Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
COCAINE 2010 <88> Database EMBASE Accession Number 2010261456 Authors Moeller S.J. Maloney T. Parvaz M.A. Alia-Klein N. Woicik P.A. Telang F. Wang G.-J. Volkow N.D. Goldstein R.Z. Institution (Moeller, Maloney) Department of Psychology, University of Michigan, Ann Arbor, MI 48109, United States. (Moeller, Parvaz, Alia-Klein, Woicik, Wang, Goldstein) Medical Department, Brookhaven National Laboratory, Upton, NY 11973, United States. (Parvaz) Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794, United States. (Telang) Intramural Program, National Institute on Alcohol Abuse and Alcoholism, Bethesda MD 20892, United States. (Volkow) Director's Office, National Institute on Drug Abuse, Bethesda, MD 20892, United States. Country of Publication United Kingdom Title Impaired insight in cocaine addiction: Laboratory evidence and effects on cocaineseeking behaviour. Source Brain. 133(5)(pp 1484-1493), 2010. Date of Publication: May 2010. Publisher Oxford University Press Abstract Neuropsychiatric disorders are often characterized by impaired insight into behaviour. Such an insight deficit has been suggested, but never directly tested, in drug addiction. Here we tested for the first time this impaired insight hypothesis in drug addiction, and examined its potential association with drug-seeking behaviour. We also tested potential modulation of these effects by cocaine urine status, an individual difference known to impact underlying cognitive functions and prognosis. Sixteen cocaine addicted individuals testing positive for cocaine in urine, 26 cocaine addicted individuals testing negative for cocaine in urine, and 23 healthy controls completed a probabilistic choice task that assessed objective preference for viewing four types of pictures (pleasant, unpleasant, neutral and cocaine). This choice task concluded by asking subjects to report their most selected picture type; correspondence between subjects' self-reports with their objective choice behaviour provided our index of behavioural insight. Results showed that the urine positive cocaine subjects exhibited impaired insight into their own choice behaviour compared with healthy controls; this same study group also selected the most cocaine pictures (and fewest pleasant pictures) for viewing. Importantly, however, it was the urine negative cocaine subjects whose behaviour was most influenced by insight, such that impaired insight in this subgroup only was associated with higher cocaine-related choice on the task and more severe actual cocaine use. These findings suggest that interventions to enhance insight may decrease drug-seeking behaviour, especially in urine negative cocaine subjects, potentially to improve their longerterm clinical outcomes. copyright The Author (2010). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. ISSN 0006-8950 Publication Type Journal: Article Journal Name Brain Volume 133 Issue Part 5 Page 1484-1493 Year of Publication 2010 Date of Publication May 2010 COCAINE 2010 <110> Database EMBASE Accession Number 2010280691 Authors Adinoff B. Devous M.D. Williams M.J. Best S.E. Harris T.S. Minhajuddin A. Zielinski T. Cullum M. Institution (Adinoff, Williams, Best, Zielinski, Cullum) Department of Psychiatry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8564, United States. (Adinoff, Best) VA North Texas Health Care System, Dallas, TX, United States. (Devous, Harris) Nuclear Medicine Center, Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, United States. (Minhajuddin) Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX, United States. Country of Publication United Kingdom Title Altered neural cholinergic receptor systems in cocaine-addicted subjects. Source Neuropsychopharmacology. 35(7)(pp 1485-1499), 2010. Date of Publication: June 2010. Publisher Nature Publishing Group Abstract Changes in the brain's cholinergic receptor systems underlie several neuropsychiatric disorders, including Alzheimer's disease, schizophrenia, and depression. An emerging preclinical literature also reveals that acetylcoholine may have an important function in addictive processes, including reward, learning, and memory. This study was designed to assess alterations in cholinergic receptor systems in limbic regions of abstinent cocaineaddicted subjects compared with healthy controls. On three separate days, 23 1-to 6-week abstinent, cocaine-(and mostly nicotine-) addicted subjects and 22 sex-, age-, and racematched control subjects were administered the muscarinic and nicotinic cholinergic agonist physostigmine, the muscarinic antagonist scopolamine, and saline. Regional cerebral blood flow (rCBF) after each infusion was determined using single photon emission-computed tomography. Both cholinergic probes induced rCBF changes (p0.005) in relatively distinct, cholinergic-rich, limbic brain regions. After physostigmine, cocaine-addicted subjects showed altered rCBF, relative to controls, in limbic regions, including the left hippocampus, left amygdala, and right insula. Group differences in the right dorsolateral prefrontal cortex, posterior cingulate, and middle temporal gyrus were also evident. Scopolamine also revealed group differences in the left hippocampus and right insula as well as the posterior cingulate and middle temporal gyrus. Cocaine addicted and controls differ in their subcortical, limbic, and cortical response to cholinergic probes in areas relevant to craving, learning, and memory. Cholinergic systems may offer a pharmacologic target for cocaine addiction treatment. copyright 2010 Nature Publishing Group All rights reserved. ISSN 0893-133X Publication Type Journal: Article Journal Name Neuropsychopharmacology Volume 35 Issue Part 7 Page 1485-1499 Year of Publication 2010 Date of Publication June 2010 COCAINE 2010 <147> Database EMBASE Accession Number 2010298938 Authors Ren Z. Sun W.L. Jiao H. Zhang D. Kong H. Wang X. Xu M. Institution (Ren, Sun, Jiao, Zhang, Kong, Xu) Department of Anesthesia and Critical Care, The University of Chicago, Chicago, IL 60637, United States. (Wang) Wyeth Research, Collegeville, PA 19426, United States. Country of Publication United Kingdom Title Dopamine D1 and N-methyl-d-aspartate receptors and extracellular signal-regulated kinase mediate neuronal morphological changes induced by repeated cocaine administration. Source Neuroscience. 