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

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

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

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

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

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

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

17 le-body plethysmography in rats administered GHB.

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

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

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

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

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

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

24 ssed by inhibitor administration 5 min after GHB.

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

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

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

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

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

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

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

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

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

34 onist, bicuculline, were administered before GHB.

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

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

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

38 ia a direct activation of GABAB receptors by GHB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 of the neuromodulator gamma-hydroxybutyrate (GHB).

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

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

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

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

63 1-enecarboxylic acid (HOCPCA) and the linear GHB analog trans-4-hydroxycrotonic acid (T-HCA).

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

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

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

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

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

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

70 or the second messenger activating action of GHB.

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

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

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

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

75 search of potential surrogate biomarkers of GHB consumption.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 200 mg/kg, intraperitoneal) had no effect on GHB-inhibited MAP kinase phosphorylation.

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

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

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

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

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

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

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

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

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

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

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

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

103 Arabidopsis genome contains two GHB dehydrogenase encoding genes.

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

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

106 n the search for metabolites associated with GHB intake.

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