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BNA2015-Abstract-Book.Pdf BNA2015: Festival of Neuroscience Poster Abstracts 12‐14 April 2015 EICC, Edinburgh, UK Citations The recommended citation for an abstract in this volume is as follows: British Neurosci. Assoc. Abstr., Vol. 23: Pxx, 2015 ISSN 1345‐8301 2015 Contents Sunday 12 April 2015 - Poster Session 1 Page Floor plan 4 Theme A: Development 5 B: Molecular, Cellular and Synaptic Mechanisms 24 C: Sensory and Motor Systems 68 D: Learning, Memory and Cognition 104 F: Nervous System Disorders 173 G: Methods and Techniques 234 H: Autonomic Nervous System 251 Monday 13 April – Poster Session 2 Page Floor plan 261 Theme A: Development 262 B: Molecular, Cellular and Synaptic Mechanisms 286 C: Sensory and Motor Systems 332 D: Learning, Memory and Cognition 368 E: Sleep, Circadian and Neuroendocrine Mechanisms 434 F: Nervous System Disorders 453 G: Methods and Techniques 518 Tuesday 14 April – Poster Session 3 Page Floor plan 537 Theme A: Development 538 B: Molecular, Cellular and Synaptic Mechanisms 560 C: Sensory and Motor Systems 605 D: Learning, Memory and Cognition 637 E: Sleep, Circadian and Neuroendocrine Mechanisms 704 F: Nervous System Disorders 723 G: Methods and Techniques 782 Conflict of interest declarations 798 Poster Reference Explanation P2-F-012 Poster board number Day Theme 1=Sunday A: Development 2=Monday B: Molecular, Cellular and Synaptic Mechanisms 3=Tuesday C: Sensory and Motor Systems D: Learning, Memory and Cognition E: Sleep, Circadian and Neuroendocrine Mechanisms F: Nervous System Disorders G: Methods and Techniques H: Autonomic Nervous System Poster Session 1 Sunday 12 April 2015 Posters P1‐A‐001 to P1‐H‐006 Theme A: Development Posters P1‐A‐001 to P1‐A‐020 Theme B: Molecular, Cellular and Synaptic Mechanisms Posters P1‐B‐001 to P1‐B‐043 Theme C: Sensory and Motor Systems Posters P1‐C‐001 to P1‐C‐031 Theme D: Learning, Memory and Cognition Posters P1‐D‐001 to P1‐D‐062 Theme F: Nervous System Disorders Posters P1‐F‐001 to P1‐F‐058 Theme G: Methods and Techniques Posters P1‐G‐001 to P1‐G‐015 Theme H: Autonomic Nervous System Posters P1‐H‐001 to P1‐H‐006 BNA 2015 POSTER DISPLAY DAY 1 SUNDAY 12 APRIL ROW 1 ROW 2 ROW 3 ROW 4 ROW 5 ROW 6 ROW 7 ROW 8 ROW 9 ROW 10 ROW 11 ROW 12 ROW 13 ROW 14 ROW 15 ROW 16 A: Development B: Molecular, Cellular and Synaptic Mechanisms C: Sensory and Motor Systems D: Learning, Memory and Cognition E: Sleep, Circadian and Neuroendocrine Mechanisms F: Nervous System Disorders G: Methods and Techniques H: Autonomic Nervous System BNA2015: FESTIVAL OF NEUROSCIENCE ABSTRACT e‐BOOK Theme A: Development Posters P1‐A‐001 to P1‐A‐020 5 ID13 BNA2015: FESTIVAL OF NEUROSCIENCE ABSTRACT e‐BOOK Poster Ref: P1-A-001 Theme: A: Development Can oxytocin be of any therapeutic use in the future? – A meta-analysis on the potential therapeutic role of oxytocin in children and youths with autism spectrum disorder (ASD). Baguiasri Mandane De Montfort University Objectives: Oxytocin is a nonapeptide hormone synthesised mostly by the neurons in the paraventricular and supraoptic nucleus of the hypothalamus; it is then released into the bloodstream by the posterior pituitary. The neuropeptide hormone, which is mainly involved in promoting maternal behaviour, has further also been widely studied as a potential for treatment of social deficit symptoms in many neurological disorders such as autism and personality disorders. This meta-analysis was carried out to examine whether the following hypothesis was true: “oxytocin enhances emotion recognition in children and youths with ASD”. The aim was to see the impact of oxytocin administration (short-term) on social deficit symptoms in children suffering from ASD on a wider scale. Review Method: The key words researched included: ASD; Autism; Oxytocin; Intranasal oxytocin; Children; Youths; RMET; Social; Short-term. The collected data was then analysed using Review Manager 5.2 program. Results: The results from this meta-analysis did not show a statistically significant benefit for the use of oxytocin in young people diagnosed with ASD compared to placebo at the 95% confidence interval (P=0.92 > 0.05). Potential reasons for these negative findings could take account of contextual and interindividual differences which might have affected the principal effects of oxytocin and its levels in the periphery. Contextual differences include for example the presence of a stranger versus a friend and interindividual factors such as gender, attachment style or the presence of existing psychiatric symptoms. Additionally, single nucleotide polymorphisms leading to a genomic deletion or unusual methylation of the oxytocin receptor gene could have also been implicated in the lack of response. Conclusion: This meta-analysis did not statistically verify the hypothesis that oxytocin enhances emotion recognition in children and youths suffering from ASD. However, this interpretation needs to be evaluated with caution, as the trials used in this meta-analysis were fairly small. Future studies comparing gender, genetics, hormonal status and also individual differences are certainly needed to further enhance our knowledge and understanding of the aetiology of autistic spectrum disorders. 