Book of abstracts - British Neuroscience Association

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15.05 Influence of sodium valproate on the EEG characteristics in epileptic children Khachidze I, Gugushvili M, Maloletnev V 14 Gotua str, I. Beritashvili Institute of Physiology, Tbilisi, 0160,GEORGIA The study was aimed to investigate the alteration of EEG characteristics in epileptic children during the treatment with anticonvulsant - depakine.146 patients aged 3 to 9 years were examined. The duration of their disease ranged from 3 months to 9 years. Absolute and Relative values of the power spectra (AVP and RVP) of standard EEG were analyzed. Expressed decrease of total AVP was observed in frontal, temporal and occipital areas. This indicates that D reduces the signs of excessive EEG. Synchronization pointing to the status of readiness to seizure activity in the CNS. This inference is confirmed by the analysis of the dynamics of the selected ranges of activity, since observation during the treatment course showed a significant decrease in AVP of Low-frequency range in temporal, parietal and occipital areas. The dynamics of high frequency fraction EEG activity requires a special consideration. It appeared that the action of D produces an advantageous decrease within the range of beta-1, and especially, beta2 activity in the parietal and occipital areas, i.e exactly in the regions where its presence is conventionally accounted for the CNS regulatory mechanisms dysfunction. The analysis of D to influence on epileptiform graphoelements shows that its effect reveals primarily in the reduction of typical epileptiform complexes peak-wave, sharp waves. The influence of D on grouped, polyphasic sharp waves, as well as on paroxysmal bursts provoked by functional tests was expressed to a less extent: these graphoelements continued to be recorded after 6-8 months after the commencement of the treatment. 15.06 Influence of sodium valproate on the EEG characteristics in epileptic children Khachidze I, Gugushvili M, Maloletnev V 14 Gotua str, I. Beritashvili Institute of Physiology, Tbilisi, 0160,GEORGIA The study was aimed to investigate the alteration of EEG characteristics in epileptic children during the treatment with anticonvulsant - depakine.146 patients aged 3 to 9 years were examined. The duration of their disease ranged from 3 months to 9 years. Absolute and Relative values of the power spectra (AVP and RVP) of standard EEG were analyzed. Expressed decrease of total AVP was observed in frontal, temporal and occipital areas. This indicates that D reduces the signs of excessive EEG. Synchronization pointing to the status of readiness to seizure activity in the CNS. This inference is confirmed by the analysis of the dynamics of the selected ranges of activity, since observation during the treatment course showed a significant decrease in AVP of Low-frequency range in temporal, parietal and occipital areas. The dynamics of high frequency fraction EEG activity requires a special consideration. It appeared that the action of D produces an advantageous decrease within the range of beta-1, and especially, beta2 activity in the parietal and occipital areas, i.e exactly in the regions where its presence is conventionally accounted for the CNS regulatory mechanisms dysfunction. The analysis of D to influence on epileptiform graphoelements shows that its effect reveals primarily in the reduction of typical epileptiform complexes peak-wave, sharp waves. The influence of D on grouped, polyphasic sharp waves, as well as on paroxysmal bursts provoked by functional tests was expressed to a less extent: these graphoelements continued to be recorded after 6-8 months after the commencement of the treatment. 16.01 Posttranslational modifications and signaling in postsynaptic densities. Schoepfer R, Trinidad J C, Thalhammer A, Burlingame A L 1. Laboratory for Molecular Pharmacology, University College London, London, UK, 2. Department of Pharmaceutical Chemistry, UCSF, San Francisco, CA, USA , Postsynaptic densities (PSDs) form a highly structured environment of signal transmission and exquisite signal processing in the nervous system. Glutamate serves as the main excitatory neurotransmitter in the mammalian central nervous system, and glutamate receptors are an integral part of excitatory PSDs. PSDs combine the receptors and channels, their downstream signaling machinery (such as kinases and phosphatases), and a cytoskeletal network into a structured environment of signaling pathways. The phosphorylation state of components of the PSD is central to the regulation of synaptic transmission and is known to play a role in synaptic plasticity, learning and memory. We purified PSDs from mouse brain on sucrose density gradients, and analyzed its protein components and phosphorylation state by mass spectrometry, following two-dimensional liquid chromatography plus immobilized metal affinity chromatography of tryptic digests. Using PSDs isolated from four different brain regions, hippocampus, cortex, midbrain and cerebellum, we examined region specific variations at both the protein and phosphorylation level. The tryptic digests of the four different PSD preparations were labeled individually with one of the four iTRAQ isobaric labels, pooled, and subjected to the same workflow as previously established for single PSD preparations. This workflow allowed us to perform relative quantitation and bioinformatic analysis of over 1000 proteins and 1376 unique phosphorylated peptides. 