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Nielsen DA, Kreek MJ
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Common and specific liability to addiction: Approaches to association studies of opioid addiction
DRUG AND ALCOHOL DEPENDENCE 2012 JUN; 123(?):S33-S41
Background: Opioid addiction, whether to opiates such as heroin and morphine, and/or to non-medical use of opioids, is a major problem worldwide. Although drug-induced and environmental factors are essential for the liability to develop opioid addiction, the genetic background of an individual is now known also to play a substantial role. Methods: The overall goal of this article is to address the common and specific liabilities to addiction in the context of approaches to studies of one addiction, opioid addiction. Literature on identifying genetic variants that may play a role in the development of opioid addiction was reviewed. Results: A substantial number of genetic variants have been reported to be associated with opioid addiction. No single variant has been found in any of the reported GWAS studies with a substantial effect size on the liability to develop heroin addiction. It appears that there is a complex interaction of a large number of variants, some rare, some common, which interact with the environment and in response to specific drugs of abuse to increase the liability of developing opioid addiction. Conclusions: In spite of the inherent difficulties in obtaining large well-phenotyped cohorts for genetic studies, new findings have been reported that are being used to develop testable hypotheses into the biological basis of opioid addiction. (C) 2012 Published by Elsevier Ireland Ltd.
Toth B, Mehes L, Tasko S, Szalai Z, Tulassay Z, Cypowyj S, Casanova JL, Puel A, Marodi L
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Herpes in STAT1 deficiency
LANCET 2012 JUN 30; 379(9835):2500-2500
Pedergnana V, Gessain A, Tortevoye P, Byun M, Bacq-Daian D, Boland A, Casanova JL, Abel L, Plancoulaine S
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A major locus on chromosome 3p22 conferring predisposition to human herpesvirus 8 infection
EUROPEAN JOURNAL OF HUMAN GENETICS 2012 JUN; 20(6):690-695
Infection with human herpesvirus 8 (HHV-8), the etiological agent of Kaposi's sarcoma, has been shown to display strong familial aggregation, in countries in which HHV-8 infection is endemic. We investigated 40 large families (608 subjects aged one to 88 years) living in an isolated area of Cameroon in which HHV-8 is highly endemic. We performed a two-step genetic analysis for HHV-8 infection status (HHV-8+/HHV-8- determined by immunofluorescence) consisting of an initial segregation analysis followed by a model-based genome-wide linkage analysis. Overall HHV-8 seroprevalence was 60%, increasing with age. Segregation analysis provided strong evidence for a recessive major gene conferring predisposition to HHV-8 infection. This gene is predicted to have a major effect during childhood, with almost all homozygous predisposed subjects (similar to 7% of the population) becoming infected by the age of 10. Linkage analysis was carried out on the 15 most informative families, corresponding to 205 genotyped subjects. A single region on chromosome 3p22 was significantly linked to HHV-8 infection (LOD score=3.83, P=2.0x10(-5)). This study provides the first evidence that HHV-8 infection in children in endemic areas has a strong genetic basis involving at least one recessive major locus on chromosome 3p22. European Journal of Human Genetics (2012) 20, 690-695; doi:10.1038/ejhg.2011.260; published online 18 January 2012
Davoli T, de Lange T
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Telomere-Driven Tetraploidization Occurs in Human Cells Undergoing Crisis and Promotes Transformation of Mouse Cells
CANCER CELL 2012 JUN 12; 21(6):765-776
Human cancers with a subtetraploid karyotype are thought to originate from tetraploid precursors, but the cause of tetraploidization is unknown. We previously documented endoreduplication in mouse cells with persistent telomere dysfunction or genome-wide DNA damage. We now report that endoreduplication and mitotic failure occur during telomere crisis in human fibroblasts and mammary epithelial cells and document the role of p53 and Rb in repressing tetraploidization. Using an inducible system to generate transient telomere damage, we show that telomere-driven tetraploidization enhances the tumorigenic transformation of mouse cells. Similar to human solid cancers, the resulting tumors evolved subtetraploid karyotypes. These data establish that telomere-driven tetraploidization is induced by critically short telomeres and has the potential to promote tumorigenesis in early cancerous lesions.
