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The British Association for Psychopharmacology Accepts No Responsibility for the Contents of the Verbal Or Any Published Proceedings of This Meeting AbstrActs A1 SUPPLEMENT TO JOURNAL OF PSYCHOPHARMACOLOGY VOL 25, SUPPLEMENT to No 8, AUGUST 2011 These papers were presented at the Summer Meeting of the BRITISH ASSOCIATION FOR PSYCHOPHARMACOLOGY 24 – 27 July, Harrogate, UK Indemnity The scientific material presented at this meeting reflects the opinions of the contributing authors and speakers. The British Association for Psychopharmacology accepts no responsibility for the contents of the verbal or any published proceedings of this meeting. BAP OFFICE 36 Cambridge Place, Hills Road Cambridge CB2 1NS bap.org.uk AA2ii AbstrcONtAENctsts Abstract Book 2011 Abstracts begin on page: SYMPOSIUM 1 A1 Evaluating the mechanisms, risks and possible benefits of MDMA (Ecstasy) and structurally-related amphetamines (S01-S04) SYMPOSIUM 2 A2 Glutamate, cognition and depression (S05-S08) SYMPOSIUM 3 A3 Improved therapies for mental illness: Greater understanding, tangible achievements and paradigm shifts (S09-S12) SYMPOSIUM 4 A5 Stress and depression: Novel approaches to treatment (S13-S16) SYMPOSIUM 5 A6 Novel approaches to understanding of brain function (S17-S20) SYMPOSIUM 6 A7 The role of histamine in cognition and psychiatric symptoms (S21-S24) SYMPOSIUM 7 A9 Offspring of depressed mothers: do the potential risks of medical treatment outweigh the costs of untreated maternal depression? (S25-S28) SYMPOSIUM 8 A10 Brain trophic factors in neuropsychiatric diseases (S29-S32) SYMPOSIUM 9 A11 Attention deficit hyperactivity disorder (ADHD) (S33-36) POSTERS Affective Disorders 1 (MA01-MA29) A13 Learning and Cognition (MB01-MB25) A24 Educational Psychopharmacology (MC01-MC06) A33 Substances of Abuse (MD01-MD20) A35 Undergraduate Abstracts (ME01-ME14) A42 Affective Disorders 2 (TA01-TA28) A47 Cont.. CAbstrONTENaTScts Aiii Abstract Book 2011 Abstracts begin on page: POSTERS Continued. Sleep and Circadian Rhythms (TB01-TB05) A56 Brain Imaging (TC01-TC14) A58 Schizophrenia (TD01-TD27) A63 Anxiety (TE01-TE11) A72 POSTDOCTORAL SYMPOSIUM (PD1-PD4) A77 SHORT ORAL PRESENTATIONS A78 Short Orals 1: Drugs of Abuse – The Next Generation? See abstracts MD15, MD14, MD07, TC06 Short Orals 2: Modelling Cognitive Dimensions in Schizophrenia See abstracts TD15, TD24, TD16, SO01 Short Orals 3: Probing the Neural Basis of Negative Emotion See abstracts MA10, TC05, TA12, TE07 GUEST LECTURE (GL1) A78 BAP PSYCHOPHARMACOLOGY AWARD WINNERS (PW1-PW3) A78 A4 AbstrActs AbstrActs A1 S01 THE IMPORTANCE OF USING CLINICALLY RELEVANT DOSES OF MDMA AND CATHINONES IN RODENT AND PRIMATES WHEN INVESTIGATING THEIR NEUROPHARMACOLOGICAL EFFECTS Green AR, School of Biomedical Sciences, Univ of Nottingham NG7 2UH [email protected] The ability of MDMA to induce both acute adverse effects and long term serotonergic neurotoxicity in laboratory animals is well documented. However most of these studies have used doses of the drug that have paid scant regard to the pharmacokinetics of the drug in either humans or animals. The recreational use of MDMA and, importantly, the current clinical investigations of the drug for therapeutic purposes demand better translational pharmacology to allow an accurate risk assessment of the drug’s ability to induce adverse events. Recently several animal and human studies have been conducted on the pharmacokinetics of MDMA and these investigations indicate that the risks of MDMA ingestion suggested by many of the earlier animal studies should be re-evaluated. MDMA-induced acute behavioural and body temperature changes result from the rapid release of monoamines by MDMA (primarily serotonin and dopamine), while long-term neurotoxicity is induced by metabolites of the drug (Esteban et al., Psychopharmacology 154: 251-60, 2001). Therefore acute physiological changes in humans can be fairly accurately mimicked in animals by appropriate dosing, although allometric dosing calculations have limited value. Long term changes however require the drug to be metabolized in a similar manner in experimental animals to that occurring in humans. This is problematic because the actual neurotoxic metabolites have not been finally identified and crucially because the rate of metabolism of MDMA and its major metabolites is very different in humans and rats or monkeys. Humans metabolize MDMA slowly in comparison to rats and squirrel monkeys. Consequently acute adverse events such as hyperthermia in humans probably limit the chance of recreational users ingesting sufficient MDMA to produce neurotoxicity, in contrast to experimental animals. Since MDMA inhibits the major enzyme responsible for its metabolism in humans this also assists in preventing neurotoxicity, particularly during binge dosing. These observations allow questions as