ライフサイエンスコーパス: ibogaine

1 t 24 hr after the administration of 40 mg/kg ibogaine.

2 ontribute to the antiaddictive properties of ibogaine.

3 d pharmacological effects mimicking those of ibogaine.

4 etabolite may mediate some of the effects of ibogaine.

5 oribogaine was identified as a metabolite of ibogaine.

6 may be involved in the behavioral effects of ibogaine.

7 y reacted at slower rates in the presence of ibogaine.

8 was administered 1 h after administration of ibogaine.

9 blocked the rescue effects of bupropion and ibogaine.

10 gues of 5may serve as useful substitutes for ibogaine.

11 U62066 (1 microM) and ibogaine (1 microM), an indole alkaloid claimed to be us

12 azepino[4,5-b]indole, 5, a major fragment of ibogaine (1), were synthesized and tested for binding to

13 However, co-administration of ibogaine (1-40 mg/kg, i.p.) and morphine (4 mg/kg, s.c.)

14 A behaviorally active dose of ibogaine (10 mg/kg, i.p.) was administered to a group of

15 Ibogaine (10, 20 or 40 mg/kg, i.p.) by itself did not al

16 tion of morphine, however, the lower dose of ibogaine (20 mg/kg, i.p.) was ineffective.

17 Ibogaine (20, 40 or 80 mg/kg, i.p.) given prior to the i

18 Ibogaine (20, 40 or 80 mg/kg, i.p.) given twice a day fo

19 rkinje cell number were observed between the ibogaine (243764[+/-32766]) and control groups (230813[+

20 similar to effects previously observed with ibogaine (40 mg/kg); however, noribogaine did not induce

21 procedure, rats were injected with saline or ibogaine (40 mg/kg, i.p.).

22 Ibogaine (40 or 80 mg/kg, i.p.) injected 10 min before e

23 died in female C57BL/6N mice pretreated with ibogaine (50 mg/kg) and sacrificed 48 h. after a single

24 Ibogaine, a hallucinogenic alkaloid proposed as a treatm

25 Ibogaine, a hallucinogenic alkaloid with purported anti-

26 Ibogaine, a hallucinogenic indole alkaloid, has been pro

27 Anecdotal reports suggest that ibogaine, a natural alkaloid, reverses behaviors associa

28 Ibogaine, a naturally occurring iboga alkaloid, has been

29 Ibogaine, a putatively anti-addictive alkaloid, binds to

30 ansient brain concentrations (100 microM) of ibogaine act at multiple cellular sites and then have a

31 The results show that ibogaine acutely potentiates morphine antinociception an

32 Ibogaine administered 4 h or 24 h prior to morphine inje

33 The results show that ibogaine administered after inferior olive ablation prod

34 for alcoholism that may mimic the effect of ibogaine against alcohol consumption but avoid the negat

35 keeping with their structural similarity to ibogaine, all five compounds displayed weak to poor affi

36 Unlike neurotensin responses, ibogaine alone did not alter DYN levels in the striatum,

37 ed HSP-72 expression, whereas treatment with ibogaine alone produced hypothermia.

38 However, ibogaine also has acute nonspecific side effects (e.g. t

39 ropeptide, the present study investigated if ibogaine also influences dynorphin (DYN) pathways.

40 Ibogaine also inhibited binding to SERT of the cocaine a

41 Ibogaine also reduced operant self-administration of eth

42 Ibogaine, an alkaloid isolated from the bark of the Afri

43 The effects of ibogaine, an alkaloid isolated from the bark of the Afri

44 Ibogaine, an indole alkaloid that causes hallucinations,

45 ception by the putative anti-addictive agent ibogaine and its active metabolite (noribogaine) was inv

46 via opioid receptor systems, the effects of ibogaine and its metabolite, noribogaine on the antinoci

47 d higher affinity at the DA transporter than ibogaine and noribogaine (4).

48 Ibogaine and noribogaine were shown to have affinity for

49 g/kg for all drugs) and i.v. (1-10 mg/kg for ibogaine and noribogaine) drug administration in awake f

50 Similar to the effects of ibogaine and other iboga alkaloids that inhibit drug sel

51 Because of the structural similarity between ibogaine and serotonin, it had been suggested that iboga

52 port describing the noncompetitive action of ibogaine and the competitive action of cocaine accounts

53 NT may contribute to an interaction between ibogaine and the DA system and may participate in the ph

54 The inhibitory actions of ibogaine and the kappa agonists were not reversed by pre

55 evant to potential anti-addictive actions of ibogaine and to the development of drugs to combat nicot

56 The effects of the antiaddictive compound, ibogaine, and its primary metabolite, noribogaine (12-hy

57 In vivo, ibogaine at 10 mg/kg completely blocked epibatidine-elic

58 studies from this laboratory had shown that ibogaine at 40 and 80 mg/kg doses inhibited tolerance to

59 s provide evidence for a mechanism of action ibogaine at the nicotinic ACh receptor.

