ライフサイエンスコーパス: GHB

1 GHB concentrations up to 1.5 mM didn't affect shoots of

2 GHB effects were mainly observed during the first 2 h af

3 GHB is produced from the reduction of succinic semialdeh

4 GHB showed preference for alpha4 over alpha(1,2,6)-subun

5 GHB was used to define non-specific binding, since it di

6 f acting directly on GABAB receptors or by a GHB-derived GABA pool (or both).

7 that Arabidopsis, but not yeast, possesses a GHB dehydrogenase activity that converts GHB back to SSA

8 in NMR-based metabolomics were applied to a GHB clinical trial on urine and serum.

9 4beta1(delta)-receptors completely abolished GHB but not GABA function, indicating nonidentical bindi

10 MKII isozymes, only CaMKIIalpha accommodates GHB ligands.

11 us neuromodulator gamma-hydroxybutyric acid (GHB) and related synthetic analogs.

12 an antagonist for gamma-hydroxybutyric acid (GHB) at GHB receptor sites.

13 ety concern, with gamma-hydroxybutyric acid (GHB) being one of the most frequently used substances du

14 gamma-Hydroxybutyric acid (GHB) binding to brain-specific high-affinity sites is we

15 e GABA metabolite gamma-hydroxybutyric acid (GHB) from pancreatic beta-cells might mediate glucose su

16 gamma-Hydroxybutyric acid (GHB) is a naturally occurring compound.

17 Gamma-hydroxybutyric acid (GHB) is a naturally occurring gamma-aminobutyric acid (G

18 gamma-Hydroxybutyric acid (GHB) is a neuroactive substance with specific high-affin

19 gamma-Hydroxybutyric acid (GHB) is a popular drug increasingly associated with case

20 oactive substance gamma-hydroxybutyric acid (GHB).

21 lso indicated the existence of an additional GHB dehydrogenase encoding gene(s) in Arabidopsis genome

22 le-body plethysmography in rats administered GHB.

23 gliosis, as a response to injury, may affect GHB neuromodulatory pathways in neurodegenerative diseas

24 receptor agonist, whereas the high affinity GHB receptor antagonist NCS-382 (200 mg/kg, intraperiton

25 at gabazine interacts with the high-affinity GHB and orthosteric GABA(A) receptor binding sites diffe

26 GABA(A) receptor and (ii) the high-affinity GHB binding site.

27 1) is a potent ligand for the high-affinity GHB binding sites in the CNS.

28 y of available ligands for the high-affinity GHB binding sites, this study identified 2-(imidazo[1,2-

29 ligand identification for the high-affinity GHB binding sites.

30 shows high specificity to the high-affinity GHB binding sites.

31 ement of the alpha4-subunit in high-affinity GHB binding.

32 ssed by inhibitor administration 5 min after GHB.

33 Administration of 50 mg/kg SCH50911 after GHB completely reversed the decrease in respiratory rate

34 Although GHB is a Schedule I drug, analogs remain widely availabl

35 e for the human SSADH deficiency disease and GHB overdose and toxicity.

36 l in which to explore the effect of GABA and GHB accumulation on central nervous system development a

37 ulation of two neuroactive species, GABA and GHB, is significant because GABA is one of the earliest

38 The results suggest that glycine and GHB provide a counterbalancing receptor-based mechanism

39 As GHB can quickly induce sedation and is rapidly eliminate

40 Moreover, as GHB can also be metabolized to GABA, it remains to be se

41 ts that reliably stimulate SW sleep, such as GHB, may represent a novel class of powerful GH secretag

42 onist for gamma-hydroxybutyric acid (GHB) at GHB receptor sites.

43 onist, bicuculline, were administered before GHB.

44 s, the physiological significance of a brain GHB signaling pathway is still unknown, and there is an

45 n and melatonin profiles were not altered by GHB administration.

46 ceptor-mediated actions of GHB are caused by GHB itself acting directly on GABAB receptors or by a GH

47 ia a direct activation of GABAB receptors by GHB.

