The Spatial Structure of Stimuli Shapes the Timescale of Correlations in Population Spiking Activity

Throughout the central nervous system, the timescale over which pairs of neural spike trains are correlated is shaped by stimulus structure and behavioral context. Such shaping is thought to underlie important changes in the neural code, but the neural circuitry responsible is largely unknown. In this study, we investigate a stimulus-induced shaping of pairwise spike train correlations in the electrosensory system of weakly electric fish. Simultaneous single unit recordings of principal electrosensory cells show that an increase in the spatial extent of stimuli increases correlations at short (~10 ms) timescales while simultaneously reducing correlations at long (~100 ms) timescales. A spiking network model of the first two stages of electrosensory processing replicates this correlation shaping, under the assumptions that spatially broad stimuli both saturate feedforward afferent input and recruit an open-loop inhibitory feedback pathway. Our model predictions are experimentally verified using both the natural heterogeneity of the electrosensory system and pharmacological blockade of descending feedback projections. For weak stimuli, linear response analysis of the spiking network shows that the reduction of long timescale correlation for spatially broad stimuli is similar to correlation cancellation mechanisms previously suggested to be operative in mammalian cortex. The mechanism for correlation shaping supports population-level filtering of irrelevant distractor stimuli, thereby enhancing the population response to relevant prey and conspecific communication inputs. © 2012 Litwin-Kumar et al

Microscale Inhomogeneity of Brain Tissue Distorts Electrical Signal Propagation

Interpretations of local field potentials (LFPs) are typically shaped on an assumption that the brain is a homogenous conductive milieu. However, microscale inhomogeneities including cell bodies, dendritic structures, axonal fiber bundles and blood vessels are unequivocally present and have different conductivities and permittivities than brain extracellular fluid. To determine the extent to which these obstructions affect electrical signal propagation on a microscale, we delivered electrical stimuli intracellularly to individual cells while simultaneously recording the extracellular potentials at different locations in a rat brain slice. As compared with relatively unobstructed paths, signals were attenuated across frequencies when fiber bundles were in between the stimulated cell and the extracellular electrode. Across group of cell bodies, signals were attenuated at low frequencies, but facilitated at high frequencies. These results show that LFPs do not reflect a democratic representation of neuronal contributions, as certain neurons may contribute to the LFP more than others based on the local extracellular environment surrounding them

フルオキセチン慢性投与は歯状回において貫通繊維-顆粒細胞シナプスの肥大化を誘導する

久留米大学2016年

High-fidelity multimode fibre-based endoscopy for deep brain in vivo imaging

Progress in neuroscience relies on new techniques for investigating the complex dynamics of neuronal networks. An ongoing challenge is to achieve minimally invasive and high-resolution observations of neuronal activity in vivo inside deep brain areas. Recently introduced methods for holographic control of light propagation in complex media enable the use of a hair-thin multimode optical fibre as an ultranarrow imaging tool. Compared to endoscopes based on graded-index lenses or fibre bundles, this new approach offers a footprint reduction exceeding an order of magnitude, combined with a significant enhancement in resolution. We designed a compact and high-speed system for fluorescent imaging at the tip of a fibre, achieving a resolution of 1.18 ± 0.04 µm across a 50-µm field of view, yielding 7-kilopixel images at a rate of 3.5 frames/s. Furthermore, we demonstrate in vivo observations of cell bodies and processes of inhibitory neurons within deep layers of the visual cortex and hippocampus of anaesthetised mice. This study paves the way for modern microscopy to be applied deep inside tissues of living animal models while exerting a minimal impact on their structural and functional properties

Dendritic spikes control synaptic plasticity and somatic output in cerebellar Purkinje cells.

Neurons receive the vast majority of their input onto their dendrites. Dendrites express a plethora of voltage-gated channels. Regenerative, local events in dendrites and their role in the information transformation in single neurons are, however, poorly understood. This thesis investigates the basic properties and functional roles of dendritic spikes in cerebellar Purkinje cells using whole-cell patch clamp recordings from the dendrites and soma of rat Purkinje cells in brain slices. I show that parallel fibre (PF) evoked dendritic spikes are mediated by calcium channels, depend on membrane potential and stimulus intensity and are highly localized to the spiny branches receiving the synaptic input. A determining factor in the localization and spread of dendritic calcium spikes is the activation of large-conductance, calcium dependent potassium (BK) channels. I provide a strong link between dendritic spikes and the endocannabinoid dependent short-term synaptic plasticity, depolarization-induced suppression of excitation (DSE). Gating the dendritic spikes using stimulus intensity or membrane potential, I show that the threshold of DSE is identical to that of the dendritic spikes and the extent of DSE depends on the number of dendritic spikes. Blocking BK channels increases the spatial spread of dendritic spikes and enables current injection or climbing fibre (CF) evoked dendritic spikes to suppress PF inputs via DSE. By monitoring dendritic spikes during strong PF stimulation-induced long-term depression (LTD), I also provide a link between long-term synaptic plasticity and dendritic excitability. By showing that blocking CB1 cannabinoid receptors reduces the intensity requirement for LTD, I provide a connection between the short- and long-term changes in PF strength triggered by dendritic spikes I also investigate the effect dendritic spikes have on somatic action potential output. Contrary to pyramidal cells, where dendritic spikes boost the output of the neuron, the average Purkinje cell output becomes independent from the output strength for inputs triggering dendritic spikes. However, the temporal pattern of the output is strongly affected by dendritic spikes. I show that this phenomenon depends on BK channel activation resulting in a pause in somatic firing following dendritic spikes. In summary, I present a description of PF evoked local dendritic spikes and demonstrate their functional role in controlling the synaptic input and action potential output of cerebellar Purkinje cells