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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  important compounds such as vinblastine and ibogaine.
8  blocked the rescue effects of bupropion and ibogaine.
9 y reacted at slower rates in the presence of ibogaine.
10 was administered 1 h after administration of ibogaine.
11 gues of 5may serve as useful substitutes for ibogaine.
12                        U62066 (1 microM) and ibogaine (1 microM), an indole alkaloid claimed to be us
13 azepino[4,5-b]indole, 5, a major fragment of ibogaine (1), were synthesized and tested for binding to
14                However, co-administration of ibogaine (1-40 mg/kg, i.p.) and morphine (4 mg/kg, s.c.)
15                A behaviorally active dose of ibogaine (10 mg/kg, i.p.) was administered to a group of
16                                              Ibogaine (10, 20 or 40 mg/kg, i.p.) by itself did not al
17 tion of morphine, however, the lower dose of ibogaine (20 mg/kg, i.p.) was ineffective.
18                                              Ibogaine (20, 40 or 80 mg/kg, i.p.) given prior to the i
19                                              Ibogaine (20, 40 or 80 mg/kg, i.p.) given twice a day fo
20 rkinje cell number were observed between the ibogaine (243764[+/-32766]) and control groups (230813[+
21  similar to effects previously observed with ibogaine (40 mg/kg); however, noribogaine did not induce
22 procedure, rats were injected with saline or ibogaine (40 mg/kg, i.p.).
23                                              Ibogaine (40 or 80 mg/kg, i.p.) injected 10 min before e
24 died in female C57BL/6N mice pretreated with ibogaine (50 mg/kg) and sacrificed 48 h. after a single
25                                              Ibogaine, a hallucinogenic alkaloid proposed as a treatm
26                                              Ibogaine, a hallucinogenic alkaloid with purported anti-
27                                              Ibogaine, a hallucinogenic indole alkaloid, has been pro
28 t in SERT we investigated its complexes with ibogaine, a hallucinogenic natural product with psychoac
29               Anecdotal reports suggest that ibogaine, a natural alkaloid, reverses behaviors associa
30                                              Ibogaine, a naturally occurring iboga alkaloid, has been
31 treatment alternatives such as the oneirogen ibogaine, a plant-derived compound known to interact wit
32                                              Ibogaine, a putatively anti-addictive alkaloid, binds to
33 ansient brain concentrations (100 microM) of ibogaine act at multiple cellular sites and then have a
34                        The results show that ibogaine acutely potentiates morphine antinociception an
35                                              Ibogaine administered 4 h or 24 h prior to morphine inje
36                        The results show that ibogaine administered after inferior olive ablation prod
37  for alcoholism that may mimic the effect of ibogaine against alcohol consumption but avoid the negat
38  keeping with their structural similarity to ibogaine, all five compounds displayed weak to poor affi
39                Unlike neurotensin responses, ibogaine alone did not alter DYN levels in the striatum,
40 ed HSP-72 expression, whereas treatment with ibogaine alone produced hypothermia.
41                                     However, ibogaine also has acute nonspecific side effects (e.g. t
42 3,4-Methylenedioxymethamphetamine (MDMA) and ibogaine also hold promise.
43 ropeptide, the present study investigated if ibogaine also influences dynorphin (DYN) pathways.
44                                              Ibogaine also inhibited binding to SERT of the cocaine a
45                                              Ibogaine also reduced operant self-administration of eth
46                                              Ibogaine, an alkaloid isolated from the bark of the Afri
47                               The effects of ibogaine, an alkaloid isolated from the bark of the Afri
48                                              Ibogaine, an indole alkaloid that causes hallucinations,
49 their derivatives), and atypical inhibitors (ibogaine analogues) bind preferentially to different sta
50                                 Notably, (-)-ibogaine and (-)-voacangine are of the opposite enantiom
51                                          (-)-Ibogaine and (-)-voacangine are plant derived psychoacti
52 ception by the putative anti-addictive agent ibogaine and its active metabolite (noribogaine) was inv
53 rials suggest that the psychoactive alkaloid ibogaine and its active metabolite noribogaine have powe
54  slices and in rat brain synaptosomes, where ibogaine and its analogs did not act as substrate-type s
55   Of the numerous pharmacological actions of ibogaine and its derivatives, the inhibition of alpha3be
56                                              Ibogaine and its main metabolite noribogaine provide imp
57  via opioid receptor systems, the effects of ibogaine and its metabolite, noribogaine on the antinoci
58 d higher affinity at the DA transporter than ibogaine and noribogaine (4).
