Book of abstracts - British Neuroscience Association

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66.03 The role of p53 in Д-Tetrahydrocannabinol-induced neuronal apoptosis. Gowran A M, Downer E J, Campbell V A Trinity College Institute of Neuroscience,, Trinity College,, Dublin 2,, Ireland. Aoife M. Gowran, Eric J. Downer, Veronica A. Campbell. Trinity College Institute of Neuroscience, Department of Physiology, Trinity College, Dublin 2, Ireland. We have previously shown that the plant-derived cannabinoid Д9- Tetrahydrocannabinol (THC) induces apoptosis via the CB1 receptor in rat cortical neurons1. In post-mitotic neurons, the tumour supressor protein, p53 may mediate apoptosis induced by a range of insults including DNA damage, hypoxia and oxidative stress. This study investigated the role of p53 in THC-induced apoptosis in cultured cortical neurons. Exposure to THC (5µM; 5 min) caused a rapid and transient increase in the activated form of p53 (phospho-p53ser15) via the CB1 receptor as determined by western immunoblot. THC caused p53 to colocalise with lysosomes, an event which co-insided with THC-induced destabilisation of the lysosomal membrane. Neurons exposed to THC (5µM; 2 h) displayed a significant increase in caspase-3 activity and DNA fragmentation (P
68.01 A comparison of carbachol and kainate-induced gamma and betaII oscillations in the rodent auditory cortex Roopun A K, Cunningham M O, Le Beau F E N, Traub R D, Whittington M A (1,2,3,5) School of Neurology, Neurobiology and Psychiatry, Medical School, Newcastle University, NE2 4HH. UK. (3) Neurology, SUNY Downstate, Med, Ctr., Brooklyn, NY, USA. High-frequency oscillatory activity at betaII (20-30Hz) and gamma (30- 80Hz) frequencies is proposed to mediate cognitive processing in the cortex. Oscillatory activity is mediated by a variety of neuromodulators, including the cholinergic and glutamatergic system. Horizontal neocortical slices (450µm) containing deafferented auditory cortex were prepared from adult male Wistar rats and maintained at the interface between artificial cerebrospinal fluid and carbogen gas at 34oC. Oscillatory activity was generated upon the application of the cholinergic agonist carbachol [25µM] or the glutamatergic agonist kainate [400nM]. Concurrent betaII and gamma oscillations were induced by carbachol (n=25), whereas only gamma oscillations were induced by kainate (n=25). Kainate-induced activity was resistant to the muscarinic-receptor blocker atropinµe [10µM] (n=6), and carbachol-induced oscillations was resistant to kainate-receptor antagonist UBP302 [10µM] (n=5), indicating two independently-driven networks producing a gamma oscillation. The similarities in gamma oscillations induced by kainate and carbachol were many-fold: the frequencies were similar, the peak power of oscillations were generated in superficial layers of the cortex, and all oscillations were abolished by carbenoxolone [100µM] (a gap-junction blocker), SYM2206 [20µM] (an AMPA-receptor antagonist) and bicuculline [2µM] (a GABAA-receptor antagonist) (n=6). Intracellular electrodes recorded gamma frequency firing from interneurons and gamma frequency IPSPs from pyramidal cells, suggesting an inhibitory-based oscillatory network. BetaII oscillations were only generated by carbachol, and may rely on intrinsically bursting (IB) cells interacting with an interneuronal network. This study indicates that cholinergic and glutamatergic systems operate independently in the auditory cortex, with the cholinergic drive exclusively producing a betaII oscillation. 68.02 Patterns of spontaneous activity in hippocampal cultures developing on multi electrode arrays: the influence of the NMDA receptor Charlesworth P, Eglen S J, Humphreys L, Morton A, Grant S G N Genes to Cognition Programme, The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, Cambridge Computational Biology Institute, University of Cambridge We have used multi electrode arrays to record action potentials from developing embryonic hippocampal cultures and a suite of software tools to analyse the resulting network activity. Action potentials are first observed at ~ 4 days in vitro (DIV) and thereafter activity increases sigmoidally until a plateau at maturity (~20+ DIV) with a period of very rapid increase between ~8 – 15 DIV. Concomitant with the rise in the number of spikes, a greater number of recording sites detect activity and also an entrainment of spikes into bursts is observed, such that by maturity most (~95+%) action potentials occur within bursts. Furthermore, these bursts show a progressively increasing degree of both temporal regularity and spatial correlation. Treating cultures with APV at DIV 6-7 (just prior to the rapid upsweep in network activity and synaptogensis) has a profound effect on this developing spike pattern: burst patterns are less regular, both spatially and temporally, and many more non-bursting, individual, spikes occur. The overall number of spikes is however unaltered. We conclude that the NMDA receptor plays an important role in the development of spike pattern in culture, with implications for the transfer of information in neuronal networks. It is the aim of the Genes to Cognition programme (www.genes2cognition.org) to employ the MEA-culture platform and analytical methods developed here to phenotype mutant mice generated within the programme (see Kopanitsa et al, this meeting). We are also currently developing statistical methods for the automated analysis of these datasets as part of the CARMEN project. 68.03 Effects of DHEA administration on auditory evoked potentials Alhaj H A, McAllister-Williams R H Psychiatry, Leazes Wing, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP Background: The adrenal steroid dehydroepiandrosterone (DHEA) has been shown to improve memory performance and modulate neural activity in rodents. Further, we have recently demonstrated beneficial effects of DHEA on long-term episodic memory performance in healthy humans. To further evaluate the effects of DHEA on attention and short-term memory in man, a study of auditory eventrelated potentials (ERPs) was conducted. Methods: Double-blind placebo-controlled crossover study in 24 healthy men (aged 18 to 34). DHEA (300 mg/day) or placebo was administered for one week. Following each treatment period, subjects participated in an auditory oddball paradigm, during which subjects heard high (frequent) and low (rare) tones and were instructed to count the number of rare tones silently. Stimulus-locked ERPs were recorded from 29 scalp electrodes. The amplitude of the N1/P2 ERP components, and the latency and amplitude of the P3 component to rare tones, were calculated. Results: DHEA treatment led to a significant increase in the amplitude of the N1 component of ERPs recorded from posterior electrodes (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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29.02 A HAP1-kinesin protein traffi
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Book of abstracts - British Neuroscience Association

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