to whether MDMA alone produces neurotoxicity in the human brain, although its combination with other recreational drugs may induce neurotoxicity. Translation of experimental animal data from studies on cathinones such as methylmethcathinone (mephedrone) to humans is even more problematical as little data exist on plasma concentrations in recreational users. Although mephedrone has a similar chemical structure and molecular weight to MDMA our studies suggest that it has a different neurochemical and behavioural profile to MDMA (King et al., this meeting; Shortall et al., this meeting). It is currently unclear whether this is due to a different pharmacodynamic or pharmacokinetic profile. S02 PRECLININCAL AND CLINICAL STUDIES ON THE INTERACTION OF MDMA WITH OTHER RECREATIONAL DRUGS O'Shea E, Pharmacology, Facultad de Medicina Univ Complutense de Madrid, 28040 [email protected] 3,4-Methylenedioxymethamphetamine (MDMA , 'ecstasy’) is a recreational drug commonly consumed with other drugs of abuse in particular among younger sections of the population. Recent trend assessment by the European Drug Monitoring Agency (EMCDDA) indicate an increase in the simultaneous consumption of MDMA with other drugs of abuse, the most common being ethanol and cannabis. Studies reveal several interactions between MDMA and ethanol exposure. Preclinical studies show that prexposure to ethanol potentiates the neurotoxic effects of MDMA in rats and may cause memory impairment. Repeated MDMA given during ethanol deprivation affects subsequent reinstatement in rats with a history of ethanol consumption in addition to increasing ethanol-induced dopamine release in the nucleus accumbens. Furthermore, the combination of ethanol and MDMA facilitated conditioned place preference and motor stimulant effects. In mice, MDMA-induced dopaminergic lesion increases consumption of and preference for ethanol while decreasing sensitivity to ethanol. In addition, in adolescent mice preexposure to ethanol prolongs the conditioned rewarding effects of MDMA. In humans, coadministration studies reveal varying psychomotor effects which may involve pharmacokinetic alterations. With regard to interactions between cannabis and MDMA, cannabinoid agonists enhance the rewarding effects of MDMA: when combined with low dose MDMA, low dose THC produces CPP, lowers the self-administration threshold dose of MDMA and attenuates the THC withdrawal syndrome. On the other hand, THC may decrease the neurotoxicity of MDMA. In humans, combined intake of MDMA and THC may impair task performance and may synergize to decrease cognitive performance. However, THC may increase the desired subjective effects of MDMA. Overall, these studies suggest that the cannabinoid system plays an important role in the rewarding effects of MDMA and that the combinations of the drugs might impair psychomotor and cognitive performance. Preclinical and clinical reports on polydrug consumption and in particular the combination of MDMA and other drugs of abuse such as ethanol and cannabis suggest that important interactions between these drugs may occur. S03 EVALUATING THE MECHANISMS, RISKS AND POSSIBLE BENEFITS OF MDMA (ECSTASY) Reneman L, Radiology Academic Medical Center, Univ of Amsterdam, NL-1105AZ [email protected] Introduction: In view of MDMA’s popularity as a recreational drug, animal studies demonstrating serotonergic neurotoxicity after MDMA administration at doses that overlap with those used by humans, and the role serotonin (5-HT) plays in several essential functions such as emotion, memory, sleep, pain, and higher order cognitive processes, it is important to determine what the risks and possible benefits of MDMA on the human brain are. Particularly also because some authors have begun to (re)advocate the use of MDMA as a therapeutic tool (e.g., anxiety and posttraumatic stress disorders). Methods: Previously, there were no methods available for directly evaluating the effects of MDMA in the living human brain. However, development of in vivo neuroimaging tools have begun to provide insights into the effects of ecstasy in human brain. These are: single photon emission computed tomography (SPECT), positron emission computed tomography (PET), proton magnetic resonance spectroscopy (1H-MRS), pharmacological magnetic resonance imaging (phMRI), in addition to structural and functional magnetic resonance imaging (fMRI and sMRI). Results: There seem to be dose-dependent and transient reductions in serotonin transporter (SERT) densities in which females may be more vulnerable than males. In addition, age (of first MDMA exposure) and use of other drugs of abuse are important confounding factors. New imaging techniques such as phMRI, fMRI and sMRI provide new insights into the effects of this popular recreational drug on the human brain. For instance, we observed
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