Book of abstracts - British Neuroscience Association

More documents

Recommendations

Info

31.03 Dopaminergic modulation of spinal neuronal excitability Han P, Michelle A. Tran, Whelan P J Rm 2068 Hotchkiss Brain Institute, University of Calgary, 3330 Hospital Drive,NW,Calgary, AB T2N4N1,CANADA Although dopamine is well known to play a role in motor control it is generally assumed that dopamine does not directly modulate spinal motor circuits. However, in recent years several studies have demonstrated a modulatory action of dopamine on spinal networks and reflexes. DA fibres and receptors are present in the spinal cord and evidence for DA release within the spinal cord has been published. A critical gap is our lack of data regarding dopaminergic modulation of intrinsic and synaptic properties of motoneurons and ventral interneurons in the mammalian spinal cord. In this study, we address this issue by examining the intracellular mechanisms underlying DA’s excitatory effect on motor systems. We examine DA’s effects on two classes of cells important for motor control, motoneurons and Hb9 interneurons located in lamina VIII. We show that DA can boost excitability in spinal motor systems by decreasing the first spike latency and the AHP. Collectively, this leads to an increase in the F-I slope. Our data suggest that these changes are due to modulation of IA and SKCa currents. We also demonstrate that DA modulates glutamatergic transmission by increasing both the amplitude and frequency of miniature and spontaneous excitatory postsynaptic currents suggesting that DA acts both pre and postsynaptically. Collectively these data suggest that DA has widespread actions on intrinsic and synaptic properties of spinal neurons consistent with its ability to modulate and stabilize spinal networks. In addition, dopaminergic therapy may provide promising perspectives on spinal cord rehabilitation. 32.01 Stimulus timing-dependent plasticity in the adult auditory system Dahmen J, Ahmed B, Hartley D E H, King A J Department of Physiology, Anatomy and Genetics, Sherrington Building, University of Oxford, Parks Road, Oxford OX1 3PT Adult cortical circuits possess considerable plasticity over different time scales, which can be induced by conditioning or task-specific training. For instance, it has been shown that repetitive pairing of stimuli that differ either in their orientation (Yao and Dan, 2001, Neuron 32:315-323) or location in space (Fu et al., 2002, Science 296:1999-2003) can induce rapid shifts in the orientation tuning and receptive field location, respectively, of neurons in the primary visual cortex. The direction of those shifts was found to depend on the order of stimulus presentation, while their magnitude depended on the interval between the stimuli in each pair, with intervals larger than about 20 ms being ineffective. This is consistent with the temporal window of spike timing-dependent synaptic plasticity. To examine whether stimulus timing-dependent plasticity also exists in the auditory system, we recorded from neurons in primary auditory cortex of anaesthetized adult ferrets. Presentation of ≥600 pairs of tones that differed in frequency resulted in shifts in the best frequencies of the neurons. These shifts were observed when stimulus onset asynchronies of up to 12 ms were used and their direction depended on the order in which the tones in a pair were presented. The shifts in frequency tuning persisted for several minutes and appeared to be most pronounced in the supragranular layers of the cortex. These data show that stimulus timing-dependent plasticity is a property of the auditory cortex and exhibits a temporal specificity similar to that observed in the visual system. 32.02 Regulation of CSPG expression in the developing barrel cortex A Petrie, Matthews R L, Kind P C 1 & 3, University of Edinburgh,, Hugh Robson Building,, George Square,, Edinburgh,, EH8 9XD,, 2, SUNY Upstate medical University, New York Chondroitin-sulphate proteoglycans (CSPGs) are a principle component of the extracellular matrix (ECM) of the CNS. In adult animals, CSPGs appears to restrict plasticity induced by monocular deprivation (Pizzorusso et al 2002) and the expression of aggrecan, a principle CSPG in adult brain, correlates well with the termination of developmental plasticity (Sur et al 1988). Aggrecan localises to perineuronal nets, a specialised ECM that surrounds soma and proximal dendrites. We have used Cat-315, an antibody that labels an epitope on aggrecan (Lander et al, 1997), to examine the role of this molecule in cortical development. In mouse neocortex, staining increases through development and, in adults, is highest in primary somatosensory cortex (S1), retrosplenial cortex and motor cortex. In S1, staining appears as two distinct bands of labelled soma, one through layer 4 and the other through lower layer 5 and layer 6. Staining with Cat-315 of tangential sections shows an intense staining in a barrel-like pattern in S1. We have previously shown that mGluR5 signalling via PLC-b1 regulates barrel formation. Aggrecan expression is known to be dependent on synaptic activity (Sur et al., 1988; Kind et al., 1995) raising the possibility that mGluR5 may regulate aggrecan expression. To determine whether mGluR5 signalling via PLC- b1 also regulates aggrecan expression we investigated Cat-315 expression in Mglur5-/- and Plc-b1-/- mice. Qualitative assessment of Mglur5-/- show fewer Cat-315 immunopositive cells and staining at a lower intensity than Mglur5+/+, indicating mGluR5 may regulate the formation of perineuronal nets in barrel cortex. 