59 d brain synaptic vesicles, we confirmed that ibogaine and noribogaine act as inhibitors of VMAT2 and
60 is is outlined and used to conceptualize why ibogaine and noribogaine do not induce catalepsy, as dem
61 ds lack the proarrhythmic adverse effects of ibogaine and noribogaine in primary human cardiomyocytes
62                               We report that ibogaine and noribogaine inhibit the transport function
63                                              Ibogaine and noribogaine were shown to have affinity for
64 g/kg for all drugs) and i.v. (1-10 mg/kg for ibogaine and noribogaine) drug administration in awake f
65                    Similar to the effects of ibogaine and other iboga alkaloids that inhibit drug sel
66 Because of the structural similarity between ibogaine and serotonin, it had been suggested that iboga
67 port describing the noncompetitive action of ibogaine and the competitive action of cocaine accounts
68 s an enantioselective total synthesis of (+)-ibogaine and the construction of four analogues.
69  NT may contribute to an interaction between ibogaine and the DA system and may participate in the ph
70                    The inhibitory actions of ibogaine and the kappa agonists were not reversed by pre
71 evant to potential anti-addictive actions of ibogaine and to the development of drugs to combat nicot
72   The effects of the antiaddictive compound, ibogaine, and its primary metabolite, noribogaine (12-hy
73 ounds bulbocapnine, chelidonine, dicentrine, ibogaine, and rotenone as novel interactors of G-quadrup
74 terpene indole alkaloids such as strychnine, ibogaine, and vinblastine.
75 f the potential therapeutic pharmacophore of ibogaine, and we use this information to engineer tabern
76                                     In vivo, ibogaine at 10 mg/kg completely blocked epibatidine-elic
77  studies from this laboratory had shown that ibogaine at 40 and 80 mg/kg doses inhibited tolerance to
78 s provide evidence for a mechanism of action ibogaine at the nicotinic ACh receptor.
79                                              Ibogaine, at low concentration (<10 microM) was found to
80                                              Ibogaine binding to SERT increases accessibility in the
81         The results presented here show that ibogaine binds to a distinct site, accessible from the c
82 esults are consistent with the proposal that ibogaine binds to and stabilizes the state of SERT from
83                                              Ibogaine binds to the central binding site, and closure
84 ne and serotonin, it had been suggested that ibogaine binds to the substrate site of SERT.
85                                              Ibogaine blocked substrate-induced currents also in DAT
86 rified voacangine, which is converted to (-)-ibogaine by heating, enabling biocatalytic production of
87   These data indicate that pretreatment with ibogaine can completely block methamphetamine-induced hy
88   O'Hearn and Molliver, however, showed that ibogaine causes degeneration of cerebellar Purkinje cell
89  cryo-electron microscopy structures of SERT-ibogaine complexes captured in outward-open, occluded an
90 pioid agonist and NMDA antagonist actions of ibogaine contribute to its putative anti-addictive effec
91                                              Ibogaine decreased ethanol intake by rats in two-bottle
92                                     Although ibogaine did not alter phosphoinositide turnover in eith
93      Every rat treated with the high dose of ibogaine displayed clear evidence of Purkinje cell degen
94 ked contrast, rats given the smaller dose of ibogaine displayed no degeneration above the level seen
95 heir effect on SERT currents, indicated that ibogaine does not inhibit by forming a long-lived comple
96 ng revealed that the unnatural enantiomer of ibogaine does not produce ibogaine-like effects on corti
97 ible, while the inhibitory effects of higher ibogaine doses persisted for at least 19 h following ibo
98 llular serotonin levels in both NAC and STR: ibogaine elicited large increases (up to 25-fold in NAC
99                                              Ibogaine (Endabuse) is a psychoactive indole alkaloid fo
100                                              Ibogaine (Endabuse) is a psychoactive indole alkaloid fo
101                   However, the metabolite of ibogaine enhances the antinociception of morphine but no
102          Here we determine whether, and how, Ibogaine exerts its long-lasting actions on GDNF express
103 a culture model, we observed that short-term Ibogaine exposure results in a sustained increase in GDN
104                                          The ibogaine followed by methamphetamine injection showed no
105 report a gram-scale, seven-step synthesis of ibogaine from pyridine.