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Mccartin J, Rios AAO, Ryckbosch D, Strobbe N, Thyssen F, Tytgat M, Vanelderen L, Verwilligen P, Walsh S, Yazgan E, Zaganidis N, Basegmez S, Bruno G, Castello R, Ceard L, Delaere C, du Pree T, Favart D, Forthomme L, Giammanco A, Hollar J, Lemaitre V, Liao J, Militaru O, Nuttens C, Pagano D, Pin A, Piotrzkowski K, Schul N, Garcia JMV, Beliy N, Caebergs T, Daubie E, Hammad GH, Alves GA, Martins MC, Damiao DD, Martins T, Pol ME, Souza MHG, Alda WL, Carvalho W, Custodio A, Da Costa EM, Martins CD, De Souza SF, Figueiredo DM, Mundim L, Nogima H, Oguri V, Da Silva WLP, Santoro A, Jorge LS, Sznajder A, Bernardes CA, Dias FA, Tomei TRFP, Gregores EM, Lagana C, Marinho F, Mercadante PG, Novaes SF, Padula SS, Genchev V, Iaydjiev P, Piperov S, Rodozov M, Stoykova S, Sultanov G, Tcholakov V, Trayanov R, Vutova M, Dimitrov A, Hadjiiska R, Kozhuharov V, Litov L, Pavlov B, Petkov P, Bian JG, Chen GM, Chen HS, Jiang CH, Liang D, Liang S, Meng X, Tao J, Wang J, Wang X, Wang Z, Xiao H, Xu M, Zang J, Zhang Z, Asawatangtrakuldee C, Ban Y, Guo S, Guo Y, Li W, Liu S, Mao Y, Qian SJ, Teng H, Wang S, Zhu B, Zou W, Avila C, Gomez JP, Moreno BG, Oliveros AFO, Sanabria JC, Godinovic N, Lelas D, Plestina R, Polic D, Puljak I, Antunovic Z, Kovac M, Brigljevic V, Duric S, Kadija K, Luetic J, Morovic S, Attikis A, Galanti M, Mavromanolakis G, Mousa J, Nicolaou C, Ptochos F, Razis PA, Finger M, Finger M, Assran Y, Elgammal S, Kamel AE, Khalil S, Mahmoud MA, Radi A, Kadastik M, Muentel M, Raidal M, Rebane L, Tiko A, Azzolini V, Eerola P, Fedi G, Voutilainen M, Harkonen J, Heikkinen A, Karimaki V, Kinnunen R, Kortelainen MJ, Lampen T, Lassila-Perini K, Lehti S, Linden T, Luukka P, Maenpaa T, Peltola T, Tuominen E, Tuominiemi J, Tuovinen E, Ungaro D, Wendland L, Banzuzi K, Karjalainen A, Korpela A, Tuuva T, Besancon M, Choudhury S, Dejardin M, Denegri D, Fabbro B, Faure JL, Ferri F, Ganjour S, Givernaud A, Gras P, de Monchenault GH, Jarry P, Locci E, Malcles J, Millischer L, Nayak A, Rander J, 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I, Foudas C, Kokkas P, Manthos N, Papadopoulos I, Patras V, Bencze G, Hajdu C, Hidas P, Horvath D, Radics B, Sikler F, Veszpremi V, Vesztergombi G, Beni N, Czellar S, Molnar J, Palinkas J, Szillasi Z, Karancsi J, Raics P, Trocsanyi ZL, Ujvari B, Beri SB, Bhatnagar V, Dhingra N, Gupta R, Jindal M, Kaur M, Mehta MZ, Nishu N, Saini LK, Sharma A, Singh J, Ahuja S, Bhardwaj A, Choudhary BC, Kumar A, Kumar A, Malhotra S, Naimuddin M, Ranjan K, Sharma V, Shivpuri RK, Banerjee S, Bhattacharya S, Dutta S, Gomber B, Jain S, Jain S, Khurana R, Sarkar S, Sharan M, Abdulsalam A, Choudhury RK, Dutta D, Kailas S, Kumar V, Mehta P, Mohanty AK, Pant LM, Shukla P, Aziz T, Ganguly S, Guchait M, Maity M, Majumder G, Mazumdar K, Mohanty GB, Parida B, Sudhakar K, Wickramage N, Banerjee S, Dugad S, Arfaei H, Bakhshiansohi H, Etesami SM, Fahim A, Hashemi M, Jafari A, Khakzad M, Mohammadi A, Najafabadi MM, Mehdiabadi SP, Safarzadeh B, Zeinali M, Abbrescia M, Barbone L, Calabria C, Chhibra SS, Colaleo A, Creanza D, De Filippis N, De Palma M, Fiore L, Iaselli G, Lusito L, Maggi