Book of abstracts - British Neuroscience Association

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65.04 Lipidomic analysis of phospholipids in mouse cerebral cortex: investigating the molecular mechanism of PUFA neuroprotection. Williams A, Nicolaou A, Obrenovitch T School of Pharmacy,, University of Bradford,, Richmond Road,, Bradford, BD7 1DP Brain phospholipids have important structural and physiological functions. They also constitute a pool of precursors for lipid mediators. Polyunsaturated fatty acids (PUFA) influence the activity of many membrane – bound proteins and receptors, regulate gene expression and participate in cell signalling. Several PUFA were neuroprotective when administered systemically to rats and mice prior to focal brain ischaemia, but the molecular mechanisms accounting for neuroprotection remain uncleart. The purpose of this study was to test whether PUFA administration causes changes in brain phospholipid composition that could account for its neuroprotective effects. Cerebral cortex phospholipids were analysed in mice treated with alphalinolenic acid (ALA) or vehicle. Following their extraction from cortical tissue samples, lipidomic analysis of phospholipids was performed by electrospray ionisation tandem mass spectrometry (ESI–MS/ MS). We detected 14 species of phosphatidylcholine (PC) and sphingomyelin (SM), 24 species of phosphatidylethanolamine (PE) species, 10 species of phosphatidylinositol (PI) and 13 species of phosphatidylserine (PS). The ALA treatment did not alter significantly the relative abundance of any of these species, suggesting that the neuroprotective effect of this PUFA is not directly linked to changes in membrane phospholipids occuring prior to the test insult. 65.05 Adenosine preconditions against ouabain but not glutamate in CA1 neurons Ferguson A L, Stone T W Institute of Biomedical and Life Sciences,, University of Glasgow, Glasgow, G12 8QQ Preconditioning is induced by exposing tissue to sublethal insults resulting in a tolerant state within the tissue protecting against further damage. To investigate the role of adenosine in excitotoxic preconditioning, we evoked responses from rat hippocampal slices exposed to glutamate and ouabain. A significant depression was observed in epsp slope, orthodromic population spike and antidromic population spike amplitudes in response to 10mM glutamate and 100µM ouabain. Antidromic population spikes showed a significantly greater recovery following ouabain exposure (82.6 ± 1.6%) (n = 6) compared with the orthodromic responses (epsps 58.6 ± 7.1%, n = 7; population spikes 56.6 ± 8.3%, n = 8) (p
65.08 The anti-inflammatory role of Interleukin-1F5 in the rat brain Watson M, Lyons A, Costello C, Lynch M Department of Physiology, Trinity College, Dublin 2, Ireland It is well established that inflammatory changes contribute to the deficits associated with the aged brain. Central to these changes is increased expression of the pro-inflammatory cytokines, interleukin-1β (IL-1β) and interleukin-6 (IL-6) and increased IL-1β-induced signaling. Recent data show that interleukin-1F5 (IL-1F5), a newly characterised member of the IL-1 ligand superfamily shares significant homologies with Interleukin-1receptor antagonist (IL-1ra), suggesting a possible anti-inflammatory action. In this study the effects of IL-1F5 on lipopolysaccharide (LPS) treatment was assessed both in vivo and in vitro. The data show that LPS increased hippocampal expression of IL-1β mRNA and protein and downstream IL-1β-induced signaling, including enhanced phosphorylation of the stress-activated protein kinases, JNK and p38. Importantly IL-1F5 abrogated this LPS-induced pro-inflammatory cytokine profile and downstream signaling. Furthermore, IL-1F5 attenuated the LPS induced increases in IL-1β and IL-6 in both mixed glial cells and astrocytes. These results demonstrate that IL-1F5 has an anti-inflammatory role in the rat brain acting to ameliorate some of the detrimental effects of LPS. 65.09 7β-hydroxyepiandrosterone (HF0220) induces neuroprotection through increased production of 15-Deoxy- 12,14-prostaglandin J2 (PGJ2) Wülfert E, Rotondo D 1. Hunter Fleming Ltd. Regus House, 1 Friary, Temple Quay, Bristol BS1 6EA, UK, 2. Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde, The John Arbuthnott Building 27 Taylor Street Glasgow G4 0NR, UK, 7β-hydroxy-epiandrosterone (HF0220) protects against neuronal cell death in vitro (organotypic hippocampal slice cultures, OTHSC, and PC12 cells) and brain damage in vivo (Pringle A et al. (2003) Eur. J. Neurosci. 