106                     The psychedelic alkaloid ibogaine has anti-addictive properties in both humans an
107                                              Ibogaine has been associated with instances of fatal car
108                         In addition, because ibogaine has been reported to interact with kappa opioid
109 se disorders, anecdotal reports suggest that ibogaine has the potential to treat addiction to various
110                                              Ibogaine (IBO) is an indole alkaloid that is reported to
111 y treatment of rats with kainic acid (KA) or ibogaine (IBO) to the neuropathology observed in mice in
112 h increased affinity (17- to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower
113 previously reported neurochemical effects of ibogaine in rodents.
114 ns have hindered the clinical development of ibogaine, including its toxicity, hallucinogenic potenti
115 face expression, we found that bupropion and ibogaine increased DAT surface expression, whereas other
116 n of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-der
117                                              Ibogaine increased the reactivity of cysteine residues p
118                                Bupropion and ibogaine increased wild type DAT protein levels and also
119 ilize inward-open conformations (e.g., 5-HT, ibogaine) increased phosphorylation.
120                            We postulate that ibogaine-induced activation of inferior olivary neurons
121 intravenous morphine self-administration and ibogaine-induced antagonism of morphine-induced locomoto
122 effects of selective dopamine antagonists on ibogaine-induced changes in NT concentrations in these b
123 sts any long-term motor deficits produced by ibogaine-induced degeneration should preferentially affe
124 eceptor antagonist, eticlopride, blocked the ibogaine-induced increase in nigral NTLI, but not in str
125                                          The ibogaine-induced increases in NTLI in striatum, nucleus
126 t (NMDA, 20 mg/kg, i.p.) partially prevented ibogaine-induced inhibition of intravenous morphine self
127 a 19 h ibogaine pretreatment, which resemble ibogaine-induced inhibition of morphine's stimulant prop
128                                      Because ibogaine influences the activity of neurotensin systems,
129           When present on the cell exterior, ibogaine inhibited SERT substrate-induced currents, but
130  mechanism of neurotransmitter transport and ibogaine inhibition.
131                         It is concluded that ibogaine inhibits selectively the development of toleran
132                            The same doses of ibogaine injected 10 min before the opioid drugs did not
133                            Microinjection of ibogaine into the ventral tegmental area (VTA), but not
134                                              Ibogaine is a naturally occurring alkaloid that has been
135                                     Notably, ibogaine is a non-competitive inhibitor of transport but
136                                              Ibogaine is an alkaloid isolated from the bark of the Af
137                                              Ibogaine is claimed to be an effective treatment for opi
138  and cocaine self-administration even though ibogaine is mostly eliminated from the body in several h
139 prevents the neurotoxicity demonstrates that ibogaine is not directly toxic to Purkinje cells, but th
140 lcoholism; however, because of side effects, ibogaine is not used clinically.
141                                              Ibogaine is the main psychoactive alkaloid produced by t
142 nuate morphine tolerance at lower doses than ibogaine, it is concluded that the attenuating effect of
143    We systematically examined the effects of ibogaine, its main metabolite noribogaine, and a series
144                          The iboga alkaloid, ibogaine, its metabolite, noribogaine, and the congener,
145                        We have proposed that ibogaine, like harmaline, excites neurons in the inferio
146          MC therefore appears to be a safer, ibogaine-like agent that might be useful in the treatmen
147 ural enantiomer of ibogaine does not produce ibogaine-like effects on cortical neuron growth, while (
148                               The effects of ibogaine-like those of other psychedelic compounds-are l
149 kg); however, noribogaine did not induce any ibogaine-like tremors.
150 cs (eg, psilocybin, MDMA, peyote, mescaline, ibogaine, LSD, ayahuasca, and DMT).
151                                 Finally, the ibogaine-mediated decrease in ethanol self-administratio
152 increased climbing fiber activity induced by ibogaine mediates excitotoxic Purkinje cell degeneration
153 sm by which the putative anti-addiction drug Ibogaine mediates its desirable action of reducing alcoh
154                                              Ibogaine noncompetitively blocked (IC50 approximately 20
155                                              Ibogaine noncompetitively inhibited transport by both SE
156                   After i.p. administration, ibogaine, noribogaine and 18-MC had very different effec
157  phosphorylation by Na(+) and stimulation by ibogaine occurred at concentrations that induced outward
158 vestigation assessed the chronic toxicity of ibogaine on cerebellar Purkinje cells in male Fischer 34
159 and NMDA alone, blocked the acute effects of ibogaine on dopamine release and metabolism in the stria
160  that GDNF in the VTA mediates the action of ibogaine on ethanol consumption.