G, Maggi M, Marangelli B, My S, Nuzzo S, Pacifico N, Pompili A, Pugliese G, Selvaggi G, Silvestris L, Singh G, Zito G, Abbiendi G, Benvenuti AC, Bonacorsi D, Braibant-Giacomelli S, Brigliadori L, Capiluppi P, Castro A, Cavallo FR, Cuffiani M, Dallavalle GM, Fabbri F, Fanfani A, Fasanella D, Giacomelli P, Grandi C, Guiducci L, Marcellini S, Masetti G, Meneghelli M, Montanari A, Navarria FL, Odorici F, Perrotta A, Primavera F, Rossi AM, Rovelli T, Siroli G, Travaglini R, Albergo S, Cappello G, Chiorboli M, Costa S, Potenza R, Tricomi A, Tuve C, Barbagli G, Ciulli V, Civinini C, D'Alessandro R, Focardi E, Frosali S, Gallo E, Gonzi S, Meschini M, Paoletti S, Sguazzoni G, Tropiano A, Benussi L, Bianco S, Colafranceschi S, Fabbri F, Piccolo D, Fabbricatore P, Musenich R, Benaglia A, De Guio F, Di Matteo L, Fiorendi S, Gennai S, Ghezzi A, Malvezzi S, Manzoni RA, Martelli A, Massironi A, Menasce D, Moroni L, Paganoni M, Pedrini D, Ragazzi S, Redaelli N, Sala S, de Fatis TT, Buontempo S, Montoya CAC, Cavallo N, De Cosa A, Dogangun O, Fabozzi F, Iorio AOM, Lista L, Meola S, Merola M, Paolucci P, Azzi P, Bacchetta N, Bellan P, Bisello D, Branca A, Carlin R, Checchia P, Dorigo T, Gasparini F, Gasparini U, Gozzelino A, Kanishchev K, Lacaprara S, Lazzizzera I, Margoni M, Meneguzzo AT, Pozzobon N, Ronchese P, Simonetto F, Torassa E, Tosi M, Vanini S, Zotto P, Zumerle G, Gabusi M, Ratti SP, Riccardi C, Torre P, Vitulo P, Biasini M, Bilei GM, Fano L, Lariccia P, Lucaroni A, Mantovani G, Menichelli M, Nappi A, Romeo F, Saha A, Santocchia A, Taroni S, Azzurri P, Bagliesi G, Boccali T, Broccolo G, Castaldi R, D'Agnolo RT, Dell'Orso R, Fiori F, Foa L, Giassi A, Kraan A, Ligabue F, Lomtadze T, Martini L, Messineo A, Palla F, Rizzi A, Serban AT, Spagnolo P, Squillacioti P, Tenchini R, Tonelli G, Venturi A, Verdini PG, Barone L, Cavallari F, Del Re D, Diemoz M, Grassi M, Longo E, Meridiani P, Micheli F, Nourbakhsh S, 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Moreno SC, Valencia FV, Ibarguen HAS, Linares EC, Pineda AM, Reyes-Santos MA, Krofcheck D, Bell AJ, Butler PH, Doesburg R, Reucroft S, Silverwood H, Ahmad M, Asghar MI, Hoorani HR, Khalid S, Khan WA, Khurshid T, Qazi S, Shah MA, Shoaib M, Brona G, Bunkowski K, Cwiok M, Dominik W, Doroba K, Kalinowski A, Konecki M, Krolikowski J, Bialkowska H, Boimska B, Frueboes T, Gokieli R, Gorski M, Kazana M, Nawrocki K, Romanowska-Rybinska K, Szleper M, Wrochna G, Zalewski P, Almeida N, Bargassa P, David A, Faccioli P, Parracho PGF, Gallinaro M, Seixas J, Varela J, Vischia P, Belotelov I, Bunin P, Gavrilenko M, Golutvin I, Gorbunov I, Kamenev A, Karjavin V, Kozlov G, Lanev A, Malakhov A, Moisenz P, Palichik V, Perelygin V, Shmatov S, Smirnov V, Volodko A, Zarubin A, Evstyukhin S, Golovtsov V, Ivanov Y, Kim V, Levchenko P, Murzin V, Oreshkin V, Smirnov I, Sulimov V, Uvarov L, Vavilov S, Vorobyev A, Vorobyev A, Andreev Y, Dermenev A, Gninenko S, Golubev N, Kirsanov M, Krasnikov N, Matveev V, 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Santaolalla J, Soares MS, Willmott C, Albajar C, Codispoti G, de Troconiz JF, Cuevas J, Menendez JF, Folgueras S, Caballero IG, Iglesias