168(1)(pp 48-60), 2010. Date of Publication: June 2010. Publisher Elsevier Ltd Abstract The development of drug addiction involves persistent cellular and molecular changes in the CNS. The brain dopamine and glutamate systems play key roles in mediating drug-induced neuroadaptation. Changes in dendritic morphology in medium spiny neurons (MSNs) in the nucleus accumbens (NAc) and caudate putamen (CPu) accompany drug-induced enduring behavioral and molecular changes. We have investigated the potential involvement of dopamine D1 and D2 receptors, the N-methyl-. d-aspartate (NMDA) receptor, and the extracellular signal-regulated kinase (ERK) in dendritic morphological changes induced by repeated cocaine administration. We show that either a genetic mutation or pharmacological blockade of dopamine D1 receptors attenuated cocaine-induced changes in both dendritic branching and spine density of MSNs in the shell of the NAc and CPu. In contrast, antagonism of dopamine D2 receptors had no obvious effect on changes in dendritic branching but had a partial effect on changes in spine density of MSNs in these brain regions following repeated cocaine injections. Pharmacological inhibition of either NMDA receptors or ERK attenuated cocaine-induced changes in both dendritic branching and spine density of MSNs in the shell of the NAc and CPu. These results suggest that dopamine D1 and NMDA receptors and ERK contribute significantly to neuronal morphological changes induced by repeated exposure to cocaine. copyright 2010 IBRO. ISSN 0306-4522 Publication Type Journal: Article Journal Name Neuroscience Volume 168 Issue Part 1 Page 48-60 Year of Publication 2010 Date of Publication June 2010 COCAINE <543> Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R) Unique Identifier 20504138 Status In-Process Authors Newport K. Coyne P. Authors Full Name Newport, Kristina. Coyne, Patrick. Institution Hospice of Lancaster County, Lancaster, Pennsylvania 17604-4125, USA. [email protected] Title Topical cocaine for relief of mucosal pain. Source Journal of Pain & Palliative Care Pharmacotherapy. 24(2):149-51, 2010 Jun. Journal Name Journal of Pain & Palliative Care Pharmacotherapy Country of Publication England Abstract Painful mucosal lesions negatively affect quality of life. When located in the oral cavity, they can cause pain that interferes with speech and swallowing. Acute pain from intra-oral lesions is difficult to treat with conventional methods such as systemic opioids or viscous lidocaine. These cases exemplify a safe, fast and effective method for treating painful mouth lesions that are not responsive to standard treatments. Mr. D and Mr. G had from painful oral lesions caused by squamous cell carcinoma. Severe pain interfered with their ability to speak and swallow, resulting in poor nutrition and dehydration. 4% liquid cocaine, self-applied topically to the open mouth sores, resulted in relief within minutes in both cases. Repeated dosing every six hours allowed both patients to restart oral nutrition without any reported side effects. Topical cocaine has not been described for repeated dosing for oral or other mucosal pain. Potential side effects of mucosal administration include gingival recession and erythematous lesions. If the recommended topical doses are exceeded, liquid cocaine may be absorbed systemically causing a stimulant response or addiction. When used appropriately, however, this intervention can result in a dramatic improvement in quality of life and functional status. Publication Type Journal Article. Date of Publication 2010 Jun Year of Publication 2010 Issue/Part 2 Volume 24 Page 149-51 COCAINE 2010 <648> Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R) Unique Identifier 20141397 Status MEDLINE Authors de Los Cobos JP. Sinol N. Banulus E. Batlle F. Tejero A. Trujols J. Authors Full Name de Los Cobos, Jose Perez. Sinol, Nuria. Banulus, Enrique. Batlle, Francisca. Tejero, Antoni. Trujols, Joan. Institution Unitat de Conductes Addictives, Servei de Psiquiatria, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. Title Personality traits of cocaine-dependent patients associated with cocaine-positive baseline urine at hospitalization. Source American Journal of Drug & Alcohol Abuse. 