60 Ibogaine, at low concentration (<10 microM) was found to

61 Ibogaine binding to SERT increases accessibility in the

62 The results presented here show that ibogaine binds to a distinct site, accessible from the c

63 esults are consistent with the proposal that ibogaine binds to and stabilizes the state of SERT from

64 ne and serotonin, it had been suggested that ibogaine binds to the substrate site of SERT.

65 Ibogaine blocked substrate-induced currents also in DAT

66 These data indicate that pretreatment with ibogaine can completely block methamphetamine-induced hy

67 O'Hearn and Molliver, however, showed that ibogaine causes degeneration of cerebellar Purkinje cell

68 pioid agonist and NMDA antagonist actions of ibogaine contribute to its putative anti-addictive effec

69 Ibogaine decreased ethanol intake by rats in two-bottle

70 Although ibogaine did not alter phosphoinositide turnover in eith

71 Every rat treated with the high dose of ibogaine displayed clear evidence of Purkinje cell degen

72 ked contrast, rats given the smaller dose of ibogaine displayed no degeneration above the level seen

73 heir effect on SERT currents, indicated that ibogaine does not inhibit by forming a long-lived comple

74 ible, while the inhibitory effects of higher ibogaine doses persisted for at least 19 h following ibo

75 llular serotonin levels in both NAC and STR: ibogaine elicited large increases (up to 25-fold in NAC

76 Ibogaine (Endabuse) is a psychoactive indole alkaloid fo

77 Ibogaine (Endabuse) is a psychoactive indole alkaloid fo

78 However, the metabolite of ibogaine enhances the antinociception of morphine but no

79 Here we determine whether, and how, Ibogaine exerts its long-lasting actions on GDNF express

80 a culture model, we observed that short-term Ibogaine exposure results in a sustained increase in GDN

81 The ibogaine followed by methamphetamine injection showed no

82 In addition, because ibogaine has been reported to interact with kappa opioid

83 Ibogaine (IBO) is an indole alkaloid that is reported to

84 y treatment of rats with kainic acid (KA) or ibogaine (IBO) to the neuropathology observed in mice in

85 h increased affinity (17- to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower

86 face expression, we found that bupropion and ibogaine increased DAT surface expression, whereas other

87 n of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-der

88 Ibogaine increased the reactivity of cysteine residues p

89 Bupropion and ibogaine increased wild type DAT protein levels and also

90 ilize inward-open conformations (e.g., 5-HT, ibogaine) increased phosphorylation.

91 We postulate that ibogaine-induced activation of inferior olivary neurons

92 intravenous morphine self-administration and ibogaine-induced antagonism of morphine-induced locomoto

93 effects of selective dopamine antagonists on ibogaine-induced changes in NT concentrations in these b

94 sts any long-term motor deficits produced by ibogaine-induced degeneration should preferentially affe

95 eceptor antagonist, eticlopride, blocked the ibogaine-induced increase in nigral NTLI, but not in str

96 The ibogaine-induced increases in NTLI in striatum, nucleus

97 t (NMDA, 20 mg/kg, i.p.) partially prevented ibogaine-induced inhibition of intravenous morphine self

98 a 19 h ibogaine pretreatment, which resemble ibogaine-induced inhibition of morphine's stimulant prop

99 Because ibogaine influences the activity of neurotensin systems,

100 When present on the cell exterior, ibogaine inhibited SERT substrate-induced currents, but

101 It is concluded that ibogaine inhibits selectively the development of toleran

102 The same doses of ibogaine injected 10 min before the opioid drugs did not

103 Microinjection of ibogaine into the ventral tegmental area (VTA), but not

104 Ibogaine is a naturally occurring alkaloid that has been

105 Ibogaine is an alkaloid isolated from the bark of the Af

106 Ibogaine is claimed to be an effective treatment for opi

107 and cocaine self-administration even though ibogaine is mostly eliminated from the body in several h

108 prevents the neurotoxicity demonstrates that ibogaine is not directly toxic to Purkinje cells, but th

109 lcoholism; however, because of side effects, ibogaine is not used clinically.

110 nuate morphine tolerance at lower doses than ibogaine, it is concluded that the attenuating effect of

111 The iboga alkaloid, ibogaine, its metabolite, noribogaine, and the congener,

112 We have proposed that ibogaine, like harmaline, excites neurons in the inferio

113 MC therefore appears to be a safer, ibogaine-like agent that might be useful in the treatmen

114 kg); however, noribogaine did not induce any ibogaine-like tremors.

