Book of abstracts - British Neuroscience Association

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33.06 FMR-Adaptation reveals a view-invariant representation for familiar faces in the fusiform face area Andrews T, Ewbank M Department of Psychology, University of York, York UK, MRC Cognition and Brain Sciences Unit, Cambridge UK Recognising complex objects, such as faces, is a simple and effortless process for most human observers. However, as we move about or as gaze or expression change, the size and shape of the face image on the retina also changes. To facilitate recognition, the visual system must take into account these sources of variation. The aim of this study was to explore whether face recognition is dependent on a viewpoint-dependent or viewpoint-invariant neural representation. Using the technique of fMR-adaptation, we measured the MR response to repeated images of the same face. We report that activity in the face-selective FFA was reduced following repeated presentations of the same face. This adaptation was similar for both familiar and unfamiliar faces. To establish if the neural representation of faces in the FFA was invariant to changes in viewpoint, we varied the viewing angle of the face between successive presentations. We found that adaptation to familiar faces was apparent across all changes in viewpoint. In contrast, we found signficant adaptation in the FFA to unfamiliar faces only occurred when the viewing angle between successive images was 2 degrees or less. Face-selective regions in the superior temporal lobe failed to adapt to repeated presentations of the same face. These results are consistent with cognitive models of face perception that predict a view-invariant neural representation underlies the recognition of familiar faces. 34.01 3-D alterations in ultrastructure of dendritic spines and postsynaptic densities after LTP and LTD induction in dentate gyrus of awake rats. Medvedev N I 1, Doyere V 2, Davies H A 1, Rodriguez J J 1, Dallérac G 2, Gabbott P L 1, Laroche S 2, Kraev I V 1,3, Popov V I 1,3, Stewart M G 1 1The Open University, Milton Keynes, UK; 2 NAMC, CNRS-UMR8620, Univ. Paris Sud, Orsay, France; 3Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, RF Using serial ultrathin sections, 3-D reconstructions of synapses and dendritic spines in dentate gyrus (DG) were prepared following induction of long-term potentiation (LTP) or heterosynaptic long-term depression (LTD) in awake rats. Control rats were pseudo-tetanized, or LTP was blocked by i.p. injection of the NMDA-receptor antagonist D,L-3[(+/-)-2- carboxypiperazin-4-yl]-propyl-1-phosphonic acid (CPP). Animals were perfused intracardially 24h later and brains prepared for electron microscopy. 3-D reconstructions enabled quantitative structural changes in dendritic spines and postsynaptic densities (PSDs) to be defined in inner, middle and outer molecular layers of the DG. A novel method enabled calculation of curvature of PSDs in each serial section. No significant changes were found in either synapse density or proportion of 4 synapse classes (thin, mushroom, stubby and shaft). However significant increases in both volume and surface area of thin spines and PSDs were found in LTP compared to control and CPP-treated animals. There was a significant reduction in volume of mushroom spines in CPP-treated animals compared to LTP and control rats. A significant reduction in concavity of spine PSD area was observed in all layers of the DG for thin and mushroom spines in LTP and LTD animals, but not CPP treatment. In LTD animals, there was a more marked reduction in concavities. Both LTP and LTD animals showed spinule growth on spine heads in all three layers examined (blocked with CPP). These data suggest substantial remodelling of large dendritic spines 24h after induction of LTP and/or LTD. Supported by EU FPVI Promemoria programme # 512012 34.02 Neuronal network oscillations in primary motor cortex Naoki Yamawaki, Gavin L. Woodhall, Ian M. Stanford School of Life and Health Sciences, Aston University, Birmingham Parkinson’s disease (PD) is associated with abnormal synchronization of neuronal network oscillations at theta (4-10Hz) and beta (15-30Hz) frequency bands across nuclei of the basal ganglia (BG) (Brown et al., 2001 J. Neurosci. 21(3):1033-8). Deep brain stimulation of specific BG nuclei appears to reduce these pathological activities, thereby alleviating PD symptoms. Recently, direct stimulation of primary motor cortex (M1) has also been shown to be effective in reducing symptoms in an animal model of PD, indicating that the cortex may pattern these pathological rhythms through its connections with BG (Drouot et al., 2004 Neuron 44(5):769-78). Here we examined properties of the M1 network oscillations in vitro. Co-application of the glutamate receptor agonist kainic acid (400nM) and muscarinic receptor agonist carbachol (50μM) induced oscillatory activity at beta frequencies in all layers (e.g. layer 5, 27.8 ± 1.1Hz, n=6). Dual extracellular recordings, local application of TTX and microsections indicate that the activity in superficial layers is strongly influenced by that within deep layers V/VI. All oscillations were abolished by the GABAA receptor antagonist picrotoxin and modulated by pentobarbital and zolpidem indicating dependence on networks of GABA interneurons. High frequency stimulation (125Hz) in superficial layers tended to generate gamma oscillations (incidence 95%, 62.2 ± 5.6Hz, n=19) whereas stimulation at 4Hz led to a higher incidence of theta oscillation (62.5%, 5.4 ± 0.5Hz, n=12). Often evoked oscillations were observed within the same recording and at the same time as the pharmacologically induced beta oscillation suggesting that they are generated by different interneuron populations. 