LL, Gomez JP, Cifuentes JAB, Cabrillo IJ, Calderon A, Chuang SH, Campderros JD, Felcini M, Fernandez M, Gomez G, Sanchez JG, Jorda C, Pardo PL, Virto AL, Marco J, Marco R, Rivero CM, Matorras F, Sanchez FJM, Rodrigo T, Rodriguez-Marrero AY, Ruiz-Jimeno A, Scodellaro L, Sanudo MS, Vila I, Cortabitarte RV, Abbaneo D, Auffray E, Auzinger G, Baillon P, Ball AH, Barney D, Bernet C, Bianchi G, Bloch P, Bocci A, Bonato A, Breuker H, Camporesi T, Cerminara G, Christiansen T, Perez JAC, D'Enterria D, Dabrowski A, De Roeck A, Di Guida S, Dobson M, Dupont-Sagorin N, Elliott-Peisert A, Frisch B, Funk W, Georgiou G, Giffels M, Gigi D, Gill K, Giordano D, Giunta M, Glege F, Garrido RGR, Govoni P, Gowdy S, Guida R, Hansen M, Harris P, Hartl C, Harvey J, Hegner B, Hinzmann A, Innocente V, Janot P, Kaadze K, Karavakis E, Kousouris K, Lecoq P, Lee YJ, Lenzi P, Lourenco 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ZJ, Hu G, Maksimovic P, Rappoccio S, Swartz M, Whitbeck A, Baringer P, Bean A, Benelli G, Grachov O, Kenny RP, Murray M, Noonan D, Sanders S, Stringer R, Tinti G, Wood JS, Zhukova V, Barfuss AF, Bolton T, Chakaberia I, Ivanov A, Khalil S, Makouski M, Maravin Y, Shrestha S, Svintradze I, Gronberg J, Lange D, Wright D, Baden A, Boutemeur M, Calvert B, Eno SC, Gomez JA, Hadley NJ, Kellogg RG, Kirn M, Kolberg T, Lu Y, Marionneau M, Mignerey AC, Peterman A, Skuja A, Temple J, Tonjes MB, Tonwar SC, Twedt E, Bauer G, Bendavid J, Busza W, Butz E, Cali IA, Chan M, Dutta V, Ceballos GG, Goncharov M, Hahn KA, Kim Y, Klute M, Krajczar K, Li W, Luckey PD, Ma T, Nahn S, Paus C, Ralph D, Roland C, Roland G, Rudolph M, Stephans GSF, Stoeckli F, Sumorok K, Sung K, Velicanu D, Wenger EA, Wolf R, Wyslouch B, Xie S, Yang M, Yilmaz Y, Yoon AS, Zanetti M, Cooper SI, Dahmes B, De Benedetti A, Franzoni G, Gude A, Kao SC, Klapoetke K, Kubota Y, Mans J, Pastika N, Rusack R, Sasseville M, Singovsky A, Tambe N, 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Stickland D, Tully C, Werner JS, Zuranski A, Acosta JG, Brownson E, Huang XT, Lopez A, Mendez H, Oliveros S, Vargas JER, Zatserklyaniy A, Alagoz E, Barnes VE, Benedetti D, Bolla G, Bortoletto D, De Mattia M, Everett A, Hu Z, Jones M, Koybasi O, Kress M, Laasanen AT, Leonardo N, Maroussov V, Merkel P, Miller DH, Neumeister N, Shipsey I, Silvers D, Svyatkovskiy A, Marono MV, Yoo HD, Zablocki J, Zheng Y, Guragain S, Parashar N, Adair A, Boulahouache C, Ecklund KM, Geurts FJM, Padley BP, Redjimi R, Roberts J, Zabel J, Betchart B, Bodek A, Chung YS, Covarelli R, De Barbaro P, Demina R, Eshaq Y, Garcia-Bellido A, Goldenzweig P, Han J, Harel A, Miner DC, Vishnevskiy D, Zielinski M, Bhatti A, Ciesielski R, Demortier L, Goulianos K, Lungu G, Malik S, Mesropian C, Arora S, Barker A, Chou JP, Contreras-Campana C, Contreras-Campana E, Duggan D, Ferencek D, Gershtein Y, Gray R, Halkiadakis E, Hidas D, Lath A, Panwalkar S, Park M, Patel R, Rekovic V, Robles J, Rose K, Salur S, Schnetzer S, Seitz C, Somalwar S, Stone R, Thomas S, Cerizza G, Hollingsworth M, Spanier S, Yang ZC, York A, Eusebi R, Flanagan W, Gilmore J, Kamon T, Khotilovich V, Montalvo R, Osipenkov I, Pakhotin Y, Perloff A, Roe