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Abstract Book 2016 Abstracts Begin on Page JOURNAL OF PSYCHOPHARMACOLOGY SUPPLEMENT TO VOLUME 30, ISSUE 8, AUGUST 2016 These papers were presented at the Summer Meeting of the BRITISH ASSOCIATION FOR PSYCHOPHARMACOLOGY 17 – 20 July, Brighton, 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 www.bap.org.uk Aii CONTENTS Abstract Book 2016 Abstracts begin on page: SYMPOSIUM 1 New paradigms and treatment approaches in schizophrenia (S01–S04) A1 SYMPOSIUM 2 New perspectives on functions of 5-HT sub-systems (S05–S08) A3 SYMPOSIUM 3 Towards a gender specific psychopharmacology: The impact of neurosteroids, gonadal steroids and oxytocin (S09–S12) A5 SYMPOSIUM 4 Bipolar disorder: Progress on many fronts (S13–S16) A7 SYMPOSIUM 5 Ketamine and addiction: Promising treatment or probable cause? (S17–S20) A9 SYMPOSIUM 6 Neuronal stem cells in mental health: Will neurogenesis and iPS cells give us the antidepressants of the future? (S21–S24) A11 SYMPOSIUM 7 Anhedonia, apathy, amotivation, anergia? Disrupted reward processing as a trans-diagnostic construct in mental illness (S25–S28) A13 SYMPOSIUM 8 Dysfunctional neuro-immune system interactions in psychiatric disorders and their relevance for novel treatment strategies (S29–S32) A15 SYMPOSIUM 9 Innovation in the treatment of obesity and binge eating (S33–S36) A18 CONTENTS Aiii POSTERS Group A: Schizophrenia/Psychosis (A01–A35) A20 Group B: Substance Use (B01–B31) A43 Group C: Affective Disorders (C01–C52) A64 Group D: Anxiety (D01–D11) A99 Group E: Developmental Disorders and Neurodegeneration (E01–E09) A106 Group F: Cognition (F01–F07) A111 Group G: Eating Disorders (G01–G04) A116 Group H: Sleep/Circadian Rhythms (H01–H04) A119 GUEST LECTURE Parsing the serotonin system into distinct functional units (GL1) A122 POSTDOCTORAL SYMPOSIUM Translational models and biomarkers for neuropsychiatric disorders (PD01–PD04) A122 SHORT ORAL PRESENTATIONS Short Orals 1: Substance Use: Neural and behavioural effects See abstracts B09, B11, B16, B24 Short Orals 2: Analysing Anhedonia: From mechanism to treatment See abstracts C12, C15, C30, C46 Short Orals 3: Neurochemical mechanisms of psychosis See abstracts A02, A03, A17, A21 2016 PSYCHOPHARMACOLOGY AWARDS (PW1–PW4) A125 ABSTRACTS A1 S01 PET IMAGING STUDIES OF MICROGLIA, A MARKER FOR NEUROINFLAMMATION IN SCHIZOPHRENIA PATIENTS: POTENTIAL AVENUES FOR NEW TREATMENT APPROACHES Talbot PS, Wolfson Molecular Imaging Centre, Univ of Manchester, 27 Palatine Road, Withington, Manchester M20 3LJ [email protected] Introduction: Positron emission tomography (PET) imaging of the 18kDa translocator protein (TSPO) has been used to investigate whether microglial activation, an indication of neuroinflammation, is evident in the brain of adults with schizophrenia. To date the results have been mixed, with early studies finding evidence for microglial activation and the majority of more recent studies refuting this. The discrepant findings may reflect differences in methodology, radiotracers, and aspects of the patient populations including severity and duration of illness. However, importantly, all of the schizophrenia patients in these previous PET studies were taking antipsychotic medication at the time of scanning, introducing a potential confound due to modulatory effects of antipsychotic medication on microglial activity. We have therefore compared TSPO availability between antipsychotic-free patients with schizophrenia, medicated patients, and matched healthy controls. Methods: we used [11C](R)-PK11195 PET to compare TSPO availability in a predominantly antipsychotic-naïve group of moderate-to-severely symptomatic unmedicated patients (n=8), similarly symptomatic medicated patients with schizophrenia taking risperidone or paliperidone by regular intramuscular injection (n=8), and healthy comparison subjects (n=16). Binding potential (BPND) was calculated using a grey matter cerebellum reference input function and the simplified reference tissue model. Results: we found no evidence for increased TSPO availability in antipsychotic- free patients compared to healthy controls (mean difference 4%, p=0.981). However, TSPO availability was significantly elevated in medicated patients (mean increase 88%, p=0.032) across dorsolateral prefrontal, ventrolateral prefrontal, orbitofrontal, anterior cingulate and parietal cortical regions. In the patients with schizophrenia, TSPO availability was also strongly correlated with negative symptoms measured using the Positive and Negative Syndrome Scale across all the brain regions investigated (r=0.651–0.741). Conclusions: we conclude that