36(1):52-6, 2010 Jan. Journal Name American Journal of Drug & Alcohol Abuse Country of Publication England Abstract BACKGROUND: Cocaine abstinence at treatment entry is considered a predictor of good response in cocaine dependence treatment. Therefore, identification of factors facilitating pretreatment cocaine abstinence could be useful for developing new therapeutic strategies. OBJECTIVE: This retrospective chart review study examines the association between personality traits and cocaine-positive baseline urinalysis (CPB) in cocaine-dependent inpatients. METHODS: All 107 participants met DSM-IV criteria for cocaine dependence, and were admitted consecutively to a closed addiction unit for detoxification treatment. Personality was assessed with the Temperament and Character Inventory and the Millon Clinical Multiaxial Inventory (MCMI-II). RESULTS: CPB was detected in 80 patients (74.8%). The logistic regression model solely based on personality dimensions showed that only the MCMIII avoidant traits were significantly associated with a decreased probability of cocainedependent patients presenting CPB. The logistic regression model based on both personality dimensions and substance use-related variables alike retained the number of days of cocaine use during the last 30 days as a risk factor, and alcohol dependence and the MCMI-II schizoid dimension as protective factors in predicting CPB results. CONCLUSION AND SCIENTIFIC SIGNIFICANCE: Avoidant and schizoid traits are personality dimensions of cocainedependent patients that are associated with cocaine abstinence prior to inpatient admission. These findings suggest an inverse relationship between social isolation and CPB. Notwithstanding, more research is needed, not only to assess the generalizability of these findings, but also to enrich the personality and substance use model with variables related to readiness to change. Publication Type Comparative Study. Journal Article. Research Support, Non-U.S. Gov't. Date of Publication 2010 Jan Year of Publication 2010 Issue/Part 1 Volume 36 Page 52-6 COCAINE 2010 <654> Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R) Unique Identifier 19491693 Status MEDLINE Authors de Millas W. Haasen C. Reimer J. Eiroa-Orosa FJ. Schaefer I. Authors Full Name de Millas, Walter. Haasen, Christian. Reimer, Jens. Eiroa-Orosa, Francisco Jose. Schaefer, Ingo. Institution Center for Interdisciplinary Addiction Research, Department of Psychiatry, University Medical Center HamburgEppendorf, Hamburg, Germany. Title Emergencies related to cocaine use: a European multicentre study of expert interviews. Source European Journal of Emergency Medicine. 17(1):33-6, 2010 Feb. Journal Name European Journal of Emergency Medicine Country of Publication England Abstract Illicit drug use can lead to acute reverse reactions leading to the admission to emergency departments. Cocaine-related emergencies have been monitored in the USA, but not in Europe so far. The study investigates patterns of cocaine emergencies in eight European cities in a multicentre cross-sectional study conducted in Barcelona, Budapest, Dublin, Hamburg, London, Rome, Vienna and Zurich. The reported frequency differs from city to city, with some emergency centres having less than one case per half year, and some centres having more than one case per month. Patterns of complaints among cocaine users are associated with the psychomotor-stimulant or cardiovascular effects of cocaine. Urine screens and referrals to the addiction services are infrequent. A closer link between the emergency departments and addiction services would help in guiding problematic drug users towards appropriate treatment at an earlier stage in the addiction process. Publication Type Journal Article. Multicenter Study. Research Support, Non-U.S. Gov't. Date of Publication 2010 Feb Year of Publication 2010 Issue/Part 1 Volume 17 Page 33-6 COCAINE 2010 <989> Database Ovid MEDLINE(R) Daily Update Unique Identifier 20030966 Status MEDLINE Authors Caselles A. Mico JC. Amigo S. Authors Full Name Caselles, Antonio. Mico, Joan C. Amigo, Salvador. Institution Departament de Matematica Aplicada, Universitat de Valencia, Spain. [email protected] Title Cocaine addiction and personality: a mathematical model. Source British Journal of Mathematical & Statistical Psychology. 63(Pt 2):449-80, 2010 May. Journal Name British Journal of Mathematical & Statistical Psychology Country of Publication England Abstract The existence of a close relation between personality and drug consumption is recognized, but the corresponding causal connection is not well known. Neither is it well known whether personality exercises an influence predominantly at the beginning and development of addiction, nor whether drug consumption produces changes in personality. This paper presents a dynamic mathematical model of personality and addiction based on the unique personality trait theory (UPTT) and the general modelling methodology. This model attempts to integrate personality, the acute effect of drugs, and addiction. The UPTT states the existence of a unique trait of personality called extraversion, understood as a dimension that ranges from impulsive behaviour and sensation-seeking (extravert pole) to fearful and anxious behaviour (introvert pole). As a consequence of drug consumption, the model provides the main patterns of extraversion dynamics through a system of five coupled differential equations. It combines genetic extraversion, as a steady state, and dynamic extraversion in a unique variable measured on the hedonic scale. The dynamics of this variable describes the effects of stimulant drugs on a short-term time scale (typical of the acute effect); while its mean time value describes the effects of stimulant drugs on a longterm time scale (typical of the addiction effect). This understanding may help to develop programmes of prevention and intervention in drug misuse. ISSN Print 0007-1102 Publication Type Journal Article. Date of Publication 2010 May Year of Publication 2010 Issue/Part Pt 2 Volume 63 Page 449-80 COCAINE / AMPHETAMINES 2010 <732> Database EMBASE Accession Number 2009650556 Authors Sofuoglu M. Institution (Sofuoglu) Yale University, Department of Psychiatry, VA Connecticut Healthcare System, 950 Campbell Avenue, West Haven, CT 06516, United States. Country of Publication United Kingdom Title Cognitive enhancement as a pharmacotherapy target for stimulant addiction. Source Addiction. 