34.03 The electrode-brain interface in deep brain stimulation is modulated by systemic and local physiological factors: A 3-dimensional computational model Yousif N, Richard Bayford, Xuguang Liu 1. Movement Disorder and Neurostimulation Unit, Department of Clinical Neuroscience, Division of Neuroscience and Mental Health, Imperial College London;, 2. Bio-modelling/Bio-informatics Group, Department of Biomedical Science, Institute of Social and Health Research, Middlesex University Deep brain stimulation (DBS) is a widely used clinical treatment for various neurological disorders, and particularly movement disorders. However, the mechanism by which these high frequency electrical pulses act on underlying neuronal activity is not understood. Once the stimulating electrode is placed in situ, an electrode-brain interface (EBI) is created. We used computational modelling to construct a three-dimensional model of the EBI using the finite element method to compensate for the clinical restrictions on the study of EBI in situ. In this way both the structural details and the biophysical properties of the EBI are retained. We focussed on systemic and local, and dynamic physiological and pathological modulation of the EBI, specifically by brain pulsation and giant cell formation. Our results show that the EBI is influenced by both the systemic and the local physiological factors. We find that there is a linear correlation between cerebral blood perfusion and the magnitude of the potential distribution induced in the tissue surrounding the electrode. Furthermore, giant cell growth at the EBI creates a ‘shielding effect’, which impedes the flow of current to the surrounding tissue. These results provide a quantitative assessment of the current flow in the brain tissue surrounding the implanted DBS electrode, the effects of the EBI on the current spreading under physiological conditions, and consequently on the therapeutic effect of DBS. The project was supported by MRC grants (id 71766 and 78512) Page 52/101 - 10/05/2013 - 11:11:03
35.01 Synchrony and sensory coding in the olivocerebellar pathway in vivo Schultz S R, Kitamura K, Hausser M 1 Dept of Bioengineering, Imperial College London, 2 Dept of Neuroscience, Osaka University, 3 Wolfson Institute for Biomedical Research, University College London The climbing fibre pathway from the inferior olive to the cerebellum has been hypothesized to provide information about non-anticipated sensory signals for the modification of motor programmes. However, the nature of the neural coding, and particularly the population coding, of this sensory information is poorly understood. To investigate this, we used two-photon imaging of calcium signals in multiple Purkinje neurons loaded with membrane-permeant dye. Rats (P18-25) were anaesthetized using urethane or ketamine/xylazine, and Purkinje cells in the Crus IIa area of the cerebellum were bulk-loaded with AM-ester calcium dye (Oregon Green BAPTA-1 AM) through a pipette inserted into the molecular layer. As previously reported, calcium transients triggered by spontaneous climbing fibre inputs were observed in the Purkinje cell dendritic tree. These signals showed fine-scale spatial structure, with synchronization between neighbouring neurons falling off over hundreds of microns transversely. We investigated the role of this synchronization in coding sensory information, by stimulating the upper or lower lip with a brief airpuff. Using the two-photon microscope, we were able to search in three dimensions for regions of tissue in which sensory evoked calcium signals were to be found. Sensory stimuli which evoked strong fluorescence responses compared to baseline accentuated synchrony between nearby cells. Periodic sensory stimuli were observed to result in the locking of calcium signals to stimulus onset. These findings suggest that sensory input modulates the fine structure of spatiotemporal patterns of synchrony in the cerebellar cortex, perhaps by changing the dynamics of oscillatory synchrony in the inferior olive. 36.01 Cholinergic neurons in human midbrain labelled with 125I Urotensin II in post-mortem tissue in Progressive Supranuclear Palsy and normal elderly Piggott M A, Muelas M W, Burn D J Dementia and Brain Ageing Group , Wolfson Research Centre , Newcastle University Institute for Ageing and Health , Newcastle General Hospital , Westgate Road , Newcastle-upon-Tyne NE4 6BE Progressive supranuclear palsy (PSP) is a disorder often misdiagnosed as Parkinson’s disease, however patients do not respond well to levodopa. Other clinical characteristics include postural instability resulting in frequent falls, and symmetric signs with trunk more than limbs affected. These features may relate to a greater pathological burden in nuclei that have bilateral influence on the basal ganglia motor loop, including the pedunculopontine