J, Safonov A, Sakuma T, Sengupta S, Suarez I, Tatarinov A, Toback D, Akchurin N, Damgov J, Dudero PR, Jeong C, Kovitanggoon K, Lee SW, Libeiro T, Roh Y, Volobouev I, Appelt E, Florez C, Greene S, Gurrola A, Johns W, Johnston C, Kurt P, Maguire C, Melo A, Sheldon P, Snook B, Tuo S, Velkovska J, Arenton MW, Balazs M, Boutle S, Cox B, Francis B, Goodell J, Hirosky R, Ledovskoy A, Lin C, Neu C, Wood J, Yohay R, Gollapinni S, Harr R, Karchin PE, Don CKK, Lamichhane P, Sakharov A, Anderson M, Bachtis M, Belknap D, Borrello L, Carlsmith D, Cepeda M, Dasu S, Gray L, Grogg KS, Grothe M, Hall-Wilton R, Herndon M, Herve A, Klabbers P, Klukas J, Lanaro A, Lazaridis C, Leonard J, Loveless R, Mohapatra A, Ojalvo I, Palmonari F, Pierro GA, Ross I, Savin A, Smith WH, Swanson J
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Observation of a New Xi(b) Baryon
PHYSICAL REVIEW LETTERS 2012 JUN 21; 108(25):? Article 252002
The observation of a new b baryon via its strong decay into Xi(-)(b)pi(+) (plus charge conjugates) is reported. The measurement uses a data sample of pp collisions at root s = 7 TeV collected by the CMS experiment at the LHC, corresponding to an integrated luminosity of 5.3 fb(-1). The known Xi(-)(b) baryon is reconstructed via the decay chain Xi(-)(b) -> J/psi Xi(-) -> mu(+)mu(-)Lambda(0)pi(-), with Lambda(0) -> p pi(-). A peak is observed in the distribution of the difference between the mass of the Xi(-)(b)pi(+) system and the sum of the masses of the Xi(-)(b) and pi(+), with a significance exceeding 5 standard deviations. The mass difference of the peak is 14.84 +/- 0.74(stat) +/- 0.28(syst) MeV. The new state most likely corresponds to the J(P) = 3/2(+) companion of the Xi(b).
Zhang XJ, Abreu JG, Yokota C, MacDonald BT, Singh S, Coburn KLA, Cheong SM, Zhang MZM, Ye QZ, Hang HC, Steen H, He X
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Tiki1 Is Required for Head Formation via Wnt Cleavage-Oxidation and Inactivation
CELL 2012 JUN 22; 149(7):1565-1577
Secreted Wnt morphogens are signaling molecules essential for embryogenesis, pathogenesis, and regeneration and require distinct modifications for secretion, gradient formation, and activity. Whether Wnt proteins can be posttranslationally inactivated during development and homeostasis is unknown. Here we identify, through functional cDNA screening, a transmembrane protein Tiki1 that is expressed specifically in the dorsal Spemann-Mangold Organizer and is required for anterior development during Xenopus embryogenesis. Tiki1 antagonizes Wnt function in embryos and human cells via a TIKI homology domain that is conserved from bacteria to mammals and acts likely as a protease to cleave eight amino-terminal residues of a Wnt protein, resulting in oxidized Wnt oligomers that exhibit normal secretion but minimized receptor-binding capability. Our findings identify a Wnt-specific protease that controls head formation, reveal a mechanism for morphogen inactivation through proteolysis-induced oxidation-oligomerization, and suggest a role of the Wnt amino terminus in evasion of oxidizing inactivation. TIKI proteins may represent potential therapeutic targets.