105(1)(pp 38-48), 2010. Date of Publication: January 2010. Publisher Blackwell Publishing Ltd Abstract Background No medications have been proven to be effective for cocaine and methamphetamine addiction. Attenuation of drug reward has been the main strategy for medications development, but this approach has not led to effective treatments. Thus, there is a need to identify novel treatment targets in addition to the brain reward system. Aim To propose a novel treatment strategy for stimulant addiction that will focus on medications enhancing cognitive function and attenuating drug reward. Methods Pre-clinical and clinical literature on potential use of cognitive enhancers for stimulant addiction pharmacotherapy was reviewed. Results and conclusions Cocaine and methamphetamine users show significant cognitive impairments, especially in attention, working memory and response inhibition functions. The cognitive impairments seem to be predictive of poor treatment retention and outcome. Medications targeting acetylcholine and norepinephrine are particularly well suited for enhancing cognitive function in stimulant users. Many cholinergic and noradrenergic medications are on the market and have a good safety profile and low abuse potential. These include galantamine, donepezil and rivastigmine (cholinesterase inhibitors), varenicline (partial nicotine agonist), guanfacine (alpha2-adrenergic agonist) and atomoxetine (norepinephrine transporter inhibitor). Future clinical studies designed optimally to measure cognitive function as well as drug use behavior would be needed to test the efficacy of these cognitive enhancers for stimulant addiction. copyright 2010 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Review Journal Name Addiction Volume 105 Issue Part 1 Page 38-48 Year of Publication 2010 Date of Publication January 2010 COCAINE / ECSTASY 2010 <754> Database EMBASE Accession Number 2009640171 Authors Alvarenga T.A. Andersen M.L. Ribeiro D.A. Araujo P. Hirotsu C. Costa J.L. Battisti M.C. Tufik S. Institution (Alvarenga, Andersen, Araujo, Hirotsu, Battisti, Tufik) Department of Psychobiology, Universidade Federal de Sao Paulo (UNIFESP), Brazil. (Ribeiro) Biosciences, Universidade Federal de Sao Paulo (UNIFESP), Brazil. (Costa) Instrumental Analysis Laboratory, Criminalistic Institute, Brazil. Country of Publication United Kingdom Title Single exposure to cocaine or ecstasy induces DNA damage in brain and other organs of mice. Source Addiction Biology. 15(1)(pp 96-99), 2010. Date of Publication: January 2010. Publisher Blackwell Publishing Ltd Abstract We evaluated the overall genetic damage induced by different doses of cocaine and MDMA (3,4-Methylenedioxymethamphetamine) in several organs. One hour after intraperitoneal drug administration, mice were euthanized; peripheral blood, liver and brain were collected, and the cellular suspensions were used for the single cell gel (comet) assay. We determined that all doses of cocaine and MDMA tested were able to induce DNA damage in blood cells. Extensive genotoxic damage was induced by cocaine or MDMA at the highest doses used in liver cells. Brain cells were affected by all doses administrated. These findings demonstrate that cocaine and MDMA are potent genotoxins. copyright 2009 Society for the Study of Addiction. ISSN 1355-6215 Publication Type Journal: Article Journal Name Addiction Biology Volume 15 Issue Part 1 Page 96-99 Year of Publication 2010 Date of Publication January 2010 COCAINE (A) 2010 <755> Database EMBASE Accession Number 2009640170 Authors Fiancette J.-F. Balado E. Piazza P.-V. Deroche-Gamonet V. Institution (Fiancette, Balado, Piazza, Deroche-Gamonet) INSERM U862, NeuroCentre Francois Magendie, Physiopathologie de la Plasticite Neuronale, 146 rue Leo Saignat, 33077 Bordeaux Cedex, France. (Fiancette, Balado, Piazza, Deroche-Gamonet) Universite de Bordeaux, Bordeaux, France. Country of Publication United Kingdom Title Mifepristone and spironolactone differently alter cocaine intravenous selfadministration and cocaine-induced locomotion in C57BL/6J mice. Source Addiction Biology. 15(1)(pp 81-87), 2010. Date of Publication: January 2010. Publisher Blackwell Publishing Ltd Abstract Corticosterone, the main glucorticoid hormone in rodents, facilitates behavioral responses to cocaine. Corticosterone is proposed to modulate cocaine intravenous self-administration (SA) and cocaine-induced locomotion through distinct receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), respectively. However, this remains debatable. On one hand, modulation of both responses by the GR was tested in different experimental conditions, i.e. light versus dark nycthemeral phase and naive versus cocaine-experienced animals. On the other hand, modulation of both responses by the MR was never tested directly but only inferred based on the ability of low plasma corticosterone levels (those for which corticosterone almost exclusively binds the MR) to compensate the effects of adrenalectomy. Our goal here was to test the involvement of the GR and the MR in cocaineinduced locomotor and reinforcing effects in the same experimental conditions. C57Bl/6J mice were trained for cocaine (1 mg/kg/infusion) intravenous SA over 40 SA sessions. The animals were then administered with mifepristone (30 mg/kg i.p.), a GR antagonist, or with spironolactone (20 mg/kg/i.p.), an MR antagonist, 2 hours before either cocaine intravenous SA or cocaine-induced locomotion. In a comparable nycthemeral period and in similarly cocaine-experienced animals, a blockade of the GR decreased cocaine-induced reinforcing effects but not cocaine-induced locomotion. A blockade of the MR decreased