48 erifused mouse islets was also unaffected by GHB at both 1 and 7 mm glucose.

49 se stimulation and interacts with alpha-cell GHB receptors, thus mediating the suppressive effect of

50 In contrast, GHB (10 mm for 15 min) was found ineffective on MAP kina

51 s a GHB dehydrogenase activity that converts GHB back to SSA.

52 or accommodation of ligands and corroborates GHB analogs as CaMKIIalpha-selective.

53 allows users to rapidly and visually detect GHB in beverages prior to consumption.

54 highly portable sensor successfully detects GHB in both alcoholic and nonalcoholic beverages, demons

55 nates using two different in-house-developed GHB-related radioligands, 3-hydroxycyclopent-1-enecarbox

56 cose from 7 to 1 mm Inhibition of endogenous GHB formation with the GABA transaminase inhibitor vigab

57 This establishes GHB analogs as powerful tools for investigating CaMKII n

58 characterize the vast majority of exogenous GHB actions mediated by GABAB receptors; and some of the

59 on GHB, we examined the effect of exogenous GHB and SSA on the growth of yeast and Arabidopsis plant

60 r (detect, identify, and quantify) exogenous GHB in almost intact body fluids and its high potential

61 a three-dimensional pharmacophore model for GHB ligands, which identified molecular features importa

62 n, represent potential treatment options for GHB-induced respiratory depression.

63 B) receptors to be primarily responsible for GHB-induced respiratory depression.

64 ted when specific ion monitoring is used for GHB on urine organic acids.

65 mma-aminobutyric acid, gammahydroxybutyrate (GHB) is a potent central nervous system depressant.

66 Advantages of using [(3)H]NCS-382 over [(3)H]GHB in radioligand binding studies are that unlike GHB,

67 Overdose of gamma-hydroxybutyrate (GHB) frequently causes respiratory depression, occasiona

68 gamma-Hydroxybutyrate (GHB) naturally occurs in the brain, but its exogenous ad

69 islets, we found that gamma-hydroxybutyrate (GHB), a potent inhibitory neurotransmitter, is generated

70 al young men, whether gamma-hydroxybutyrate (GHB), a reliable stimulant of slow-wave (SW) sleep in no

71 mally desorbed sodium gamma-hydroxybutyrate (GHB), and the second sample was a liquid mixture of dicy

72 om the drugs of abuse gamma-hydroxybutyrate (GHB), gamma-hydroxypentanoate(GHP), in addition to the o

73 of the neuromodulator gamma-hydroxybutyrate (GHB).

74 rvous system GABA and gamma-hydroxybutyrate (GHB).

75 to the natural substance y-hydroxybutyrate (GHB) bind selectively to CaMKIIa.

76 s as 4-hydroxybutyric (gamma-hydroxybutyric, GHB) aciduria.

77 To determine the receptors involved in GHB-induced respiratory depression, a specific GABA(B) r

78 alpha4delta-containing GABA(A) receptors in GHB pharmacology and physiology.

79 ion of the MCT inhibitor l-lactate increased GHB renal and total clearance, also improving respirator

80 In human islets, GHB tended to stimulate glucagon secretion at 1 mm gluco

81 1-enecarboxylic acid (HOCPCA) and the linear GHB analog trans-4-hydroxycrotonic acid (T-HCA).

82 st wild-type strain with 10 mM SSA and 10 mM GHB didn't affect the growth.

83 ed by the same concentration of SSA, but not GHB.

84 oped; GABAB receptor knockout mice and novel GHB analogs have helped to characterize the vast majorit

85 Conversely, the accumulation of GHB in Arabidopsis plants subjected to abiotic stresses

86 The accumulation of GHB in ssadh mutants led to the speculation that GHB is

87 kg, intraperitoneal) prevented the action of GHB, and the effect of GHB was mimicked by baclofen, a s

88 or the second messenger activating action of GHB.

89 the many GABAB receptor-mediated actions of GHB are caused by GHB itself acting directly on GABAB re

90 ccinic semialdehyde (SSA) by the activity of GHB dehydrogenase.