115 Finally, the ibogaine-mediated decrease in ethanol self-administratio

116 increased climbing fiber activity induced by ibogaine mediates excitotoxic Purkinje cell degeneration

117 sm by which the putative anti-addiction drug Ibogaine mediates its desirable action of reducing alcoh

118 Ibogaine noncompetitively blocked (IC50 approximately 20

119 Ibogaine noncompetitively inhibited transport by both SE

120 After i.p. administration, ibogaine, noribogaine and 18-MC had very different effec

121 phosphorylation by Na(+) and stimulation by ibogaine occurred at concentrations that induced outward

122 vestigation assessed the chronic toxicity of ibogaine on cerebellar Purkinje cells in male Fischer 34

123 and NMDA alone, blocked the acute effects of ibogaine on dopamine release and metabolism in the stria

124 that GDNF in the VTA mediates the action of ibogaine on ethanol consumption.

125 sm that mediates the desirable activities of ibogaine on ethanol intake.

126 study, we first characterized the actions of ibogaine on ethanol self-administration in rodents.

127 In this study, the effects of ibogaine on local cerebral glucose utilization (LCGU) we

128 ated prolonged (one or more days) effects of ibogaine on morphine and cocaine self-administration eve

129 is concluded that the attenuating effect of ibogaine on morphine tolerance may be mediated by its co

130 as designed to determine: (1) the effects of ibogaine on striatal, nigral, cortical, and accumbens ne

131 The effects of noribogaine, a metabolite of ibogaine, on the development of tolerance to the antinoc

132 e show that the initial exposure of cells to Ibogaine or GDNF results in an increase in GDNF mRNA, le

133 e anti-addictive actions of these drugs; (2) ibogaine (or an unidentified metabolite) may release ser

134 Ibogaine pretreatment (40 mg/kg, i.p., 19 h) significant

135 Interestingly, ibogaine pretreatment dramatically enhanced cocaine-indu

136 in these brain areas; and (3) the effects of ibogaine pretreatment on cocaine-induced changes in stri

137 Ibogaine pretreatment significantly blocked the striatal

138 However, the inhibitory effects of a 19 h ibogaine pretreatment, which resemble ibogaine-induced i

139 However, in morphine-dependent animals, ibogaine produced a global decrease in LCGU that was gre

140 In drug-naive animals, ibogaine produced significant increases in LCGU in the p

141 These findings indicate that ibogaine produces distinctly different effects on LCGU i

142 These data suggest that bupropion and ibogaine promote maturation of DAT by acting as pharmaco

143 enerative and "anti-addictive' properties of ibogaine reflect different actions of the drug.

144 ereas many of the responses by NT systems to ibogaine resembled those which occur after cocaine, ther

145 s have shown that a single administration of Ibogaine results in a long-lasting reduction of drug cra

146 f kappa-opioid and NMDA actions in mediating ibogaine's (40 mg/kg, i.p.) behavioral and neurochemical

147 her kappa receptor antagonists could reverse ibogaine's effects on catecholamine release.

148 ynthetic iboga alkaloid congener that mimics ibogaine's effects on drug self-administration without a

149 gests that different mechanisms may underlie ibogaine's hallucinogenic and anti-addictive effects.

150 he ascending serotonergic system may mediate ibogaine's hallucinogenic effect; and (4) 18-MC probably

151 elf-administration without appearing to have ibogaine's other adverse effects.

152 uggest that noribogaine may be a mediator of ibogaine's putative anti-addictive effects.

153 ted that the action of the natural alkaloid, ibogaine, to reduce alcohol (ethanol) consumption is med

154 In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indic

155 cantly increased in the frontal cortex after ibogaine treatment.

156 Ibogaine treatments profoundly affected NT systems by in

157 ed cerebellar responses to the high doses of ibogaine used by O'Hearn and Molliver (100 mg/kg or 3 x

158 e attributed to subsequent administration of ibogaine was analyzed using immunocytochemical markers f

159 The blockade of nicotinic responses by ibogaine was only partially reversible in PC12 cells.

160 Ibogaine was relatively weak as a blocker (IC50 approxim

161 doses persisted for at least 19 h following ibogaine washout.

162 action of the putative anti-addictive agent ibogaine, we have measured its effects on catecholamine

163 posing effects of the inhibitors cocaine and ibogaine were each reversed by an excess of the other in

164 The effects of low dose (10 microM) ibogaine were rapidly reversible, while the inhibitory e

165 It is concluded that ibogaine, which has been suggested to decrease the self-

166 ds (9 and 17a) exhibited higher potency than ibogaine, while the rest had weaker binding affinities t

167 een provided for the possible interaction of ibogaine with mu-opioid receptor following its metabolis