the pathophysiology of schizophrenia is not associated with microglial activation in the 2–6 year period following diagnosis, but that antipsychotic treatment with risperidone or paliperidone may induce microglial activation. It remains to be determined whether this activation represents a pro- or anti-inflammatory state, its association with primary negative symptoms and treatment resistance, and whether there are significant differences between antipsychotics. Implications for novel treatment strategies will be discussed. S02 EVIDENCE THAT PARVALBUMIN PATHOLOGY IN SCHIZOPHRENIA CAN BE RESCUED BY NOVEL DRUG TARGETS Harte MK, Manchester Pharmacy School, Univ of Manchester, Stopford Building, Oxford Road, Manchester M13 9PL [email protected] Cognitive deficits remain an unmet clinical need in a number of neuropsychiatric and neurodegenerative disorders. With an improved understanding of the pathology related to these deficits comes the hope of novel treatment strategies. Current evidence from both clinical and preclinical studies suggests a strong involvement of GABAergic interneurons (particularly the parvalbumin (PV) subset) in regulating cognitive function in vivo. Alongside this are numerous reports of dysfunction of these GABAergic neurons in schizophrenia (Lewis et al., Trends Neurosci. 2012; 35(1): 57–67), with a number of relevant preclinical models recapitulating this deficit (e.g. sub-chronic phencyclidine model (Neill et al., 2010; 128(3):419–32)). This emerging understanding of the pathophysiology of schizophrenia offers us the potential to identify novel drug targets through which it may be possible to treat the underlying neural dysfunction and potentially alleviate the cognitive deficits. One such target is the Kv3.1 voltage-gated potassium channel. These channels are expressed on PV interneurons, where they confer the ability of the neurons to fire rapidly and accurately, allowing synchronisation of cortical circuits. A recent post- mortem study found reduction in Kv3.1 protein in un-medicated schizophrenia patients (Yanagi et al. Mol Psychiatry 2014; 19: 573–579). Modulation of this channel may therefore provide a novel target A2 ABSTRACTS for restoration of cognitive function in schizophrenia patients. The presentation will cover data from behavioural, immunohistochemical, electrophysiological and imaging studies in validated preclinical models aimed at investigating the efficacy of this approach for treating cognitive deficits in schizophrenia. Briefly, we demonstrate that treatment (acute and/or chronic) with: - AUT00206, a novel Kv3.1 modulator (Autifony Therapeutics Limited) significantly attenuated the sub-chronic phencyclidine (scPCP) induced social behaviour deficits. - AUT00206 significantly attenuated scPCP induced deficits in different cognitive domains. - AUT00206 significantly enhanced the power of fast network oscillations in the prelimbic cortex from scPCP treated rats. - AUT00206 significantly reversed the scPCP induced PV deficit, an effect dependent on the presence of AUT00206. - AUT00206 significantly reduced ketamine induced BOLD signal changes in cortical and subcortical regions of the rat brain Taken together these results suggest that the modulation of Kv3 channels on PV neurons by AUT00206 could be an important novel approach for improving cognitive deficits and function in schizophrenia patients. Financial Sponsorship: These studies were funded by Innovate UK. S03 UTILITY OF COGNITIVE AND BOLD FMRI BIOMARKERS IN INDIVIDUALS WITH HIGH SCHIZOTYPY TO ASSESS NEW THERAPIES FOR SCHIZOPHRENIA Dourish CT, P1vital, Manor House, Howbery Park, Wallingford, Oxfordshire OX10 8BA [email protected] Schizophrenia is a debilitating, life-long, psychiatric disorder affecting approximately 1% of the world’s population. Antipsychotic drug therapies do not treat all the symptoms of the illness (including positive, negative and cognitive symptoms) and cause significant side-effects including dyskinesia, obesity and diabetes. Therefore, there is a significant unmet need to develop new treatments for schizophrenia that have improved efficacy and fewer side-effects. However, few new compounds have emerged and often promising pre-clinical data have not translated to efficacy in clinical trials. Use of experimental medicine efficacy biomarkers offers a potential way forward for antipsychotic drug development and this presentation reviews a series of recent schizophrenia efficacy biomarker validation studies. Two potential models were examined, an “intermediate phenotype” model and a drug challenge model. The intermediate
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