161 sm that mediates the desirable activities of ibogaine on ethanol intake.
162 study, we first characterized the actions of ibogaine on ethanol self-administration in rodents.
163                In this study, the effects of ibogaine on local cerebral glucose utilization (LCGU) we
164 ated prolonged (one or more days) effects of ibogaine on morphine and cocaine self-administration eve
165  is concluded that the attenuating effect of ibogaine on morphine tolerance may be mediated by its co
166 as designed to determine: (1) the effects of ibogaine on striatal, nigral, cortical, and accumbens ne
167  The effects of noribogaine, a metabolite of ibogaine, on the development of tolerance to the antinoc
168 e show that the initial exposure of cells to Ibogaine or GDNF results in an increase in GDNF mRNA, le
169 e anti-addictive actions of these drugs; (2) ibogaine (or an unidentified metabolite) may release ser
170                                              Ibogaine pretreatment (40 mg/kg, i.p., 19 h) significant
171                               Interestingly, ibogaine pretreatment dramatically enhanced cocaine-indu
172 in these brain areas; and (3) the effects of ibogaine pretreatment on cocaine-induced changes in stri
173                                              Ibogaine pretreatment significantly blocked the striatal
174    However, the inhibitory effects of a 19 h ibogaine pretreatment, which resemble ibogaine-induced i
175      However, in morphine-dependent animals, ibogaine produced a global decrease in LCGU that was gre
176                       In drug-naive animals, ibogaine produced significant increases in LCGU in the p
177                 These findings indicate that ibogaine produces distinctly different effects on LCGU i
178        These data suggest that bupropion and ibogaine promote maturation of DAT by acting as pharmaco
179 enerative and "anti-addictive' properties of ibogaine reflect different actions of the drug.
180 ereas many of the responses by NT systems to ibogaine resembled those which occur after cocaine, ther
181 s have shown that a single administration of Ibogaine results in a long-lasting reduction of drug cra
182 f kappa-opioid and NMDA actions in mediating ibogaine's (40 mg/kg, i.p.) behavioral and neurochemical
183 her kappa receptor antagonists could reverse ibogaine's effects on catecholamine release.
184 ynthetic iboga alkaloid congener that mimics ibogaine's effects on drug self-administration without a
185 gests that different mechanisms may underlie ibogaine's hallucinogenic and anti-addictive effects.
186 he ascending serotonergic system may mediate ibogaine's hallucinogenic effect; and (4) 18-MC probably
187 elf-administration without appearing to have ibogaine's other adverse effects.
188                               Unfortunately, ibogaine's promiscuity and cardiotoxicity limit the unde
189 uggest that noribogaine may be a mediator of ibogaine's putative anti-addictive effects.
190 e, non-hallucinogenic, non-toxic analogue of ibogaine that can be prepared in a single step.
191                                 For decades, ibogaine-the main psychoactive alkaloid found in Taberna
192 pective observational study of the Magnesium-Ibogaine: the Stanford Traumatic Injury to the CNS proto
193 ted that the action of the natural alkaloid, ibogaine, to reduce alcohol (ethanol) consumption is med
194    In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indic
195 cantly increased in the frontal cortex after ibogaine treatment.
196                                              Ibogaine treatments profoundly affected NT systems by in
197 ed cerebellar responses to the high doses of ibogaine used by O'Hearn and Molliver (100 mg/kg or 3 x
198 e attributed to subsequent administration of ibogaine was analyzed using immunocytochemical markers f
199       The blockade of nicotinic responses by ibogaine was only partially reversible in PC12 cells.
200                                              Ibogaine was relatively weak as a blocker (IC50 approxim
201  doses persisted for at least 19 h following ibogaine washout.
202  action of the putative anti-addictive agent ibogaine, we have measured its effects on catecholamine
203 posing effects of the inhibitors cocaine and ibogaine were each reversed by an excess of the other in
204          The effects of low dose (10 microM) ibogaine were rapidly reversible, while the inhibitory e
205 r bulbocapnine, chelidonine, dicentrine, and ibogaine, whereas with the 5'-end G-quartet region for r
206                         It is concluded that ibogaine, which has been suggested to decrease the self-
207 ibitors target the outward-open state except ibogaine, which has unusual anti-depressant and substanc
208 ds (9 and 17a) exhibited higher potency than ibogaine, while the rest had weaker binding affinities t
209 een provided for the possible interaction of ibogaine with mu-opioid receptor following its metabolis

 
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