both cocaineinduced reinforcing (but to a much lesser extent than the GR blockade) and locomotor effects. Altogether, our results comforted the hypothesis that the GR modulates cocaine-related operant conditioning, while the MR would modulate cocaine-related unconditioned effects. The present data also reveal mifepristone as an interesting tool for manipulating the impact of corticosterone on cocaine-induced reinforcing effects in mice. copyright 2009 Society for the Study of Addiction. ISSN 1355-6215 Publication Type Journal: Article Journal Name Addiction Biology Volume 15 Issue Part 1 Page 81-87 Year of Publication 2010 Date of Publication January 2010 COCAINE (A) 2010 <784> Database EMBASE Accession Number 2009627141 Authors Rodriguez-Borrero E. Rivera-Escalera F. Candelas F. Montalvo J. Munoz-Miranda W.J. Walker J.R. Maldonado-Vlaar C.S. Institution (Rodriguez-Borrero, Rivera-Escalera, Candelas, Montalvo, Munoz-Miranda, Maldonado-Vlaar) University of Puerto Rico, Department of Biology, P.O. Box 23360, San Juan, PR 00931, United States. (Walker) Novartis Genome Institute, San Diego, CA, United States. Country of Publication United Kingdom Title Arginine vasopressin gene expression changes within the nucleus accumbens during environment elicited cocaine-conditioned response in rats. Source Neuropharmacology. 58(1)(pp 88-101), 2010. Date of Publication: January 2010. Publisher Elsevier Ltd Abstract It is known that changes in gene expression within the nucleus accumbens (NAc) occur during cocaine dependence development. However, identification of specific genes involved in cocaine conditioning awaits further investigation. We conducted a high throughput gene expression profile analysis of the NAc, during different stages of the environment-elicited cocaine conditioning. Rats were assigned to two different environmental conditions. Cocaine conditioned group received a cocaine injection (10 mg/kg, i.p.) prior to being placed in the activity chambers. Control rats received saline injections before being exposed to their environment. Both groups received a saline injection in their home cage. Conditioning training lasted for 10 days. Animals were then re-exposed to their previously paired environments only on day 12 (test session). We found that the gene for arginine vasopressin (AVP) was differentially expressed on experimental subjects during all stages of environment-elicited cocaine conditioning. To further validate our molecular results, biochemical and immunolocalization experiments were conducted. We found the presence of AVP within accumbal fibers and changes in AVP protein levels following cocaine conditioning. Moreover, we tested the effects of accumbal microinfusions of either AVP receptor V1A agonist [pGlu4, Cyt6, Arg8] AVP 4-9 1.0 ng/0.5 mul, or V1A antagonist (CH2) 5[Tyr (Me) 2] AVP, 1.0 ng/0.5 mul or vehicle solution (0.9% saline solution) during different stages of the cocaine conditioning. Blockade of V1A receptors within the NAc during acquisition interrupted the expression of the conditioned response, while activation leads to an increase in this response. Our findings propose a new role for AVP in cocaine addiction. copyright 2009 Elsevier Ltd. All rights reserved. ISSN 0028-3908 Publication Type Journal: Article Journal Name Neuropharmacology Volume 58 Issue Part 1 Page 88-101 Year of Publication 2010 Date of Publication January 2010 COCAINE 2010 <785> Database EMBASE Accession Number 2009627138 Authors Smith R.J. Tahsili-Fahadan P. Aston-Jones G. Institution (Smith, Tahsili-Fahadan, Aston-Jones) Department of Neurosciences, Medical University of South Carolina, 173 Ashley Ave., 403 Basic Science Bldg, Charleston, SC 29425-5100, United States. Country of Publication United Kingdom Title Orexin/hypocretin is necessary for context-driven cocaine-seeking. Source Neuropharmacology. 58(1)(pp 179-184), 2010. Date of Publication: January 2010. Publisher Elsevier Ltd Abstract Orexin/hypocretin signaling at the orexin 1 receptor (OX1R) has recently been implicated in addiction and relapse. We examined the role of the orexin system in cocaine-seeking elicited by a drug-associated context following abstinence or extinction from chronic cocaine selfadministration. Male Sprague-Dawley rats self-administered cocaine in 2-h sessions for 10 days, followed by extinction training or extended abstinence in the home cage. The OX1R antagonist SB-334867 (SB; 10, 20, or 30 mg/kg, i.p.) was administered prior to re-exposure to the cocaine self-administration environment. We found that pretreatment with SB significantly attenuated cocaine-seeking when rats were placed back into the self-administration environment following either 1 day or 2 weeks of abstinence (no extinction), or following extinction of cocaine-seeking in an alternative environment (distinct from the training environment). These results indicate that orexin signaling at OX1R is critical for conditioned cocaine-seeking elicited by a drug-associated context, following either extinction or abstinence. copyright 2009 Elsevier Ltd. All rights reserved. ISSN 0028-3908 Publication Type Journal: Article Journal Name Neuropharmacology Volume 58 Issue Part 1 Page 179-184 Year of Publication 2010 Date of Publication January 2010 COCAINE (A) 2010 <787> Database EMBASE Accession Number 2009627126 Authors Xi Z.-X. Kiyatkin M. Li X. Peng X.-Q. Wiggins A. Spiller K. Li J. Gardner E.L. Institution (Xi, Kiyatkin, Li, Peng, Wiggins, Spiller, Li, Gardner) Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, United States. Country of Publication United Kingdom Title N-acetylaspartylglutamate (NAAG) inhibits intravenous cocaine self-administration and cocaine-enhanced brain-stimulation reward in rats. Source Neuropharmacology. 