupled glomus cells and carotid nerve endings.

31 Glomus cells and carotid sinus afferents are anatomicall

32 uring Na2S2O4 occur by direct effects on the glomus cells and feedback action through released ACh an

33 -like immunoreactivity was localized to many glomus cells and nerve fibers and the concentration of S

34 stablished, the presence of TRPC channels in glomus cells and sensory nerves of the carotid body sugg

35 Glomus cells and sheath cells were immunocytochemically

36 rk, we quantify functional differences among glomus cells and show reciprocal sensitivity to acidosis

37 le similar to mammalian carotid body Type I (glomus) cells and pulmonary neuroepithelial cells.

38 (glomus cells, sheath cells, and subtypes of glomus cells) and oxygen sensitivity of potassium channe

39 amniote respiratory reflexes - carotid body glomus cells, and 'pulmonary neuroendocrine cells' (PNEC

40 ar effects on cytosolic calcium ([Ca2+]i) in glomus cells, and if so, whether a heterogenous response

41 n experiments, induces calcium transients in glomus cells, and stimulates carotid sinus nerve activit

42 ly connected, and the chemical events in the glomus cells are expected to be conveyed reflexly as aff

43 Glomus cells are present in normal numbers and appear st

44 Carotid body glomus cells are the primary sites of chemotransduction

45 : (a) hypoxia increases cytosolic calcium in glomus cells; (b) response patterns were heterogeneous i

46 not affect the basal [Ca(2+) ]i in isolated glomus cells bathed in 5 mm KClo , but elicited transien

47 hus, hypoxia may suppress the K+ currents in glomus cells but K+ current suppression of itself does n

48 calcium currents accompany calcium inflow in glomus cells, but calcium influx may not depend exclusiv

49 v) are highly expressed in carotid body (CB) glomus cells, but their role in hypoxia-induced excitati

50 ate that this selective chemotransduction of glomus cells by either stimulus may result in the activa

51 und K(+) channels that mediate activation of glomus cells by hypoxia.

52 changes in arterial O(2) with activation of glomus cells by inhibition of unidentified background K(

53 est the redox inhibition of K(+) channels of glomus cells by reduced glutathione (GSH), dithiothreito

54 metabolic model postulates that the rise in glomus cell [Ca2+]i, the initiating reaction in the sign

55 tissues most commonly studied, i.e. carotid glomus cells, central neurons, smooth muscle cells, and

56 and resting potential (Em) of cultured mouse glomus cells (clustered and isolated) were simultaneousl

57 physiologically or pharmacologically induced glomus cell depolarization or hyperpolarization may not

58 our results show that BK/Kv are activated as glomus cells depolarize in response to hypoxia, which th

59 forming next-generation sequencing on single glomus cell-derived cDNAs to eliminate contamination of

60 from intracellular store in the carotid body glomus cells during hypoxia, we stimultaneously measured

61 lux both contribute to the depolarization of glomus cells during moderate to severe hypoxia.

62 o, 4-AP did not evoke any rise in [Ca2+]i in glomus cells either during normoxia and hypoxia, althoug

63 ypertensive rats (SHRs) carotid body type I (glomus) cells exhibit hypersensitivity to chemosensory s

64 Chemosensitive carotid body glomus cells exhibited toll-like receptor (TLR-2 and TLR

65 Cultured glomus cells expressed immunoreactivity for alpha3, alph

66 morphology and size of these cells resemble glomus cells found in amphibians, mammals, tortoises, an

67 ve O2-sensing cells were similar to those of glomus cells found in other vertebrates.

68 Experiments were performed on glomus cells from adult rat carotid bodies, rat pheochro

69 r normoxic conditions were blunted in the CB glomus cells from CHF rabbits compared with sham rabbits

70 tage-gated K+ (Kv) channels to hypoxia in CB glomus cells from CHF rabbits, and whether endogenous an

71 sensitivity of Kv channels to hypoxia in CB glomus cells from CHF rabbits; (2) high concentrations o

72 e NO donor SNAP (100 microm) increased IK in glomus cells from HF rabbits to a greater extent than th

73 results demonstrate that IK is reduced in CB glomus cells from HF rabbits.

74 Pairs of electrically coupled glomus cells from rat carotid bodies were impaled with m

75 Carotid body (CB) glomus cells from rat express a TASK-like background K+

76 of Ang II (> 1 nM) directly inhibit IK in CB glomus cells from sham and CHF rabbits; (3) changes in K

77 ker iberiotoxin (IbTx, 100 nm) reduced IK in glomus cells from sham rabbits, but had no effect on IK

78 the pH sensitivity of isolated carotid body glomus cells from young spontaneously hypertensive rats

79 In the case of glomus cells (GC/GC coupling), it was mostly resistive a

80 osed of the neurotransmitter (NT)-containing glomus cells (GCs) and the sensory afferent fibers synap

81 cell RNA-Seq results characterized novel CB glomus cell genes, including members of the G protein-co

82 Glomus cells had less negative Em and lower Ro.

83 Glomus cells harvested from Wistar rat carotid bodies we

84 Although carotid chemosensitive glomus cells have been the most extensively studied from

85 lished the first transcriptome profile of CB glomus cells, highlighting genes with potential implicat

86 the most specifically expressed genes in CB glomus cells, highlighting their potential roles in mito

87 we compared the outward K+ currents (IK) of glomus cells in sham rabbits with that in HF rabbits and

88 Glomus cells in the carotid body respond to decreases in

89 sible for the oxygen-sensitive properties of glomus cells in the rat carotid body (CB) we used Ba2+,

90 formation between peripheral chemoreceptors (glomus cells) in the carotid body and relay neurons in t

91 [Ca2+]i in glomus cells increased in response to hypoxia (pO2 = 35

92 a2+]i seemed to play a significant a role in glomus cell intercellular communication.