Muller M, Mentel M, van Hellemond JJ, Henze K, Woehle C, Gould SB, Yu RY, van der Giezen M, Tielens AGM, Martin WF
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Biochemistry and Evolution of Anaerobic Energy Metabolism in Eukaryotes
MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS 2012 JUN; 76(2):444-495
Proudnikov D, Randesi M, Levran O, Crystal H, Dorn M, Ott J, Ho A, Kreek MJ
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Association of Polymorphisms of the Mu Opioid Receptor Gene with the Severity of HIV Infection and Response to HIV Treatment
JOURNAL OF INFECTIOUS DISEASES 2012 JUN 1; 205(11):1745-1756
Mu opioid receptor (OPRM1) ligands may alter expression of chemokines and chemokine receptors involved in penetration of human immunodeficiency virus (HIV) type 1 into the cell. We suggest that OPRM1 variants may affect the pathophysiology of HIV infection. DNA samples from 1031 eligible African Americans, Hispanics, and whites from the Women's Interagency HIV Study (WIHS) who were alive as of April 2006 were analyzed. We performed regression analysis of association of 18 OPRM1 variants with a change of viral load and CD4 cell count during 2 periods: between admission to WIHS and the start of highly active antiretroviral therapy (HAART) (interval X) and between the start of HAART and the most recent WIHS visit (interval Y), and examined the association of these variants with HIV status. Regardless of genotype, a significant decrease in viral load during interval X was found for each ethnicity. Whites with allele G of the functional polymorphism 118A > G (reference sequence rs1799971) showed a smaller decrease in viral load; those bearing minor alleles IVS1 + 1050A, IVS1 + 14123A, and IVS2 + 31A showed a larger decrease in viral load over interval X (0.01 < P < .05). Hispanics with the same alleles showed a greater increase in CD4 cell count over interval Y (0.01 < P < .05). We found an association between OPRM1 variants and HIV status in African Americans and whites. OPRM1 polymorphisms may alter the severity of HIV infection before and after HAART.
Bieniasz PD
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An overview of intracellular interactions between immunodeficiency viruses and their hosts
AIDS 2012 JUN 19; 26(10):1243-1254
Many studies have documented how extensively HIV-1 and related viruses interact with host cells. Virus-host interactions are of two conceptual types. First, viruses have evolved to make use of numerous host-cell functions to facilitate their own replication. Second, hosts have evolved a number of activities to inhibit virus replication. Understanding the scope and details of HIV-host interactions has been an extraordinary rich scientific endeavor, and in addition to their biomedical importance, studies in this area have established HIV as a model system in virology. Here, I present an overview of how HIV-1 interacts with some key host cell factors during its replication cycle. (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
Butelman ER, Caspers M, Lovell KM, Kreek MJ, Prisinzano TE
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Behavioral Effects and Central Nervous System Levels of the Broadly Available kappa-Agonist Hallucinogen Salvinorin A Are Affected by P-Glycoprotein Modulation In Vivo
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2012 JUN; 341(3):802-808
Active blood-brain barrier mechanisms, such as the major efflux transporter P-glycoprotein (mdr1), modulate the in vivo/central nervous system (CNS) effects of many pharmacological agents, whether they are used for nonmedical reasons or in pharmacotherapy. The powerful, widely available hallucinogen salvinorin A (from the plant Salvia divinorum) is a high-efficacy, selective kappa-opioid agonist and displays fast-onset behavioral effects (e. g., within 1 min of administration) and relatively short duration of action. In vitro studies suggest that salvinorin A may be a P-glycoprotein substrate; thus, the functional status of P-glycoprotein may influence the behavioral effects of salvinorin A or its residence in CNS after parenteral administration. We therefore studied whether a competing P-glycoprotein substrate (the clinically available agent loperamide; 0.032-0.32 mg/kg) or a selective P-glycoprotein blocker, tariquidar (0.32-3.2 mg/kg) could enhance unconditioned behavioral effects (ptosis and facial relaxation, known to be caused by kappa-agonists in nonhuman primates) of salvinorin A, as well as its entry and residence in the CNS, as measured by cerebrospinal fluid sampling. Pretreatment with either loperamide or tariquidar dose-dependently enhanced salvinorin A-induced ptosis, but not facial relaxation. In a control study, loperamide and tariquidar were inactive when given as a pretreatment to ((+)-(5 alpha,7 alpha,8 beta)-N-methyl-N-[7-(1-pyrrolidinyl)-1-oxaspiro[4.5]dec-8-yl]-benzeneacetamide (U69,593), a kappa-agonist known to be a very poor P-glycoprotein substrate. Furthermore, pretreatment with tariquidar (3.2 mg/kg) also enhanced peak levels of salvinorin A in cerebrospinal fluid after intravenous administration. These are the first studies in vivo showing the sensitivity of salvinorin A effects to modulation by the P-glycoprotein transporter, a major functional component of the blood-brain barrier.