Book of abstracts - British Neuroscience Association

More documents

Recommendations

Info

40.07 Neurotransmitter interaction and the adaptive response to the absence of food in the pharynx of C. elegans Luedtke S, Walker R, Hopper N, O`Connor V, Holden-Dye L University of Southampton; School of Biological Sciences, Bassett Crescent East,, Southampton,, SO16 7PX We are interested in peptidergic and classical neurotransmitter interaction and how these modulate behaviour as a response to internal and external signals. As a model behaviour we are using the pharyngeal pumping in the nematode C. elegans. The pharyngeal nervous system regulates feeding behaviour in C. elegans. This neural network regulates muscle pumping via a number of different classical transmitters and neuropeptides. We are trying to delineate a mechanism that controls pharyngeal pumping in the intact worm under differing environmental conditions (on food and increasing time off food). Placing worms off food identified 3 distinct behavioural phases of pharyngeal pumping with increasing time. Subsequent analyses of several mutants have shown modified responses to the absence of food. In particular a number of mutants in classical and peptidergic inhibitors support the notion that pharynx is under negative regulation that is lessened with increasing time of food. We are currently trying to correlate the distinct phases of pharyngeal behaviour with the metabolic status of the worm (measuring fat storage) and switches in the locomotory behaviours worms use when foraging for food. In doing so we hope to develop an integrated view of cellular and behavioural adaptive responses underlying feeding behaviour. Funded by the Gerald Kerkut Charitable Trust. We are grateful to the C. elegans Genetics Centre for providing strains. 40.08 Distinguishing between error detection and error awareness: implications for clinical research O’Connell R G, Dockree P M, Bellgrove M A, Lau A, Fitzgerald M, Foxe J J, Robertson I H School of Psychology and Trinity College Institute of Neuroscience, Trinity College Dublin In everyday life our ability to detect errors is critical for smooth and dynamic interaction with our environment, providing us with the opportunity to realign our behaviour with prevailing goals and to learn the consequences of different behaviours. Error processing is reliant, in part, on communication between anterior cingulate and lateral prefrontal cortices and is impaired in a number of putatively frontal conditions including schizophrenia, ADHD and OCD. A common limitation of error processing studies, and particularly those involving clinical groups, has been a failure to distinguish between error detection and conscious error awareness. Damage to the frontal lobes has been associated with decreased awareness of one’s deficits including a tendency to ‘miss’ errors during neuropsychological tasks. The present study constitutes a systematic electrophysiological investigation of error processing networks in a group of adults diagnosed with ADHD. Eighteen patients and 21 matched controls performed a Go/No-go response inhibition paradigm that was specially designed to ascertain levels of error awareness. This experiment reveals that adults with ADHD are significantly less likely to consciously detect their errors and identifies a number of ERP abnormalities relating to aspects of performance monitoring and conscious error processing. The Error Positivity (Pe) is identified as a key marker of conscious error processing and is found to be attenuated in the patient group even following consciously detected errors. In addition, the results of source analysis indicate de-activation of midline frontal regions during conscious error processing in the ADHD group. 40.09 Effects of early life deprivation and fluoxetine treatment on central dopamine D2 receptors in adult Wistar rats Leventopoulos M (1), Lukito S (1),, Russig H (2), Feldon J (2), Pryce C R (2), Opacka–Juffry J. (1) (1)Roehampton University, London, UK., (2)Behavioural Neurobiology Laboratory, Swiss Federal Institute of Technology, Zurich, Switzerland., Studies on animal models of depression have shown that early life stress affects monoamine status in adult rats. The present study on adult Wistar rats exposed to early life deprivation (ED) assessed the level of postsynaptic dopamine D2 receptor binding in the subregions of cortex, striatum and nucleus accumbens (NAc). Male Wistar rat P1–14 pups were isolated for 4h/day (ED) or were handled for 1 minute (CON). They were weaned at P21 and left undisturbed until 4-6 months old. The ED and CON groups were halved to receive either vehicle or fluoxetine (FLX, 10 mg/kg, 31 days). Thus gave four treatment groups: CON-VEH, CON-FLX, ED-VEH and ED-FLX, n=8 each. ED-VEH rats showed significantly reduced motivation to obtain sucrose in a progressive ratio schedule (vs CON- VEH); FLX reversed this deficit. Quantitative receptor autoradiography was used to determine D2 receptor binding with [3H]raclopride. D2 binding in dorsolateral