58(1)(pp 304-313), 2010. Date of Publication: January 2010. Publisher Elsevier Ltd Abstract Pharmacological activation of group II metabotropic glutamate (mGlu2 and mGlu3) receptors inhibits reward-seeking behavior and/or rewarding efficacy induced by drugs (cocaine, nicotine) or natural rewards (food, sucrose). In the present study, we investigated whether elevation of brain N-acetylaspartylglutamate (NAAG), an endogenous group II mGlu receptor agonist, by the NAAG peptidase inhibitor 2-PMPA attenuates cocaine's rewarding effects, as assessed by intravenous cocaine self-administration and intracranial electrical brainstimulation reward (BSR) in rats. Systemic administration of 2-PMPA (10, 30, 100 mg/kg, i.p.) or intranasal administration of NAAG (100, 300 mug/10 mul/nostril) significantly inhibited intravenous cocaine self-administration under progressive-ratio (PR), but not under fixed-ratio 2 (FR2), reinforcement conditions. In addition, 2-PMPA (1, 10, 30 mg/kg, i.p) or NAAG (50, 100 mug/10 mul/nostril) significantly inhibited cocaine-enhanced BSR, but not basal BSR. Pretreatment with LY341495 (1 mg/kg, i.p.), a selective mGlu2/3 receptor antagonist, prevented the inhibitory effects produced by 2-PMPA or NAAG in both the self-administration and BSR paradigms. In vivo microdialysis demonstrated that 2-PMPA (10, 30, 100 mg/kg) dose-dependently attenuated cocaine-enhanced extracellular dopamine (DA) in the nucleus accumbens (NAc). 2-PMPA alone inhibited basal NAc DA release, an effect that was prevented by LY341495. These findings suggest that systemic administration of 2-PMPA or intranasal administration of NAAG inhibits cocaine's rewarding efficacy and cocaineenhanced NAc DA - likely by activation of presynaptic mGlu2/3 receptors in the NAc. These data suggest a potential utility for 2-PMPA or NAAG in the treatment of cocaine addiction. ISSN 0028-3908 Publication Type Journal: Article Journal Name Neuropharmacology Volume 58 Issue Part 1 Page 304-313 Year of Publication 2010 Date of Publication January 2010 COCAINE 2010 <804> Database EMBASE Accession Number 2009627911 Authors Grakalic I. Panlilio L.V. Quiroz C. Schindler C.W. Institution (Grakalic, Panlilio, Quiroz, Schindler) DHHS, NIH, NIDA Intramural Research Program, Baltimore, MD, United States. Country of Publication United Kingdom Title Effects of orbitofrontal cortex lesions on cocaine self-administration. Source Neuroscience. 165(2)(pp 313-324), 2010. Date of Publication: 20 Jan 2010. Publisher Elsevier Ltd Abstract Previous research has implicated limbic and prefrontal cortical areas in the control of drugseeking behavior. The present study examined the effects of orbitofrontal-cortex (OFC) lesions on acquisition, dose-dependence, within-session patterning, and reinstatement of cocaine self-administration. Rats received OFC or sham lesions before or after acquisition (0.3 mg/kg/injection, paired with a visual stimulus), then were tested with a range of doses (0, 0.03, 0.1, 0.3 and 1). Compared to controls, rats lesioned before acquisition acquired the behavior sooner, responded more at low doses, and responded more on the first day of extinction. Rats that were lesioned after acquisition showed an even larger increase in responding ([similar to]250%) at the lowest dose, and they also showed increased timeout responding and drug "loading" at low doses. Pre-acquisition lesions were tested and found to have no effect on cocaine-induced reinstatement. In parallel experiments examining effects of pre-acquisition OFC lesions on food-reinforced responding, lesions did not alter acquisition, maintenance, or reinstatement, but accelerated the course of extinction. The increased cocaine self-administration seen in OFC-lesioned rats did not resemble the dysregulated drug intake observed in long-access models of addiction but might be due to impaired response inhibition or impaired tracking of the reward value of drug-related cues. ISSN 0306-4522 Publication Type Journal: Article Journal Name Neuroscience Volume 165 Issue Part 2 Page 313-324 Year of Publication 2010 Date of Publication 20 Jan 2010 COCAINE 2010 <853> Database EMBASE Accession Number 2010051720 Authors Espana R.A. Oleson E.B. Locke J.L. Brookshire B.R. Roberts D.C.S. Jones S.R. Institution (Espana, Oleson, Locke, Brookshire, Roberts, Jones) Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157, United States. Country of Publication United Kingdom Title The hypocretin-orexin system regulates cocaine self-administration via actions on the mesolimbic dopamine system. Source European Journal of Neuroscience. 31(2)(pp 336-348), 2010. Date of Publication: January 2010. Publisher Blackwell Publishing Ltd Abstract Recent evidence suggests that the hypocretin-orexin system participates in the regulation of reinforcement processes. The current studies examined the extent to which hypocretin neurotransmission regulates behavioral and neurochemical responses to cocaine, and behavioral responses to food reinforcement. These studies used a combination of fixed ratio, discrete trials, progressive ratio and threshold self-administration procedures to assess whether the hypocretin 1 receptor antagonist, SB-334867, reduces cocaine selfadministration in rats. Progressive ratio sucrose self-administration procedures were also used to assess the extent to which SB-334867 reduces responding to a natural reinforcer in food-restricted and food-sated rats. Additionally, these studies used microdialysis and in vivo voltammetry in rats to examine whether SB-334867 attenuates the effects of cocaine on dopamine signaling within the nucleus accumbens core. Furthermore, in