33.01 Space-Time Spike triggered covariance analysis of fly motion selective neuron Saleem A, Schultz S R Department of Bioengineering,, Imperial College London,, UK SW7 2AZ The H1 neuron of the fly lobula plate has been widely studied with an interest to understand the motion detection systems of the visual system. Most properties of H1 have been studied in the steady state through tuning curve functions of the cells, which assume separability of the response properties along the different dimensions. The spike triggered covariance (STC) analysis of these cells avoids this. STC in the velocity-time domain is also limited as it assumes velocity tuning of a neuron that is known to be temporal frequency tuned. We carry out STC in the space-time domain, thus making fewer assumptions about the properties of the cells. We recorded extracellular activity of the H1 cells of blowflies while presenting a bar stimulus: the contrasts of the bars changing as ternary noise. We carry out STC analysis on this data. We recovered the spacetime receptive fields of the cell. These show a temporal frequency tuning of about 120 cycles/deg, which matches previous studies. We also observe that the cell responds to changes is position that are within 8msec. We recovered spatially separated excitatory and suppressive filters. We also recovered the non-linear stage of a stochastic linear-nonlinear model of the cell. We present a complete model of the cell recovered from the data. The space-time STC analysis has been used to build models of cells in the MT/V5 of the primate visual cortex, and hence we can directly compare our results between the two systems. Page 50/101 - 10/05/2013 - 11:11:03
33.02 Noradrenaline reuptake inhibitors inhibit neuroinflammation induced by a systemic inflammatory challenge O`Sullivan J B, Harkin A, Connor T J Trinity College Institute of Neuroscience, University of Dublin, Trinity College, Dublin 2, Ireland. Evidence suggests that the monoamine neurotransmitter noradrenaline elicits anti-inflammatory actions in the central nervous system (CNS), and consequently may play an endogenous neuroprotective role in CNS disorders where inflammatory events contribute to pathology. In line with this hypothesis, we demonstrate that noradrenaline suppresses expression of the pro-inflammatory cytokines IL-1beta and TNF-alpha and induction of iNOS/nitric oxide production from mixed glial cultures prepared from rat cortex, in response to the inflammagen bacterial lipopolysaccharide (LPS). As previous studies indicate that the noradrenaline reuptake inhibitor (NRI) desipramine has anti-inflammatory properties, we examined the ability of desipramine and more selective NRI’s to alter glial proinflammatory cytokine production. However, treatment of mixed glial cells with NRI’s largely failed to alter inflammatory events induced by LPS. In contrast to the in vitro situation, acute in vivo treatment of rats with NRI’s elicited an anti-inflammatory effect in the CNS characterised by reduced mRNA expression of the pro-inflammatory cytokines IL-1beta and TNF-alpha and iNOS in cortex in response to systemic LPS administration. The data also suggest that in vivo treatment with NRI’s inhibited microglial activation in the cortex indicated by reduced expression of the microglial activation makers CD40 and CD11b. These data indicate that NRI’s do not have a direct modulatory effect on the inflammatory response in glial cells, however when administered in vivo can limit inflammatory events in the brain. Overall, this study has yielded significant insights into the ability of noradrenaline augmentation strategies to limit neuroinflammation. 33.03 Functional segregation of synaptic GABA(A) and GABA(C) receptors in retinal bipolar cell terminals Palmer M J Institute for Science and Technology in Medicine, Keele University The transmission of light responses to retinal ganglion cells is regulated by inhibitory input from amacrine cells to bipolar cell (BC) synaptic terminals. GABAA and GABAC receptors in BC terminals mediate currents with different kinetics and are likely to have distinct functions in limiting BC output but the synaptic properties and localisation of the receptors are currently poorly understood. By recording endogenous GABA receptor currents directly from BC terminals in goldfish retinal slices, I show that spontaneous GABA release activates rapid GABAA receptor mIPSCs in addition to a tonic GABAC receptor current. The GABAC receptor antagonist TPMPA has no effect on the amplitude or kinetics of the rapid GABAA mIPSCs. In addition, inhibition of the GAT-1 GABA transporter, which strongly regulates GABAC receptor currents in BC terminals, fails to reveal a GABAC component in the mIPSCs. These data suggest that GABAA and GABAC receptors are highly unlikely to be synaptically colocalised. Using non-stationary noise analysis of the mIPSCs, I estimate that GABAA receptors in BC terminals have a single-channel conductance of 17 pS and that an average of just seven receptors mediates a quantal event. From noise analysis of the tonic current, GABAC receptor singlechannel conductance is estimated to be 4 pS. Identified GABAC receptor mIPSCs exhibit a slow decay and are mediated by approximately 42 receptors. The distinct properties and localisation of synaptic GABAA and GABAC receptors in BC terminals are likely to facilitate their specific roles in regulating the transmission of light responses in the retina. 