93 7BL/6J) strain measuring the ventilatory and glomus cell intracellular calcium ([Ca(2+)](i)) response

94 s fully consistent with release of Ca2+ from glomus cell intracellular stores according to metabolic

95 cular machinery and signalling pathway in CB glomus cells is still limited.

96 of O2 sensing by carotid body chemoreceptor (glomus) cells is that hypoxia inhibits the outward K(+)

97 ody pH sensing by recording the responses of glomus cells isolated from rat carotid body to rapid cha

98 toplasmic Ca(2+) concentration in individual glomus cells, isolated in clusters from rat carotid bodi

99 in expression (Kv3.4 versus Kv4.3) in the CB glomus cell may contribute to the suppression of IK and

100 Carotid body (CB) glomus cells mediate acute oxygen sensing and the initia

101 Accordingly, K(+) channel inhibition of the glomus cell membrane is expected to be followed by excit

102 ed cells and strings of cells, but clustered glomus cells never responded.

103 s Ca2+-activated K+ (K+(Ca)) currents in the glomus cell of neonatal rat carotid body.

104 550 Torr) on the pHi and [Ca2+]i in cultured glomus cells of adult rat carotid body (CB) as a test of

105 IK was attenuated in glomus cells of HF rabbits, and their resting membrane p

106 g cells of fish (5HT) and those found in the glomus cells of mammals (acetylcholine, adenosine, and c

107 These results suggest that most glomus cells of the adult cat carotid body possess oxyge

108 The chemosensory glomus cells of the carotid body (CB) detect changes in

109 ialized for rapid functional oxygen sensing: glomus cells of the carotid body (peripheral respiratory

110 decrease in P(O2) (hypoxia) oxygen-sensitive glomus cells of the carotid body release ATP to activate

111 nd selectively expressed in oxygen-sensitive glomus cells of the carotid body, a chemosensory organ a

112 ia with a heterogenous pattern in individual glomus cells of the carotid body.

113 nd protein, which was primarily localized to glomus cells of the carotid body.

114 racterize the gap junctions between cultured glomus cells of the rat carotid body and to assess the e

115 enign neuroendocrine tumors derived from the glomus cells of the vegetative nervous system.

116 ammasome and interleukin-1beta expression in glomus cells (p < 0.01).

117 These results indicate that cultured cat glomus cells possess functional nAChRs, and that their c

118 heath cells and possibly a small fraction of glomus cells possess oxygen-insensitive potassium channe

119 e excitability of afferent nerve endings and glomus cells (putative chemoreceptor cells).

120 etermine the correlation between cell types (glomus cells, sheath cells, and subtypes of glomus cells

121 Dual voltage clamping of coupled glomus cells showed a mean macrojunctional conductance (

122 Nicotinic AChRs of glomus cells showed high affinity for ACh.

123 essed in glomus cells, which contained novel glomus cell-specific genes.

124 ensitive ion channels have been described in glomus cells that respond directly to extracellular acid

125 acidosis evoked transient inward current in glomus cells that was inhibited by the acid-sensing ion

126 Glomus cells, the site of O2 sensing in the carotid body

127 Type I (also called glomus) cells, the site of O2 sensing in the carotid bod

128 creased outward potassium current (Ik) in CB glomus cells to levels similar to those that were observ

129 h bilateral carotid body resections (BR) for glomus cell tumours.

130 Short-term cultures of glomus cells (up to seven days), were employed to study

131 Ik was measured in glomus cells using conventional and perforated whole-cel

132 tinic ACh receptors (nAChRs) in cultured cat glomus cells using immunocytochemistry and whole cell pa

133 tracellular calcium ([Ca(2+)](i)) release in glomus cells via ryanodine receptor (RyR) activation by

134 gs and glomus cells was more complex, When a glomus cell was stimulated, current spread to the nerve

135 Coupling between nerve endings and glomus cells was more complex, When a glomus cell was st

136 us to conclude that the redox modulation of glomus cells was not conveyed to the afferents, and this

137 ypoxic chemotransduction in the carotid body glomus cells was tested by using 4-aminopyridine (4-AP),

138 Glomus cells were identified by catecholamine fluorescen

139 Dissociated rat glomus cells were loaded with Fura-2 AM to study the eff

140 olarizing effect of low pH in SHR versus WKY glomus cells which was caused by overexpression of 2 aci

141 elease of an excitatory transmitter from the glomus cell, which is a secretory cell that is presynapt

142 Homology has been proposed between glomus cells, which are neural crest-derived, and the hy

143 ified a set of genes abundantly expressed in glomus cells, which contained novel glomus cell-specific

144 y a drop in intracellular pH of carotid body glomus cells, which inhibits a K+ current.

145 is a major arterial chemoreceptor containing glomus cells whose activities are regulated by changes i

146 of TASK by external acid, depolarization of glomus cells with high external KCl (20 mm) or opening o

147 current clamping after impaling two adjacent glomus cells with microelectrodes, and alternate stimula

148 constant normoxic conditions in sham and CHF glomus cells, with threshold concentrations of about 900