18: 117- 124; Dudas B et al. (2004) Neurobiology of Disease 15: 262-8). HF0220 also reduces the level of soluble amyloid peptide Abeta42 in the brain of 8- months old TgAPP/717I mice, and facilitates neurite growth from mouse sensory neurones and spinal cord motor neurones in culture. Recent findings show that incubation of PC12 cells and mouse sensory neurones with indomethacin, a cyclooxygenase (COX) inhibitor, abrogates the effects of HF0220 suggesting that COX activity is required for HF0220- induced neuroprotection and neurite out-growth. Moreover, incubation of human monocytic blood cells (hMBC) with nanomolar concentrations of HF0220 caused a 10-12-fold increase in the production of 15-deoxy- 12,14- prostaglandin J2 (15d-PGJ2), but did not significantly alter the production of prostaglandin E2 (PGE2). In contrast, incubation of hMBC with the proinflammatory cytokine TNFα increased the production of both prostaglandins approx. 3-fold. Addition of nanomolar concentrations of HF0220 caused a further increase in TNF-α-induced 15d-PGJ2 similar to the increase observed with HF0220 alone, but completely abolished the increases in PGE2 by TNFα. Our results suggest that HF0220 could have beneficial effects in numerous inflammatory degenerative disorders such as stroke and AD and that the effects of HF0220 are mediated by 15d-PGJ2. The clinical safety of HF0220 is currently assessed in patients with mild-to-moderate Alzheimer’s disease. 66.01 Excess porphyrin excretion in childhood autistic disorder, a marker of environmental toxicity Lathe R (1), Skorupka C (2), Springbett A (3), Lam A (4), Amet L (2), Nataf, R. (4) (1) Pieta Research, Edinburgh, UK; (2) Association ARIANE, Clichy, France; (3) Dept. Statistics, Roslin Institute, Roslin, UK; (4) Laboratoire Philippe Auguste,Paris, France Urinary porphyrin levels increase in response to inhibition of heme synthesis enzymes. To address possible environmental toxicity in autism porphryin levels were studied in a 269 children referred to a Paris clinic for neurodevelopmental disorders. Subjects with autistic disorder had elevated levels of porphyrins relative to control groups (p
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1.0 Paths to recovery: Modulating P
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3.07 Congenital hypothyroidism alte
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4.01 The effect of hippocampal slic
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4.09 ß-adrenergic modulation of in
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5.03 Constitutively active Ras and
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6.07 Proteomic identification of bi
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8.01 Dietary flavonoids stimulate P
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9.04 Inducing neural differentiatio
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10.02 The effect of PAT (thymulin r
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10.10 Immuno-regulatory T cell func
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11.04 Expression profile of mesench
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12.01 Use of capillary chip based p
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13.06 Contribution of synaptic cond
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15.01 L-serine enhances the inhibit
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16.03 Quantitative analysis of memb
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18.03 Finding cells for replacement
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20.01 Cannabinoid neuropharmacology
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21.05 Spatial arrangement of cortic
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23.04 Adenosine, astrogliosis and e
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25.04 The L1 cell adhesion family a
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28.05 The effects of the FAAH inhib
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28.13 Genetic determinants of ethan
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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
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Page 63 and 64: 41.01 A polymorphism at the 3’ un
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Page 75 and 76: 51.04 The use of MRI for tracking d
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Page 79 and 80: 56.06 Dissecting exploratory behavi
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Page 85 and 86: 57.17 An analysis of DJ-1 (PARK7) a
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Book of abstracts - British Neuroscience Association

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