91 Acute administration of GHB (500 mg/kg, intraperitoneal) induced a fast and long

92 We observed increased amounts of GHB and total GABA in urine, brain and liver homogenates

93 Furthermore, we show that binding of GHB and related analogs to this site promotes concentrat

94 search of potential surrogate biomarkers of GHB consumption.

95 eritoneal), which inhibits the conversion of GHB into GABA, failed to block the effect of GHB on MAP

96 The distribution of GHB binding sites as defined by [(3)H]NCS-382 suggests t

97 GHB into GABA, failed to block the effect of GHB on MAP kinase phosphorylation.

98 The primary effect of GHB on respiration was a dose-dependent decrease in resp

99 evented the action of GHB, and the effect of GHB was mimicked by baclofen, a selective GABAB receptor

100 However, the direct effects of GHB on alpha-cell signaling and glucagon release have no

101 ered to assess the dose-dependent effects of GHB on respiration.

102 In the present study, the effects of GHB on the activation (phosphorylation) of mitogen-activ

103 of analysis and having forensic evidence of GHB intake in a long term are mandatory.

104 r mechanisms behind the proposed function of GHB as a neurotransmitter and its unique therapeutic eff

105 istration of placebo, 2.5, 3.0, and 3.5 g of GHB.

106 GHBR has been cloned; a transgenic model of GHB aciduria has been developed; GABAB receptor knockout

107 In the presence of GHB, Fe(3+) forms a stable complex, preventing its reduc

108 nderlying the dependence/abuse properties of GHB, and its ability to elicit absence seizures and an i

109 osteric factor in determining selectivity of GHB analogs for CaMKIIalpha.

110 portant developments in our understanding of GHB neurobiology: a putative GHBR has been cloned; a tra

111 Chronic use of GHB or its analogs is associated with a withdrawal syndr

112 200 mg/kg, intraperitoneal) had no effect on GHB-inhibited MAP kinase phosphorylation.

113 f potential overdose treatment strategies on GHB-induced respiratory depression.

114 To resolve these contrasting views on GHB, we examined the effect of exogenous GHB and SSA on

115 ub domain and small molecule brain-penetrant GHB analogs.

116 odel of cerebral ischemia with the selective GHB analog, HOCPCA (3-hydroxycyclopent-1-enecarboxylic a

117 two-electrode voltage clamp technique showed GHB to be a partial agonist at alphabetadelta- but not a

118 To identify molecular targets for specific GHB high-affinity binding, we undertook photolinking stu

119 Our data link specific GHB forebrain binding sites with alpha4-containing GABA(

120 dioligand binding studies using the specific GHB radioligand [(3)H](E,RS)-(6,7,8,9-tetrahydro-5-hydro

121 We conclude that GHB does not mediate the inhibitory effect of glucose on

122 Taken together, we conclude that GHB is less toxic than SSA.

123 Here, we found that GHB (4-10 mum) lacked effects on the cytoplasmic concent

124 in ssadh mutants led to the speculation that GHB is the cause of aberrant phenotypes.

125 Altogether, these data suggest that GHB, administered in vivo, reduces MAP kinase phosphoryl

126 es as defined by [(3)H]NCS-382 suggests that GHB may play a role in neuromodulation or neurotransmiss

127 The GHB receptor agonist 3-chloropropanoic acid and the anta

128 finity analogs (medium nanomolar Ki) for the GHB high-affinity binding sites as the most high-affinit

129 Moreover, the GHB dehydrogenase inhibitor valproate (500 mg/kg, intrap

130 Arabidopsis genome contains two GHB dehydrogenase encoding genes.

131 radioligand binding studies are that unlike GHB, NCS-382 does not appear to bind to, activate, or in

132 glucose suppression of glucagon release via GHB receptors on alpha-cells.

133 s in synaptogenesis and myelination, whereas GHB displays a vast array of pharmacological actions.

134 n the search for metabolites associated with GHB intake.

135 Acute intoxication with GHB or its analogs leads to coma and respiratory depress