striatum and NAc, both core and shell, was significantly reduced (by 16-20%) in ED vs CON. Although fluoxetine treatment did not significantly affect these changes, it caused a significant reduction in D2 binding in the prelimbic cortex, dorsolateral and ventromedial striatum and NAc core and shell in CON-FLX vs CON-VEH. Correlation analysis of D2 binding between NAc core and shell in each of the treatment groups indicated a different response to fluoxetine between NAc core and NAc shell in ED rats when compared with CON. This is of interest, considering the putative differential involvement of NAc core versus shell in reward-related behaviour 40.10 Changes in 5HT1A and 5HT2C receptor binding in response to early life deprivation and fluoxetine treatment in adult Wistar rats Leventopoulos M (1), Opacka–Juffry J (1), Russig H (2), Feldon J (2), Pryce C R (2) (1)Roehampton University, London, UK., (2)Behavioural Neurobiology Laboratory, Swiss Federal Institute of Technology, Zurich, Switzerland., Early life deprivation (ED) can act as a risk factor in aetiology of depression; in rats, it leads to depression-like behaviour in adulthood. The central serotonergic system is a putative player in such long-term responses. The present study hypothesised that ED would reduce postsynaptic 5HT receptor binding in the brain regions that regulate depression-like behaviour, and that the antidepressant fluoxetine would correct receptor responses in adult rats. Male Wistar rat P1–14 pups were isolated for 4h/day (ED) or were handled for 1 minute (CON). They were weaned at P21 and left undisturbed until 4- 6 months old. The ED and CON groups were halved to receive either vehicle or fluoxetine (FLX, 10 mg/kg, 31 days). Thus, four treatment groups were studied: CON-VEH, CON-FLX, ED-VEH and ED-FLX, n=8 each. ED- VEH rats showed significantly reduced motivation to obtain sucrose in a progressive ratio schedule (vs CON-VEH); FLX reversed this deficit. Quantitative receptor autoradiography was used to determine 5HT1A and 5HT2C receptor binding with [3H]WAY100635 and [3H]mesulergine (added spiperone and 8-OH-DPAT), respectively. 5HT1A binding was significantly reduced in anterior cingulate, premotor cortex and ventral hippocampal CA1 in ED-VEH vs CON-VEH specifically. Same regions and, additionally, prelimbic and frontal cortices, and accumbens had significantly reduced 5HT2C binding. Whilst fluoxetine reversed the ED-dependent changes in 5HT1A binding in cortices, it did not correct those of 5HT2C. These results indicate that the depression-like behavioural phenotype studied here implicates abnormal serotonergic regulation. 5HT1A receptor acts as a selective therapeutic target for behavioural improvement achieved with antidepressant treatment. Page 62/101 - 10/05/2013 - 11:11:03
41.01 A polymorphism at the 3’ untranslated region of the human clock gene is associated with adult Attention-Deficit Hyperactivity Disorder Kissling C, Retz W, Wieman S, Hunnerkopf R, Conner A C, Freitag C, Rosler M, Coogan A N, Thome J The Institute of Life Science and School of Medicine, Swansea University, United Kingdom. Institute for Forensic Psychology and Psychiatry, University of the Saarland, Germany. , Division of Molecular Genome Analysis, German Cancer Research Centre, Heidelberg, Germany Attention-Deficit Hyperactivity Disorder (ADHD) is commonly found in subjects with antisocial personality disorders and predicts criminal activity in adulthood. Several studies demonstrate a relationship between ADHD and sleep problems indicating an increased nocturnal activity and significant daytime somnolence in unmedicated ADHD patients. Since ADHD is a very complex disease with a high genetic load involving multiple genes of moderate effect we hypothesized a link of between adult ADHD to and genes involved in the circadian timekeeping system. We performed an association of this polymorphism with ADHD in 238 male adult detainees with German background suffering of from clinically defined ADHD. We examined a previously characterised C/T SNP in the 3’ UTR of the Clock gene, a polymorphism postulated to be associated with evening preference. Our results reveal a strong association of adult ADHD with a genotype of the SNP rs1801260, with the C mutation being the risk allele. To our knowledge, this is the first study to link adult ADHD to polymorphisms of a biological clock gene. This finding confirms that the Clock gene represents a potential candidate gene and susceptibility factor for disturbed circadian rhythmicity and sleep disorders, both of which are frequently observed in patients with ADHD. 41.02 Characterising SH-SY5Y cells as a model to study the molecular effects of ethanol on the brain. Hodder E J M, Rulten S L, King S L, Mayne L V Trafford Centre for Medical Research, University of Sussex, Falmer, Brighton, UK., , Neuronal cell culture provides a powerful system to study the molecular actions of drugs of abuse in the brain. This study aimed to characterize and exploit SH-SY5Y cells as an in vitro model to explore the effects