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Abstract Book 2013.Indd JOURNAL OF PSYCHOPHARMACOLOGY SUPPLEMENT TO VOLUME 27, ISSUE 8, AUGUST 2013 These papers were presented at the Summer Meeting of the BRITISH ASSOCIATION FOR PSYCHOPHARMACOLOGY 28 – 31 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. All contributors completed a Declaration of Interests form when submitting their abstract BAP Office 36 Cambridge Place Hills Road Cambridge CB2 1NS bap.org.uk Aii CONTENTS Abstract Book 2013 Abstracts begin on page: SYMPOSIUM 1 The neurobiology of social behaviour: pharmacological manipulation and A1 recent advances in therapy (S01-S04) SYMPOSIUM 2 Brain-derived neurotrophic factor (BDNF) and synaptic plasticity as a drug A2 target for cognitive dysfunction in CNS disorders (S05-S08) SYMPOSIUM 3 Experimental medicine approaches in developing new treatments for anxiety A3 disorders (S09-S12) SYMPOSIUM 4 Imaging dopamine in the living brain (S13-S16) A5 SYMPOSIUM 5 Computational psychopharmacology (S17-S20) A6 SYMPOSIUM 6 Alzheimer’s disease early detection and early effective treatment (S21-S24) A7 SYMPOSIUM 7 Can psychological constructs make good drug targets? The example of salience A9 dysregulation in schizophrenia (S25-S28) SYMPOSIUM 8 Novel innovation in monitoring symptoms and treatments for schizophrenia and A10 bipolar disorder (S29-S32) SYMPOSIUM 9 The impact of inflammatory challenges on mental function (S33-S36) A11 CONTENTS Aiii Abstract Book 2013 (Continued) Abstracts begin on page: POSTERS Affective Disorders 1 (MA01-MA24) A13 Sleep and Circadian Rhythms (MB01-MB04) A23 Learning and Cognition (MC01-MC21) A24 Dementia (MD01-MD07) A33 Anxiety (ME01-ME09) A36 Educational Psychopharmacology (MF01-MF05) A40 Brain Imaging (MG01-MG12) A42 Affective Disorders 2 (TA01-TA18) A46 Neuropharmacology (TB01-TB09) A53 Psychomotor Stimulants (TC01-TC06) A57 Substances of Abuse (TD01-TD19) A59 Schizophrenia (TE01-TE25) A65 POSTDOCTORAL SYMPOSIUM Translational autism research for drug discovery (PD1-PD4) A76 SHORT ORAL PRESENTATIONS Short Orals 1: Special K – New Horizons See abstracts TE22, TA07, MC13, MG01 Short Orals 2: Windows on the Brain See abstracts MC19, TE19, TE25, ME08 Short Orals 3: Reward and Choice See abstracts TD03, MG08, TA10, MC04, MC14 PRIZE WINNER ABSTRACTS (PW1-PW4) A77 ABSTRACTS A1 S01 SOCIAL BEHAVIOUR AND TOP-DOWN CONTROL IN AUTISM Hamilton A, School of Psychology University of Nottingham, University Park, Nottingham, NG7 2RD, [email protected] Introduction: Autism spectrum condition is characterised by difficulties in social interaction and communication. In recent years, there has been a major focus on the role of mirror neurons in autism and the possibility that imitation behaviour provides a marker of mirror neuron function. Here, I present data arguing against this thesis. Method: I will review brain imaging and behavioural studies showing that mirror neuron systems are intact in autism. These include a systematic review of neuroimaging studies and new behavioural studies of imitation in children with autism. Results: The systematic review reveals no evidence that mirror neuron systems are abnormal in autism. The behavioural studies show that children with autism can imitate goal directed actions but do not overimitate actions in order to affiliate with other people. Conclusions: These data suggest that brain and cognitive systems for top-down control of social responding are abnormal in autism. There are also important links between top-down control and social motivation. This new model of autism can help to move the field forwards. S02 PRENATAL VALPROATE AS A RODENT MODEL FOR AUTISM Scheel-Krüger J, CFIN Aarhus University, DCN Building, DK8000 Aarhus, Denmark, [email protected] Social dysfunction represents a key feature in several psychiatric disorders, including autism, schizophrenia, depression and drug dependence. Unfortunately this most debilitating human behavioural disorder remains largely untreated by current medication. Social interaction is performed by all species of the animal kingdom and their complex social interactions are an essential part of survival of the organism. It is thus imperative for the development of effective drug treatments of social dysfunctions that we study social behaviour across species, which can later be translated to the human condition. Recent data from our team suggest that prenatal exposure of valproate (VPA) could provide an animal model for autism and or reduced social interaction. In the clinic, it is well known that prenatal exposure to the antiepileptic drug VPA is associated with a high risk factor for cognitive dysfunction in the offspring, which may include autism