nucleus (PPN). Degeneration of the PPN could also be implicated in the absence of REM sleep in PSP. The PPN is severely affected in PSP, with approximately 60% neuronal loss. The PPN is located in the rostral midbrain and has connections with the basal ganglia, thalamus, lower brainstem and spinal cord. Urotensin II receptor transcripts and radioligand binding have been detected in cholinergic neurones of rat midbrain, especially in PPN and the laterodorsal tegmentum (LDTg) (Clark SD et al, 2001) where their presence may relate to sensory-motor integration. We have taken frozen sections from midbrain in PSP and normal elderly controls at levels incorporating the PPN and LDTg. Sections have been stained for acetylcholinesterase, with relative density of staining quantified. Areas with strong staining include the PPN, LDTg, substantia nigra, raphe nuclei, pontine nuclei, and cuneiform nucleus. Radioligand receptor autoradiography has been carried out to visualise urotensin receptors (125I urotensin II) showing binding localised to acetylcholinesterase-rich areas. Specific binding was demonstrated by displacement with the antagonist palosuran (gift from Actelion Pharmaceuticals Ltd), and unlabelled urotensin. Urotensin II binding in PSP compared to control cases is presented. 36.02 Computational Modelling of Neostriatal Neurons Hoyland D, Wood R B, Overton P G, Gurney K Department of Psychology, University of Sheffield, Sheffield, , United Kingdom Computational modelling at the biophysical level often encounters a severe limitation in that the modelling enterprise is divorced from the gathering of physiological data, and hence generic parameters, and membrane behaviour gathered from the work of others, have to be used. Here we present the results of an exercise to model certain neuronal types from the neostriatum - medium spiny neurons (MSNs) and fast spiking interneurons (FSNs) - using data gathered in parallel with the modelling. Brain slices (250-400µm) were prepared from rats at P14-19, containing the neostriatum in coronal section. Electrophysiological data were acquired under current clamp in the whole cell patch configuration. The acquired data consisted of measurements of voltage responses to short current pulses (to determine passive membrane properties) and responses to longer duration subthreshold and suprathreshold pulses (to activate voltage gated conductances). Medium spiny neurons (N = 11) were identified by their hyperpolarised membrane potential (-81.95mV ± 2.78) and long delay to first spike (216.45ms ± 42.77) at rheobase. Fast spiking interneurons (N = 4) were identified by high maximum firing frequency (typically around 75 Hz) and faster spike responses at threshold (132.50ms ± 58.10). Passive membrane and voltage response data were used to drive a parameter search algorithm developed previously by our group, which refines models of the cell concerned until target voltage behaviour is achieved. These models of MSNs and FSNs, and refinements that take into account neuronal morphology, will be used to build large scale striatal models for the investigation of striatal functionality. 36.03 How visual stimuli activate subthalamic neurones at short latency. Graham J H, Coizet V, Overton P G, Redgrave P Biology Dept., King College, Bristol, TN, USA, Dept. Psychology, University of Sheffield, S10 2TP The midbrain superior colliculus (SC) is one of a number of brainstem sensorimotor structures that provides input to and receives output from the basal ganglia (BG). Recently, the status of the subthalamic nucleus (STN) as a major input station of the BG has been firmly established. Although the STN is known to receive many afferents from the cerebral cortex, comparatively little is known about inputs from subcortical sensorimotor structures. We have recently described a pronounced projection to the STN from the SC (Redgrave et al., 2005); however, the functional implications of this connectivity are unknown. The purpose of the present electrophysiological investigation was, therefore, to determine whether short-latency visual signals are relayed to the STN from the visually responsive SC. In the anaesthetised rat, cells in the intermediate and deep layers of the SC, as well as cells in the STN, were found to be unresponsive to a bright wholefield light flash. However, following a local disinhibitory injection of the GABAA antagonist bicuculline into the SC, both SC and STN neurons exhibited phasic, short latency responses to the flash. These results demonstrate the SC is a major source of short latency visual signals to the STN. This route could enable unexpected events to interrupt ongoing behaviour. (Supported by BBSRC and Wellcome Trust) Page 53/101 - 10/05/2013 - 11:11:03
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Page 5 and 6: 4.01 The effect of hippocampal slic
Page 7 and 8: 4.09 ß-adrenergic modulation of in
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Page 11 and 12: 6.07 Proteomic identification of bi
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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 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
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Page 73 and 74: 49.04 Regulation of synaptic functi
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