vitro voltammetry was used to examine whether hypocretin knockout mice display attenuated dopamine responses to cocaine. Results indicate that when SB-334867 was administered peripherally or within the ventral tegmental area, it reduced the motivation to self-administer cocaine and attenuated cocaine-induced enhancement of dopamine signaling. SB-334867 also reduced the motivation to self-administer sucrose in food-sated but not food-restricted rats. Finally, hypocretin knockout mice displayed altered baseline dopamine signaling and reduced dopamine responses to cocaine. Combined, these studies suggest that hypocretin neurotransmission participates in reinforcement processes, likely through modulation of the mesolimbic dopamine system. Additionally, the current observations suggest that the hypocretin system may provide a target for pharmacotherapies to treat cocaine addiction. copyright 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd. ISSN 0953-816X Publication Type Journal: Article Journal Name European Journal of Neuroscience Volume 31 Issue Part 2 Page 336-348 Year of Publication 2010 Date of Publication January 2010 COCAINE 2010 <871> Database EMBASE Accession Number 2010077310 Authors Tannu N.S. Howell L.L. Hemby S.E. Institution (Tannu, Hemby) Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, United States. (Howell) Neuroscience Division, Yerkes National Primate Research Center, Emory University, Atlanta, GA, United States. (Howell) Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, United States. (Hemby) Department of Psychiatry and Behavioral Medicine, Wake Forest University School of Medicine, WinstonSalem, NC, United States. Country of Publication United Kingdom Title Integrative proteomic analysis of the nucleus accumbens in rhesus monkeys following cocaine self-administration. Source Molecular Psychiatry. 15(2)(pp 185-203), 2010. Date of Publication: January 2010. Publisher Nature Publishing Group Abstract The reinforcing effects and long-term consequences of cocaine self-administration have been associated with brain regions of the mesolimbic dopamine pathway, namely the nucleus accumbens (NAc). Studies of cocaine-induced biochemical adaptations in rodent models have advanced our knowledge; however, unbiased detailed assessments of intracellular alterations in the primate brain are scarce, yet essential, to develop a comprehensive understanding of cocaine addiction. To this end, two-dimensional difference in gel electrophoresis (2D-DIGE) was used to compare changes in cytosolic protein abundance in the NAc between rhesus monkeys self-administering cocaine and controls. Following image normalization, spots with significantly differential image intensities (P<0.05) were identified, excised, trypsin digested and analyzed by matrix-assisted laser-desorption ionization time-offlight time-of-flight (MALDI-TOF-TOF). In total, 1098 spots were subjected to statistical analysis with 22 spots found to be differentially abundant of which 18 proteins were positively identified by mass spectrometry. In addition, approximately 1000 protein spots were constitutively expressed of which 21 proteins were positively identified by mass spectrometry. proteins in the cocaine-exposed monkeys include glial fibrillary acidic protein, syntaxinbinding protein 3, protein kinase C isoform, adenylate kinase isoenzyme 5 and mitochondrialrelated proteins, whereas decreased levels of proteins included B-soluble N-ethylmaleimidesensitive factor attachment protein and neural and non-neural enolase. Using a complimentary proteomics approach, the differential expression of phosphorylated proteins in the cytosolic fraction of these subjects was examined. Two-dimensional gel electrophoresis (2DGE) was followed by gel staining with Pro-Q Diamond phosphoprotein gel stain, enabling differentiation of approximately 150 phosphoprotein spots between the groups. Following excision and trypsin digestions, MALDI-TOF-TOF was used to confirm the identity of 15 cocaine-altered phosphoproteins. Significant increased levels were detected for gammaaminobutyric acid type A receptor-associated protein 1, 14-3-3 gamma-protein, glutathione Stransferase and brain-type aldolase, whereas significant decreases were observed for Bactin, Rab GDP-dissociation inhibitor, guanine deaminase, peroxiredoxin 2 isoform b and several mitochondrial proteins. Results from these studies indicate coordinated dysregulation of proteins related to cell structure, signaling, metabolism and mitochondrial function. These data extend and compliment previous studies of cocaine-induced biochemical alterations in human postmortem brain tissue, using an animal model that closely recapitulates the human condition and provide new insight into the molecular basis of the disease and potential targets for pharmacotherapeutic intervention. copyright 2010 Nature Publishing Group All rights reserved. ISSN 1359-4184 Publication Type Journal: Article Journal Name Molecular Psychiatry Volume 15 Issue Part 2 Page 185-203 Year of Publication 2010 Date of Publication January 2010 COCAINE 2010 <937> Database EMBASE Accession Number 2010113003 Authors Wang L. Lv Z. Hu Z. Sheng J. Hui B. Sun J. Ma L. Institution (Wang, Lv, Hu, Sheng, Hui, Sun, Ma) Pharmacology Research Center, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai, Shanghai 200032, China. Country of Publication United Kingdom Title Chronic cocaine-induced H3 acetylation and transcriptional activation of CaMKIIalpha in the nucleus accumbens is critical for motivation for drug reinforcement. Source Neuropsychopharmacology. 