spectrum disorder. In our model, pregnant rats received a sub- chronic daily administration of VPA at 20 or 100mg/kg from day 9 until the end of pregnancy. This model is thus designed to mimic the human clinical condition with VPA administered chronically to pregnant women with epilepsy. Our model differs from the original VPA model in which only one single high neurotoxic dose of VPA (600mg/kg) is injected at day 12.5 of pregnancy. This model shows reduced numbers of neurones and various behavioural changes. In contrast, we observe increases in neuronal cortical cell numbers in the offspring, a finding we suggest may be related to the stimulatory trophic effect of GABA on the migration of early embryonic cells in the fetal brain tissue. Our finding of increased cell number is consistent with the results of Courchesne et al (Courchesne E, et al. Neuron number and size in prefrontal cortex of children with autism. JAMA. 2011;306(18):2001-2010) reporting an abnormal excess of neurons in the prefrontal cortex of autistic males. In our model, we also observe decreased juvenile play behavior in young, male VPA rats, consistent with the social deficit observed in human autism. These VPA-rats had a marked decrease in the level of striatal serotonin, a finding consistent with the involvement of serotonin in social play behavior. The adult VPA rats showed enhanced performance in the object recognition test. These findings and our latest results on the receptor binding profile of the essential social neurotransmitters oxytocin and vasopressin will be presented. S03 THE NEUROBIOLOGY OF SOCIAL PLAY BEHAVIOR IN RATS Vanderschuren LJMJ, Dept. of Animals in Science and Society, Faculty of Veterinary Medicine Utrecht University, Yalelaan 2 Utrecht The Netherlands, 3584CM, [email protected] In between weaning and puberty, the young of all mammalian species, including humans, display a characteristic form of social interaction known as social play behaviour or rough-and-tumble play. This form of social behaviour is highly rewarding and essential for the development of social and cognitive skills. Indeed, social traumas in early life greatly enhance the risk for later psychopathology. Conversely, social play is known to be impaired in child and adolescent psychiatric disorders, including autism and early-onset schizophrenia. Despite its abundance and importance, however, the neural underpinnings of social play are incompletely understood. Recent pharmacological analysis of the neurotransmitter systems involved has revealed an important role for interacting opioid, cannabinoid and dopaminergic neurotransmission in the modulation of social play behaviour. This is in keeping with the rewarding properties of social play, as these neurotransmitter systems have been widely implicated in the positive emotional properties of food, sex and drugs. Investigation of the brain regions involved has identified the nucleus accumbens and basolateral amygdala, respectively, as important sites of action for opioids and endocannabinoids on social play. On the other hand, psychostimulant drugs, such as amphetamine and methylphenidate, reduce social play through stimulation of alpha2-adrenoceptors. These effects are exerted through the anterior cingulate cortex, amygdala and habenula. Consistent with a role for corticostriatal mechanisms in social play, pharmacological inactivation of medial prefrontal cortex, dorsomedial striatum and nucleus accumbens core alters social play behaviour. Last, our recent work has indicated that the positive subjective (‘pleasurable’) and incentive motivational properties of social play can be pharmacologically dissociated. In conclusion, there is emerging evidence to indicate that social play behaviour is modulated through opioid, cannabinoid and monoamine neurotransmission within limbic corticostriatal mechanisms that are involved in reward, motivation and cognitive control over behaviour. Identifying the neural underpinnings of social play behaviour will increase our understanding of normal social development as well as of the etiology of child and adolescent psychiatric disorders. A2 ABSTRACTS S04 DISCOVERING NOVEL THERAPIES FOR NEGATIVE SYMPTOMS OF SCHIZOPHRENIA BY USING RODENT MODELS OF SOCIAL WITHDRAWAL Prinssen EP, pRED, Pharma Research & Early Development, DTA Neuroscience F. Hoffmann-La Roche Ltd., , Basel, Switzerland, B72/148, Grenzacherstrasse 124 CH-4070, Basel, Switzerland, 4070, [email protected] Biemans B1, Leahy E2, Alberati D1 1 F. Hoffmann-La Roche Ltd., pRED, Pharma Research & Early Development, DTA Neuroscience, Basel, Switzerland; 2 Psychogenics Inc, Tarrytown, NJ, US Negative
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