16.02 Synapse evolution is linked to neuroanatomical diversity Grant S G N, Anderson C N G, Emes R D, Pocklington A J, Vickers C A, Croning M D R, Armstrong J D A † The Wellcome Trust Sanger Institute, Genes to Cognition Program, Hinxton, Cambridge CB10 1SA UK, Present address: Department of Biology, University College London, Darwin Building, Gower Street, London, WC1E 6BT UK, ‡ University of Edinburgh, Institute for Adaptive and Neural Computation, 5 F Increasing brain size and number of synaptic connections is thought to be the primary mechanism underlying evolution of intelligence. Here we examine the molecular evolution of the synapse in 19 species and focus on postsynaptic signaling complexes essential for learning and memory. Striking increases in number of synapse components preceded the evolution of large vertebrate brains. Key synapse components predate the origins of nerve cells and later molecular innovations at the metazoan and chordate boundaries contribute novel signaling functions and greater molecular and signaling complexity. mRNA and protein expression patterns in mouse brain show recently evolved synapse proteins preferentially contribute to differences between brain regions. Progressive elaboration upon an ancestral synapse signaling structure leading to increased synapse diversity and signaling complexity was further supported by analyses of protein function and interactions. We propose that evolution of synapses and brain size are linked and synergistically important for species differences in behaviour. Support Contributed By: NIH NCRR grants RR12961, RR14606, and RR01614 to ALB and grants from the Wellcome Trust (UK) to RS Page 28/101 - 10/05/2013 - 11:11:03
16.03 Quantitative analysis of membrane microdomains-associated proteins in the DLPFC in the schizophrenic and bipolar disorder brain Áine T. Behan*, Kieran Wynne#, Connie Byrne#, Patricia Maguire#, Niaobh O`Donoghue$, Michael J. Dunn$, Gerard Cagney#, David R. Cotter* *Department of Psychiatry, Royal College of Surgeons in Ireland ERC, Beaumont Hospital, Dublin 9., $Proteome Research Centre, UCD Conway Institute of Biomolecular and Biomedical Research, UCD, #School of Biomolecular, and Biomedical Science, Conway Institute, UCD. Membrane microdomains (MM) are defined by their cholesterol and sphingolipid-rich nature with numerous roles been ascribed them such as their involvement as vehicles of endocytosis and trafficking during signaling. Studies analysing protein changes potentially contributing to human brain diseases have identified numerous MM associated proteins as candidate players. We reason that by identifying and quantifying MMs in the dorsolateral prefrontal cortex (DLPFC), an area implicated in schizophrenia (SCZ), we may better understand the molecular mechanisms underlying dysfunction in the SCZ and bipolar disorder (BPD) brain. A 10/10/10 series of the best matched brains (pH. PMI etc.) were chosen from the 35/35/35 Stanley Foundation frozen post-mortem brain tissue from DLPFC grey matter. Ten samples were pooled for each of the groups (control, SCZ, BPD) and MMs were isolated and analysed using two proteomic methods, (i) 2D-DIGE and MALDI-TOF and (ii) 1D SDS PAGE and ion-trap MS. Proteins of interest were validated in whole cell lysates (10/10/10 series – not pooled) using Western blotting. 21 proteins were found to be differentially expressed by both proteomic methods in our pooled samples. Further validation by Western blotting demonstrated this differential expression for 3 synaptic/neuroplasticity proteins, namely brain acid soluble protein 1(BASP1), limbic system associated membrane protein(LAMP) and syntaxin binding protein 1(STXBP1). BASP1, STXBP1 and LAMP are increased in the SCZ and BPD brain. This suggests a dysfunction in synaptic function and/or neuroplasticity in these psychiatric disorders. 16.04 Cellular and proteomics approaches to protein synthesis in axons. Minnen Jv Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research (CNCR), Vrije Universiteit, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands. Recent studies have begun to focus on axonal protein synthesis and the functional significance of localized protein synthesis. However, identification of proteins that are synthesized in mammalian axons has not been rigorously addressed. Here, we used axons purified from cultures of injuryconditioned adult dorsal root ganglion (DRG) neurons and proteomics methodology to identify axonally synthesized proteins. Proteins and the encoding mRNAs for cytoskeletal proteins were identified in glial cell free axonal preparations. In addition to the cytoskeletal elements, several heat shock proteins, resident endoplasmic reticulum (ER) proteins, proteins associated with neurodegenerative diseases (ubiquitin C-terminal hydrolase L1, rat ortholog of human DJ-1/Park7, -synuclein, superoxide dismutase 1), anti-oxidant proteins and metabolic proteins were identified among the axonally synthesized proteins. Detection of the mRNAs encoding each of the axonally synthesized proteins identified by mass spectrometry in the axonal compartment indicates that the DRG axons have the potential to synthesize a complex population of proteins. Ultrastructural studies on in vivo injured and regenerating axons demonstrated that these axons harbor high numbers of polyribosomes, indicating active protein synthesis. Surprisingly, by creating GFP-tagged ribosomes in Schwann cells, we demonstrated that the axonal polyribosomes have originated in the Schwann cells. These data indicate that mammalian axons have the ability to synthesize a large variety of proteins, of which part of the encoding mRNAs and synthetic machinery have originated in Schwann cells. 