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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-11-4
pubmed:abstractText
The psychoactive indole alkaloid, ibogaine (IBO), has been investigated for over a decade concerning its reported anti-addictive properties for opioids as well as psychomotor stimulants. The mechanism for the anti-addictive action of IBO is still unclear. IBO interactions with opioid, NMDA, nicotinic, adrenergic, and serotonergic receptor sites have been suggested. The involvement of the dopaminergic system in IBO action is well documented. Increased or decreased levels of dopamine (DA) in specific brain regions following IBO pretreatment have been seen concomitantly with increased or decreased motor activity after subsequent amphetamine or cocaine administration. In this report, in vivo electrophysiological measures were monitored in awake adult male rats in order to investigate alterations of the electrocorticogram (ECoG) resulting from interactions between IBO and cocaine (COC). Rats were implanted bilaterally with bipolar ECoG electrodes. They were either injected with saline, COC alone (20 mg/kg, i.p.) or IBO (50 mg/kg, i.p.) and COC 1 hr later. The concentrations of DA, 5-HT, and their metabolites DOPAC, HVA, and 5-HIAA were assessed in the caudate nucleus in separate groups of saline-, COC-, and IBO/COC-treated rats. An alpha1 power increase was observed within 10 min after COC injection, which lasted for less than 20 min. A desynchronization over alpha2 and both beta power bands was observed throughout the recording. In IBO/COC-treated rats, a significant increase in delta, theta, and alpha1 power occurred within 20 min after COC injection (p <0.05). This effect lasted for up to an hour. DA levels significantly increased after COC only and decreased after IBO administration. A further decrease in levels of DA was observed in IBO/COC-treated rats. DA turnover increased significantly after IBO alone but was not observed after IBO/COC treatment. The alterations in ECoG and neurotransmitter levels suggest a decreased response to COC following IBO pretreatment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
914
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
387-93
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11085337-3,4-Dihydroxyphenylacetic Acid, pubmed-meshheading:11085337-Analysis of Variance, pubmed-meshheading:11085337-Animals, pubmed-meshheading:11085337-Brain Chemistry, pubmed-meshheading:11085337-Cerebral Cortex, pubmed-meshheading:11085337-Cocaine, pubmed-meshheading:11085337-Dopamine, pubmed-meshheading:11085337-Dopamine Uptake Inhibitors, pubmed-meshheading:11085337-Drug Interactions, pubmed-meshheading:11085337-Electroencephalography, pubmed-meshheading:11085337-Excitatory Amino Acid Antagonists, pubmed-meshheading:11085337-Homovanillic Acid, pubmed-meshheading:11085337-Hydroxyindoleacetic Acid, pubmed-meshheading:11085337-Ibogaine, pubmed-meshheading:11085337-Male, pubmed-meshheading:11085337-Rats, pubmed-meshheading:11085337-Rats, Sprague-Dawley, pubmed-meshheading:11085337-Serotonin, pubmed-meshheading:11085337-Time Factors, pubmed-meshheading:11085337-Wakefulness
pubmed:year
2000
pubmed:articleTitle
Application of electrophysiological method to study interactions between ibogaine and cocaine.
pubmed:affiliation
Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, Arkansas 72079, USA. zbinienda@nctr.fda.gov
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't