6 ID13 BNA2015: FESTIVAL OF NEUROSCIENCE ABSTRACT e‐BOOK Poster Ref: P1-A-003 Theme: A: Development An in vitro model of the impact of chemotherapy on neural stem cells and the protection provided by cells in the neurogenic niche. Entedhar Kadhum Huss Rabiaa, Ayesha Maqbool, Ayoub Al-Bayati, Paul Smith and Peter Wigmore University of Nottingham Numerous patient reports have complained about cognitive decline after chemotherapy treatment. These effects have been called “chemobrain” or “chemofog” and while not affecting all patients can persist for many years after the completion of treatment. Animal studies have found that the systemic chemotherapy causes a persistent reduction in adult hippocampal neurogenesis. As hippocampal neurogenesis is required for the consolidation of long term memory this is likely to be one of the causes of cognitive decline. Hippocampal neurogenesis requires the proliferation of neural stem cells in the subgranular zone of the dentate gyrus. Many of these stem cells are in close contact with blood vessels and astrocytes which form components of the neurogenic niche which regulates neurogenesis. After chemotherapy, proliferating cells in contact with blood vessels, survive better than cells some distance from blood vessels suggesting that association with this tissue provides protection from chemotherapy. We have developed an in-vitro model to study the protective effect of different combinations of neural and non neural cells. Neural stem cells are more sensitive to chemotherapy (5-Fluorouracil) in comparison to endothelial or glial cells. Co-culture of neural cells with endothelial and glial cells protects neural stem cells from chemotherapy in contrast to co-culture with non neural cells (3T3). Both endothelial and glial cells require cell to cell contact with neural stem cells to provide protection with glial cells providing the most protection. We are currently studying the mechanisms by which endothelial and glial cells regulate neural stem cell proliferation via cell to cell contact. 7 ID24 BNA2015: FESTIVAL OF NEUROSCIENCE ABSTRACT e‐BOOK Poster Ref: P1-A-004 Theme: A: Development The role of transcription factor Pax6 in the development of the ventral lateral geniculate nucleus. Ziwen Li, Tian Tian, Martine Manuel, Tom Pratt and David Price University of Edinburgh The development of diencephalon can be summarized as a process in which cells that initially appear similar give rise to a complex structure that contains a variety of cell groups called nuclei. The nuclei execute distinct functions. The ventral lateral geniculate nucleus (vLGN) is involved in the visual system. The transcription factor Pax6 is involved in the development of structures including cortex, diencephalon and major axonal tracts in the forebrain. Pax6-/- mouse mutants, also known as Small eye (Sey) mutants, show severe defects in the embryonic forebrain. The disrupted structure of the diencephalon hinders us from further investigating its detailed structures. In this study, we use the Cre-loxP system to mutate Pax6 conditionally using Zic4Cre, with a GFP reporter to show the Cre activity. Zic4 is a transcription factor mainly expressed in septum, hem, thalamus and prethalamus. The deletion of Pax6 is restricted to lineages that express Zic4. A relatively normal forebrain is maintained. With the help of this model, we investigated the development of specific thalamic nuclei, including the vLGN. Staining of GFP on postnatal day (P) 0 coronal brain sections showed a distinct distribution of Zic4 lineage cells: they aggregate in greater density into the vLGN than into the adjacent nuclei such as dorsal lateral geniculate nuclei (dLGN) and ventral posterior nuclei (VP). We found Pax6 deletion causes Zic4 lineage cell density to decrease in the vLGN of the Pax6fl/fl mutants but to increase in that of the Pax6fl/+mutants. An increase of Zic4 lineage cell density was also observed in dLGN of both the Pax6fl/fl and Pax6fl/+ mutants. VP is not significantly affected by the Pax6 deletion. These findings indicated that the transcription factor Pax6 is involved in the development of the lateral geniculate complex and may play a role in cell parcellation in the diencephalon by regulating cell distribution. Figure GFP staining on P0 coronal sections from Zic4Cre:Pax6+/+ (wt), Zic4Cre:Pax6fl/+ (het) and Zic4Cre:Pax6fl/fl (hom) mouse brains. There are more GFP+ve cells in the vLGN in het (arrow, B) than in that of wt (arrow, A) and the fewest in hom vLGN (arrow, C). Comparisons of GFP+ve cell density (cells/100 miron2) in vLGN (D) and dLGN (E) between genotypes at a range of rostrocaudal positions. 8 ID28 BNA2015: FESTIVAL OF NEUROSCIENCE ABSTRACT e‐BOOK Poster Ref: P1-A-005 Theme: A: Development Influence of white matter connections on cortical gyrification. Yujiang Wang, Peter Taylor and Marcus Kaiser Newcastle University Purpose: The mechanisms underlying cortical gyrification have been subject of debate for nearly two decades.
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