17.01 Molecular regulation of thalamocortical axonal navigation Price D Centres for Integrative Physiology and Neuroscience Research, Edinburgh University, Hugh Robson Building, George Square, Edinburgh EH8 9XD The cerebral cortex receives most of its sensory innervation via thalamocortical axons, whose development requires interactions between advancing thalamic growth cones and guidance cues that they encounter, attracting them towards or repelling them from specific regions. We have been studying the regulation of guidance molecules in thalamic neurons and in the environment through which their growth cones navigate. Regarding control of navigation in thalamic cells, we found that thalamic growth cones and neurons contain β-catenin mRNA and that manipulations predicted to affect β-catenin levels cause major disruption to thalamic axonal navigation. (1) In vivo, loss of adenomatous polyposis coli (APC) in the forebrain blocks completely thalamic axonal navigation from ventral to dorsal telencephalon. (2) In vitro, application of lithium blocks thalamic axonal growth in thalamocortical co-cultures. Regarding control of the environment that thalamic axons navigate, we found direct evidence that telencephalic expression of the transcription factor Pax6 is required for thalamic axon guidance. We made mice with loxP sites flanking exons encoding Pax6’s paired DNA binding domain (Pax6loxP), so that exposure to Cre recombinase excises this crucial domain and knocks the remainder of the protein out of frame, creating a null-allele. We removed Pax6 from some cells in ventral telencephalon using a Six3Cre allele that drives Cre recombinase expression in cells around the developing internal capsule but neither in diencephalon nor in cortex. In Pax6loxP/loxP;Six3Cre embryos, a 60-70% depletion of Pax6-expressing cells around the internal capsule correlates with a ventral misrouting of a significant proportion of thalamic axons. 17.02 Tangential neuronal migration controls axon guidance: a role for neuregulin-1 in thalamocortical axon navigation López-Bendito G Instituto de Neurociencias de Alicante, CSIC & Universidad Miguel Hernández, 03550 San Joan d’Alacant, Spain Neuronal migration and axon guidance constitute fundamental processes in brain development that are generally studied independently. Although both share common mechanisms of cell biology and biochemistry, little is known about their coordinated integration in the formation of neural circuits. Using several in vitro coculture assays, in situ hybridation and immunohistochemistry, here we show that the development of the thalamocortical projection, one of the most prominent tracts in the mammalian brain, depends on the early tangential migration of a population of neurons derived from the ventral telencephalon. This tangential migration contributes to the establishment of a permissive corridor that is essential for thalamocortical axon pathfinding. Our results also demonstrate that in this process two different products of the Neuregulin-1 gene, CRD-NRG1 and Ig-NRG1, mediate the guidance of thalamocortical axons. These results have been demonstrated in part by the analysis of specific mutant mice deficient on either or all isoforms of Ngr1. TCAs fail to extend normally through the telencephalon in mice with a loss of function mutation in the Nrg1 gene. We have also demonstrated that this function seems to be mediated by the tyrosine kinase receptor ErbB4. In sum, these results show that neuronal tangential migration constitutes a novel mechanism to control the timely arrangement of guidance cues required for axonal tract formation in the mammalian brain Page 29/101 - 10/05/2013 - 11:11:03
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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
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Page 23 and 24: 12.01 Use of capillary chip based p
Page 25 and 26: 13.06 Contribution of synaptic cond
Page 27: 15.01 L-serine enhances the inhibit
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
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Page 49 and 50: 29.18 Supporting study skills: work
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56.06 Dissecting exploratory behavi
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57.01 Opioid Receptor Agonists’-
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57.09 Cognitive rigidity and altere
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57.17 An analysis of DJ-1 (PARK7) a
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58.05 Differential effects of Inter
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59.05 Blockade of paw incision-indu
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60.07 2-Dimensional gel electrophor
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63.02 Subpyrogenic systemic inflamm
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64.08 Modulation of ketamine-induce
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65.08 The anti-inflammatory role of
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