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Application of Electrophysiological Method to Study Interactions between Ibogaine and Cocaine
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, nicotini...
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Published in: | Annals of the New York Academy of Sciences 2000-09, Vol.914 (1), p.387-393 |
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description | 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 |
doi_str_mv | 10.1111/j.1749-6632.2000.tb05212.x |
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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.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/j.1749-6632.2000.tb05212.x</identifier><identifier>PMID: 11085337</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>3,4-Dihydroxyphenylacetic Acid - metabolism ; Analysis of Variance ; Animals ; Brain Chemistry - drug effects ; Cerebral Cortex - drug effects ; Cocaine - pharmacology ; Dopamine - metabolism ; Dopamine Uptake Inhibitors - pharmacology ; Drug Interactions ; Electroencephalography - methods ; Excitatory Amino Acid Antagonists - pharmacology ; Homovanillic Acid - metabolism ; Hydroxyindoleacetic Acid - metabolism ; Ibogaine - pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Serotonin - metabolism ; Time Factors ; Wakefulness</subject><ispartof>Annals of the New York Academy of Sciences, 2000-09, Vol.914 (1), p.387-393</ispartof><rights>2000 The New York Academy of Sciences</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4427-632aa147cec49f548bbe9c24653b43bd4b32e013b7c5674d2cd0a6cd57cd0c493</citedby><cites>FETCH-LOGICAL-c4427-632aa147cec49f548bbe9c24653b43bd4b32e013b7c5674d2cd0a6cd57cd0c493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11085337$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BINIENDA, ZBIGNIEW</creatorcontrib><creatorcontrib>BEAUDOIN, MICHAEL A.</creatorcontrib><creatorcontrib>THORN, BRETT T.</creatorcontrib><creatorcontrib>SADOVOVA, NATALYA</creatorcontrib><creatorcontrib>SKINNER, ROBERT D.</creatorcontrib><creatorcontrib>SLIKKER JR, WILLIAM</creatorcontrib><creatorcontrib>ALI, SYED F.</creatorcontrib><title>Application of Electrophysiological Method to Study Interactions between Ibogaine and Cocaine</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>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.</description><subject>3,4-Dihydroxyphenylacetic Acid - metabolism</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Brain Chemistry - drug effects</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cocaine - pharmacology</subject><subject>Dopamine - metabolism</subject><subject>Dopamine Uptake Inhibitors - pharmacology</subject><subject>Drug Interactions</subject><subject>Electroencephalography - methods</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Homovanillic Acid - metabolism</subject><subject>Hydroxyindoleacetic Acid - metabolism</subject><subject>Ibogaine - pharmacology</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Serotonin - metabolism</subject><subject>Time Factors</subject><subject>Wakefulness</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqVkF1v0zAUhq0JtJWxv4AsrrhJ8GfscIOq7oOK0SENNLhAlu2cbilpnMWu1v57ErUa1_ONj3Te97H1IPSekpwO5-Mqp0qUWVFwljNCSJ4ckYyyfHuEJs-rV2hCiFKZLhk_QW9iXBFCmRbqGJ1QSrTkXE3Qn2nXNbW3qQ4tDkt80YBPfegedrEOTbgfVg3-BukhVDgFfJs21Q7P2wS99WMnYgfpCaDFcxfubd0Ctm2FZ8GP81v0emmbCGeH-xT9vLz4MfuSXd9czWfT68wLwVQ2_NZaKpQHL8qlFNo5KD0TheROcFcJxxkQyp3yslCiYr4itvCVVMMwVPgp-rDndn143EBMZl1HD01jWwibaKjWulRCF3qIftpHfR9i7GFpur5e235nKDGjXrMyo0MzOjSjXnPQa7ZD-d3hnY1bQ_W_evA5BD7vA091A7sXoM3i9_SW65GQ7Ql1TLB9Jtj-rykUV9LcLa7M-feZ_LqQv0zJ_wHKeJrZ</recordid><startdate>200009</startdate><enddate>200009</enddate><creator>BINIENDA, ZBIGNIEW</creator><creator>BEAUDOIN, MICHAEL A.</creator><creator>THORN, BRETT T.</creator><creator>SADOVOVA, NATALYA</creator><creator>SKINNER, ROBERT D.</creator><creator>SLIKKER JR, WILLIAM</creator><creator>ALI, SYED F.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7ST</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope><scope>SOI</scope></search><sort><creationdate>200009</creationdate><title>Application of Electrophysiological Method to Study Interactions between Ibogaine and Cocaine</title><author>BINIENDA, ZBIGNIEW ; 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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.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>11085337</pmid><doi>10.1111/j.1749-6632.2000.tb05212.x</doi><tpages>7</tpages></addata></record> |
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subjects | 3,4-Dihydroxyphenylacetic Acid - metabolism Analysis of Variance Animals Brain Chemistry - drug effects Cerebral Cortex - drug effects Cocaine - pharmacology Dopamine - metabolism Dopamine Uptake Inhibitors - pharmacology Drug Interactions Electroencephalography - methods Excitatory Amino Acid Antagonists - pharmacology Homovanillic Acid - metabolism Hydroxyindoleacetic Acid - metabolism Ibogaine - pharmacology Male Rats Rats, Sprague-Dawley Serotonin - metabolism Time Factors Wakefulness |
title | Application of Electrophysiological Method to Study Interactions between Ibogaine and Cocaine |
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