35(4)(pp 913-928), 2010. Date of Publication: March 2010. Publisher Nature Publishing Group Abstract The regulation of gene expression in the brain reward regions is known to contribute to the pathogenesis and persistence of drug addiction. Increasing evidence suggests that the regulation of gene transcription is mediated by epigenetic mechanisms that alter the chromatin structure at specific gene promoters. To better understand the involvement of epigenetic regulation in drug reinforcement properties, rats were subjected to cocaine selfadministration paradigm. Daily histone deacetylase (HDAC) inhibitor infusions in the shell of the nucleus accumbens (NAc) caused an upward shift in the dose-response curve under fixed-ratio schedule and increased the break point under progressive-ratio schedule, indicating enhanced motivation for self-administered drug. The effect of the HDAC inhibitor is attributed to the increased elevation of histone acetylation induced by chronic, but not acute, cocaine experience. In contrast, neutralizing the chronic cocaine-induced increase in histone modification by the bilateral overexpression of HDAC4 in the NAc shell reduced drug motivation. The association between the motivation for cocaine and the transcriptional activation of addiction-related genes by H3 acetylation in the NAc shell was analyzed. Among the genes activated by chronic cocaine experiences, the expression of CaMKIIalpha, but not CaMKIIB, correlated positively with motivation for the drug. Lentivirus-mediated shRNA knockdown experiments showed that CaMKIIalpha, but not CaMKIIB, in the NAc shell is essential for the maintenance of motivation to self-administered cocaine. These findings suggest that chronic drug-use-induced transcriptional activation of genes, such as CaMKIIalpha, modulated by H3 acetylation in the NAc is a critical regulatory mechanism underlying motivation for drug reinforcement. copyright 2010 Nature Publishing Group All rights reserved. ISSN 0893-133X Publication Type Journal: Article Journal Name Neuropsychopharmacology Volume 35 Issue Part 4 Page 913-928 Year of Publication 2010 Date of Publication March 2010 COCAINE / OPIOIDS 2010 <991> Database EMBASE Accession Number 2010123969 Authors McCance-Katz E.F. Jatlow P. Rainey P.M. Institution (McCance-Katz) Department of Psychiatry, University of California San Francisco, San Francisco, CA, United States. (Jatlow) Department of Laboratory Medicine, Yale University, New Haven, CT, United States. (Rainey) Department of Laboratory Medicine, University of Washington, Seattle, WA, United States. (McCance-Katz) San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110, United States. Country of Publication United Kingdom Title Effect of cocaine use on methadone pharmacokinetics in humans. Source American Journal on Addictions. 19(1)(pp 47-52), 2010. Date of Publication: January February 2010. Publisher Wiley-Blackwell Abstract Chronic cocaine use has been shown to significantly decrease buprenorphine concentrations in the blood with potential for adverse events and poor treatment response. In this study, we investigated whether a similar drug interaction occurred between cocaine and methadone. In a retrospective analysis, methadone pharmacokinetics were compared for those who were either regular cocaine users (N = 16) or with intermittent or no cocaine use (N = 23). Participants who used cocaine regularly showed a significant decrease in Cmin (p =.04) and a trend for decreased AUC (p =.09) and more rapid methadone clearance (p =.08). Regular cocaine use may adversely impact treatment outcomes for opioid dependence in those receiving methadone maintenance by decreasing methadone exposure. copyright American Academy of Addiction Psychiatry. ISSN 1055-0496 Publication Type Journal: Article Journal Name American Journal on Addictions Volume 19 Issue Part 1 Page 47-52 Year of Publication 2010 Date of Publication January - February 2010 COCAINE / OPIOIDS 2010 <1000> Database EMBASE Accession Number 2010123958 Authors McCance-Katz E.F. Rainey P.M. Moody D.E. Institution (McCance-Katz) Department of Psychiatry, University of California San Francisco, San Francisco, CA, United States. (Rainey) Department of Laboratory Medicine, University of Washington, Seattle, WA, United States. (Moody) Center for Human Toxicology, University of Utah, Salt Lake City, UT, United States. (McCance-Katz) San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110, United States. Country of Publication United Kingdom Title Effect of cocaine use on buprenorphine pharmacokinetics in humans. Source American Journal on Addictions. 19(1)(pp 38-46), 2010. Date of Publication: January February 2010. Publisher Wiley-Blackwell Abstract The effect of chronic cocaine use on buprenorphine pharmacokinetics was investigated to identify drug interactions and potential toxicities. In a retrospective analysis, pharmacokinetics were compared for 16 studies completed on subjects who were regular cocaine users and 74 studies on subjects who used cocaine only occasionally or not at all. All participants were stably maintained on buprenorphine/naloxone 16/4 mg daily. Participants who used cocaine regularly had lower buprenorphine exposure (AUC 34% lower; Cmax 27% lower and C24 37% lower; p [less-than or equal to].001 for all comparisons). Regular cocaine users were younger (p =.0007), and used more heroin (p =.004) and cocaine (p <.0001). Regular cocaine use may result in lower buprenorphine plasma concentrations with potential for adverse clinical outcomes. copyright American Academy of Addiction Psychiatry. ISSN 1055-0496 Publication TypeJournal: Article Journal Name American Journal on Addictions Volume 19 Issue Part 1 Page 38-46 Year of Publication 2010 Date of Publication January - February 2010