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Tiesinga, P.

Publications and source records attributed to Tiesinga, P..

3 recordsLinked to original sources

Why not record from every channel with a CMOS scanning probe?

It is an uninformative truism to state that the brain operates at multiple spatial and temporal scales, each with each own set of emergent phenomena. More worthy of attention is the point that our current understanding of it cannot clearly indicate which of these phenomenological scales are the significant contributors to the brains function and primary output (i.e. behaviour). Apart from the sheer complexity of the problem, a major contributing factor to this state of affairs is the lack of instrumentation that can simultaneously address these multiple scales without causing function altering damages to the underlying tissue. One important facet of this problem is that standard neural recording devices normally require one output connection per electrode. This limits the number of electrodes that can fit along the thin shafts of implantable probes generating a limiting balance between density and spread. Sharing a single output connection between multiple electrodes relaxes this constraint and permits designs of ultra-high density probes. Here we report the design and in-vivo validation of such a device, a complementary metal-oxide-semiconductor (CMOS) scanning probe with 1344 electrodes; the outcome of the European research project NeuroSeeker. We show that this design targets both local and global spatial scales by allowing the simultaneous recording of more than 1000 neurons spanning 7 functional regions with a single shaft. The neurons show similar recording longevity and signal to noise ratio to passive probes of comparable size and no adverse effects in awake or anesthetized animals. Addressing the data management of this device we also present novel visualization and monitoring methods. Using the probe with freely moving animals we show how accessing a number of cortical and subcortical brain regions offers a novel perspective on how the brain operates around salient behavioural events. Finally, we compare this probe with lower density, non CMOS designs (which have to adhere to the one electrode per output line rule). We show that an increase in density results in capturing neural firing patterns, undetectable by lower density devices, which correlate to self-similar structures inherent in complex naturalistic behaviour. To help design electrode configurations for future, even higher density, CMOS probes, recordings from many different brain regions were obtained with an ultra-dense passive probe.

neuroscience

Feature Specific Prediction Errors and Surprise across Macaque Fronto-Striatal Circuits during Attention and Learning

Prediction errors signal unexpected outcomes indicating that expectations need to be adjusted. For adjusting expectations efficiently prediction errors need to be associated with the precise features that gave rise to the unexpected outcome. For many visual tasks this credit assignment proceeds in a multidimensional feature space that makes it ambiguous which object defining features are relevant. Here, we report of a potential solution by showing that neurons in all areas of the medial and lateral fronto-striatal networks encode prediction errors that are specific to separate features of attended multidimensional stimuli, with the most ubiquitous prediction error occurring for the reward relevant features. These feature specific prediction error signals (1) are different from a non-specific prediction error signal, (2) arise earliest in the anterior cingulate cortex and later in lateral prefrontal cortex, caudate and ventral striatum, and (3) contribute to feature-based stimulus selection after learning. These findings provide strong evidence for a widely-distributed feature-based eligibility trace that can be used to update synaptic weights for improved feature-based attention.\n\nHighlightsO_LINeural reward prediction errors carry information for updating feature-based attention in all areas of the fronto-striatal network.\nC_LIO_LIFeature specific neural prediction errors emerge earliest in anterior cingulate cortex and later in lateral prefrontal cortex.\nC_LIO_LIVentral striatum neurons encode feature specific surprise strongest for the goal-relevant feature.\nC_LIO_LINeurons encoding feature-specific prediction errors contribute to attentional selection after learning.\nC_LI

neuroscience

Molecules of map plasticity in the somatosensory cortex

Sensory maps are representations of the sensory epithelia in the brain. Despite the intuitive explanatory power behind sensory maps as being neuronal precursors to sensory perception, and sensory cortical plasticity as a neural correlate of perceptual learning, molecular mechanisms that regulate map plasticity are not well understood. Here we perform a meta-analysis of transcriptional and translational changes during altered whisker use to nominate the major molecular correlates of experience-dependent map plasticity in the barrel cortex. We argue that brain plasticity is a systems level response, involving all cell classes, from neuron and glia to non-neuronal cells including endothelia. Using molecular pathway analysis, we further propose a gene regulatory network that could couple activity dependent changes in neurons to adaptive changes in neurovasculature, and finally we show that transcriptional regulations observed in major brain disorders target genes that are modulated by altered sensory experience. Thus understanding the molecular mechanisms of experience-dependent plasticity of sensory maps might help to unravel the cellular events that shape brain plasticity in health and disease.\n\nHighlightsO_LIExperience alters gene transcription in all major cell types of the brain\nC_LIO_LIGene expression profile during brain plasticity is cell-type specific\nC_LIO_LITemporal profile of gene expression is dynamic, regulated by recent experience\nC_LIO_LINeural activity-dependent gene regulation might cause neurovascular reorganization\nC_LIO_LIGenes that are regulated by experience are commonly dysregulated in brain disorders\nC_LI

neuroscience