33.04 Immunocytochemical studies of GABA receptors and transporters at amacrine cell to bipolar cell terminal synapses in the goldfish retina. Jones S, Palmer M, Furness D ISTM, Huxley Building, Keele University, Keele, Staffordshire, ST5 5BG The vertebrate retina transduces light and carries out the initial stages of visual signal processing. The visual signal is transmitted from photoreceptors to bipolar cells and then to ganglion cells, the output cells of the retina. Transmission between bipolar cells and ganglion cells is modulated by a class of lateral inhibitory interneurones, amacrine cells, which form both reciprocal and conventional GABAergic synapses with bipolar cell terminals. GABA transporters are likely to be associated with these synapses to control receptor activation properties and recycling of GABA. We have therefore attempted to determine the ultrastructural distribution of GABA transporters on and around the bipolar cell terminal using postembedding immunogold labelling of freezesubstituted, Lowicryl embedded goldfish retina. Preliminary results show that labelling for GAT-1 is found at relatively high density in putative amacrine cell processes, some distance from their contact with bipolar cell terminals, and at a lower density around the periphery of GABAergic synapses with bipolar cell terminals. Labelling for GAT-3 is weaker and more diffuse. 33.05 Using SSVEPs to investigate the half-life of attentional lapses Dockree P M, O’Connell R G, Shalgi S, Kelly S P, Bellgrove M A, Robertson I H The Lloyd Building, Trinity College Institute of Neuroscience, Trinity College Dublin , Dublin 2, Ireland Traditional measures of vigilance have shown that time-on-task decrements emerge after several tens of minutes; however more recent research suggests that the half-life of sustained attention failures is apparent over shorter periods of minutes and seconds (Pardo et al., 1991; Robertson et al., 1997; Weissman et al., 2006). The present study utilises a steady-state visual evoked potential (SSVEP) measure of sensory facilitation in the visual cortical pathways and behavioral data of momentary lapses of attention to examine the temporal dynamics of sustained attention modulation. Importantly, SSVEPs are ongoing oscillatory waveforms that provide a continuous record of cortical facilitation suited to capturing fluctuations in sustained attention over time. Ten neurologically healthy participants were presented with flickering (25Hz) pattern-reversal stimuli. Participants monitored standard stimuli presented for 800ms and responded with a key press to target stimuli presented for the longer duration of 1040ms. Temporal Spectral Evolution (TSE) analysis was conducted for the time window prior to detected versus undetected targets and transient ERP analysis of targets and standards and relationship to SSVEP modulation was investigated. Results are discussed in the context of fronto-parietal modulation of visual cortical pathways. Both GABAA and GABAC receptors can be identified physiologically in bipolar cell terminals and the terminals exhibit response properties which suggest that these receptor subtypes may be located at different sites in the postsynaptic membrane. The above technique will be applied to enable us to determine where the receptor subtypes are located in relation to the synapse and the GABA transporters. Page 51/101 - 10/05/2013 - 11:11:03
Page 1 and 2: 1.0 Paths to recovery: Modulating P
Page 3 and 4: 3.07 Congenital hypothyroidism alte
Page 5 and 6: 4.01 The effect of hippocampal slic
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
Page 21 and 22: 11.04 Expression profile of mesench
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
Page 43 and 44: 28.13 Genetic determinants of ethan
Page 45 and 46: 29.02 A HAP1-kinesin protein traffi
Page 47 and 48: 29.10 Identification of molecular d
Page 49: 29.18 Supporting study skills: work
Page 53 and 54: 35.01 Synchrony and sensory coding
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
Page 61 and 62: 40.03 Live imaging of Per1 driven G
Page 63 and 64: 41.01 A polymorphism at the 3’ un
Page 65 and 66: 43.02 Neuroleptic treatment worsens
Page 67 and 68: 43.10 Biochemical estimates of SNAR
Page 69 and 70: 45.01 Mutant SOD1-PUMA knockout dou
Page 71 and 72: 47.03 VAP proteins Skehel P Center
Page 73 and 74: 49.04 Regulation of synaptic functi
Page 75 and 76: 51.04 The use of MRI for tracking d
Page 77 and 78: 53.04 The role of the pedunculopont
Page 79 and 80: 56.06 Dissecting exploratory behavi
Page 81 and 82: 57.01 Opioid Receptor Agonists’-
Page 83 and 84: 57.09 Cognitive rigidity and altere
Page 85 and 86: 57.17 An analysis of DJ-1 (PARK7) a
Page 87 and 88: 58.05 Differential effects of Inter
Page 89 and 90: 59.05 Blockade of paw incision-indu
Page 91 and 92: 60.07 2-Dimensional gel electrophor
Page 93 and 94: 63.02 Subpyrogenic systemic inflamm
Page 95 and 96: 64.08 Modulation of ketamine-induce
Page 97 and 98: 65.08 The anti-inflammatory role of
Page 99 and 100: 68.01 A comparison of carbachol and
Page 101:
69.06 Comparison of data analysis t
show all

Book of abstracts - British Neuroscience Association

Create successful ePaper yourself

Delete template?

Save as template?