of ethanol on the NMDA receptor and genomic integrity. SH-SY5Y cells are derived from a human neuroblastoma cell line and can be differentiated to a mature neuronal phenotype in a novel modified method involving growth in low serum and addition of retinoic acid. Behavioural changes resulting from ethanol intoxication have been linked to changes in NMDA receptor function and expression in the brain. Here we show that SH-SY5Y cells express functional NMDA receptors with NR1, NR2B, NR2C and NR2D subunit expression measured by qualitative real time PCR. We have examined expression patterns of specific subtypes of the NR1 subunit in response to ethanol exposure, using primers designed to splice-variants of the C-terminal region and examined whether ethanol exposure has an effect on the expression of any one splice variant. We have also explored whether ethanol toxicity was associated with DNA strand breaks in SH- SY5Y cells. Using the alkaline comet assay, we demonstrated that ethanol itself caused negligible DNA damage. However, acetaldehyde, the metabolic by-product of ethanol, caused significant dose and time dependent DNA damage in SH-SY5Y cells consistent with DNA damage arising through the metabolic break down of ethanol and the actions of acetaldehyde. 41.03 Cyclin D1 protein downregulation in high grade brain tumors Farizan A 1, Abdullah J 1, Jaafar H 2, Asmarina K 1, Aini I 3, Manaf A 3, Rahman A O 3, Khatijah Y 3, Mohd Azmi M L 3, Fauziah O 3 1Department of Neurosciences, 2Department of Pathology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia. , 3Universiti Putra Malaysia, Serdang, Selangor, Malaysia. Overexpression of cyclin D1 has been observed in various malignancies including breast cancer, colorectal cancer, parathyroid adenoma and prostate cancer. However, there is no systematic immunohistochemical study of the protein expression in brain tumors. This study was thus performed to better understand the expression pattern of cyclin D1 in brain tumors, particularly in Malaysian patients. For the purposes, 24 meningiomas and 23 gliomas samples were collected. All samples were analyzed by immunohistochemistry analysis to determine cyclin D1 protein expression. Our results revealed equal expression of cyclin D1 in low grades of gliomas, and the expression decreased in higher grades of gliomas with 76.9% (10/13) were low expressers (
Page 1 and 2:
1.0 Paths to recovery: Modulating P
Page 3 and 4:
3.07 Congenital hypothyroidism alte
Page 5 and 6:
4.01 The effect of hippocampal slic
Page 7 and 8:
4.09 ß-adrenergic modulation of in
Page 9 and 10:
5.03 Constitutively active Ras and
Page 11 and 12: 6.07 Proteomic identification of bi
Page 13 and 14: 8.01 Dietary flavonoids stimulate P
Page 15 and 16: 9.04 Inducing neural differentiatio
Page 17 and 18: 10.02 The effect of PAT (thymulin r
Page 19 and 20: 10.10 Immuno-regulatory T cell func
Page 21 and 22: 11.04 Expression profile of mesench
Page 23 and 24: 12.01 Use of capillary chip based p
Page 25 and 26: 13.06 Contribution of synaptic cond
Page 27 and 28: 15.01 L-serine enhances the inhibit
Page 29 and 30: 16.03 Quantitative analysis of memb
Page 31 and 32: 18.03 Finding cells for replacement
Page 33 and 34: 20.01 Cannabinoid neuropharmacology
Page 35 and 36: 21.05 Spatial arrangement of cortic
Page 37 and 38: 23.04 Adenosine, astrogliosis and e
Page 39 and 40: 25.04 The L1 cell adhesion family a
Page 41 and 42: 28.05 The effects of the FAAH inhib
Page 43 and 44: 28.13 Genetic determinants of ethan
Page 45 and 46: 29.02 A HAP1-kinesin protein traffi
Page 47 and 48: 29.10 Identification of molecular d
Page 49 and 50: 29.18 Supporting study skills: work
Page 51 and 52: 33.02 Noradrenaline reuptake inhibi
Page 53 and 54: 35.01 Synchrony and sensory coding
Page 55 and 56: 37.01 Nitric oxide inhibition incre
Page 57 and 58: 37.09 Behavioural and electrophysio
Page 59 and 60: 39.06 The role of glutamate recepto
Page 61: 40.03 Live imaging of Per1 driven G
Page 65 and 66: 43.02 Neuroleptic treatment worsens
Page 67 and 68: 43.10 Biochemical estimates of SNAR
Page 69 and 70: 45.01 Mutant SOD1-PUMA knockout dou
Page 71 and 72: 47.03 VAP proteins Skehel P Center
Page 73 and 74: 49.04 Regulation of synaptic functi
Page 75 and 76: 51.04 The use of MRI for tracking d
Page 77 and 78: 53.04 The role of the pedunculopont
Page 79 and 80: 56.06 Dissecting exploratory behavi
Page 81 and 82: 57.01 Opioid Receptor Agonists’-
Page 83 and 84: 57.09 Cognitive rigidity and altere
Page 85 and 86: 57.17 An analysis of DJ-1 (PARK7) a
Page 87 and 88: 58.05 Differential effects of Inter
Page 89 and 90: 59.05 Blockade of paw incision-indu
Page 91 and 92: 60.07 2-Dimensional gel electrophor
Page 93 and 94: 63.02 Subpyrogenic systemic inflamm
Page 95 and 96: 64.08 Modulation of ketamine-induce
Page 97 and 98: 65.08 The anti-inflammatory role of
Page 99 and 100: 68.01 A comparison of carbachol and
Page 101: 69.06 Comparison of data analysis t
show all

Book of abstracts - British Neuroscience Association

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?