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Sredniawa, W.

Publications and source records attributed to Sredniawa, W..

7 recordsLinked to original sources

Mapping Large-scale Spatiotemporal Dynamics of Synaptic Plasticity and LTP for Memory Encoding in the Hippocampal Network

Understanding memory formation requires elucidating the intricate dynamics of neuronal networks in the hippocampus, where information is encoded and processed through specific activity patterns and synaptic plasticity. Here, we introduce "EVOX," an advanced network electrophysiology platform equipped with high-density microelectrode arrays to capture critical network-level synaptic dynamics integral to learning and memory. This platform surpasses traditional methods by enabling label-free, high-order mapping of neural interactions, providing unprecedented insights into network Long-Term Potentiation (LTP) and evoked synaptic transmission within the hippocampal network. Utilizing EVOX, we demonstrate that high-frequency stimulation induces network-wide LTP, revealing enhanced synaptic efficacy in previously inactive cell assemblies in hippocampal layers. Our platform enables the real-time observation of network synaptic transmission, capturing the intricate patterns of connectivity and plasticity that underpin memory encoding. Advanced computational techniques further elucidate the mesoscale transmembrane generators and the dynamic processes that govern network-level memory encoding mechanisms. These findings uncover the complex dynamics that underlie learning and memory, showcasing EVOXs potential to explore synaptic and cellular phenomena in aging circuits. EVOX not only advances our understanding of hippocampal memory mechanisms but also serves as a powerful tool to investigate the broader scope of neural plasticity and network interactions in healthy and diseased states.

neuroscience↗

Local contribution to the somatosensory evoked potentials in rat's thalamus

Local Field Potential (LFP), despite its name, often reflects remote activity. Depending on the orientation and synchrony of their sources, both oscillations and more complex waves may passively spread in brain tissue over long distances and be falsely interpreted as local activity at such distant recording site. Current Source Density method was proposed to recover locally active currents from multi-site LFP recordings. Here we use a model-based kernel CSD (kCSD) to study the contribution of local and distant currents to LFP recorded with dense multichannel probes from rat thalamic nuclei and barrel cortex, activated by whisker stimulation. We show that the evoked potential wave seen in the thalamic nuclei around 7-15 ms post-stimulus has a substantial negative component reaching from cortex. This component can be analytically removed and truly local thalamic LFP, with purely thalamic contributions, can be recovered reliably using kCSD. In particular, concurrent recordings from the cortex are not essential for reliable thalamic CSD estimation. Proposed framework can be used to analyse LFP from other brain areas and has consequences for general LFP interpretation and analysis. 1 BRIEF SUMMARYWhile recording LFP simultaneously in multiple structures, we often see significant correlations between the observed waves. A natural question is if they are propagated passively from one structure to another or if they are simultaneously generated by different, separated sets of sources. We argue this can be answered reliably using CSD analysis. We focus on the case of thalamic and cortical recordings in the somatosensory system in response to whisker stimulation where we observe significant correlations between early thalamic and cortical responses to whisker deflection.

neuroscience↗

What we can and what we cannot see with extracellular multielectrodes

Extracellular recording is an accessible technique used in animals and humans to study the brain physiology and pathology. As the number of recording channels and their density grows it is natural to ask how much improvement the additional channels bring in and how we can optimally use the new capabilities for monitoring the brain. Here we show that for any given distribution of electrodes we can establish exactly what information about current sources in the brain can be recovered and what information is strictly unobservable. We demonstrate this in the general setting of previously proposed kernel Current Source Density method and illustrate it with simplified examples as well as using evoked potentials from the barrel cortex obtained with a Neuropixels probe and with compatible model data. Author SummaryEvery set of measurements is a window into reality rendering its incomplete or distorted picture. It is often difficult to relate the obtained representation of the world to underlying ground truth. Here we show, for brain electrophysiology, for arbitrary experimental setup (distribution of electrodes), and arbitrary analytical setup (function space of current source densities), that one can identify distributions of current sources which can be recovered precisely, and those which are invisible in the system. This shows what is and what is not observable in the studied system for a given setup, allows to improve the analysis results by modifying analytical setup, and facilitates interpretation of the measured sets of LFP, ECoG and EEG recordings.

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Nasal respiration is necessary for the emergence of ketamine-induced high frequency network oscillations and behavioral hyperactivity in freely moving rats.

Changes in oscillatory activity are widely reported after subanesthetic ketamine, however their mechanisms of generation are unclear. Here, we tested the hypothesis that nasal respiration underlies the emergence of high-frequency oscillations (130-180 Hz, HFO) and behavioral activation after ketamine in freely moving rats. We found ketamine 20 mg/kg provoked "fast" theta sniffing in rodents which correlated with increased locomotor activity and HFO power in the OB. Bursts of ketamine-dependent HFO were coupled to "fast" theta frequency sniffing. Theta coupling of HFO bursts were also found in the prefrontal cortex and ventral striatum which, although of smaller amplitude, were in phase with OB activity. Haloperidol 1 mg/kg pretreatment prevented ketamine-dependent increases in fast sniffing and instead HFO coupling to slower basal respiration. Consistent with ketamine-dependent HFO being driven by nasal respiration, unilateral naris blockade led to an ipsilateral reduction in ketamine-dependent HFO power compared to the control side. Bilateral nares blockade reduced ketamine-induced hyperactivity and HFO power and frequency. In conclusion, nasal entrainment of ketamine-dependent HFO across cortical and subcortical regions at theta frequencies represents a mechanism of orchestrated neural activity across distinct brain regions. The dense divergent connectivity of the olfactory system serves to broadcast this HFO to limbic areas.

neuroscience↗

Network and synaptic mechanisms underlying high frequency oscillations in the rat and cat olfactory bulb under ketamine-xylazine anesthesia.

High frequency oscillations (HFO) are receiving increased attention for their role in health and disease. Ketamine-dependent HFO have been identified in cortical and subcortical regions in rodents, however, the mechanisms underlying their generation and whether they occur in higher mammals is unclear. Here, we show under ketamine-xylazine anesthesia, classical gamma oscillations diminish and a prominent > 80 Hz oscillation emerges in the olfactory bulb of rats and cats. In cats negligible HFO was observed in the thamalus and visual cortex indicating the OB was a suitable site for further investigation. Simultaneous local field potential and thermocouple recordings demonstrated HFO was dependent on nasal airflow. Silicon probe mapping studies spanning almost the entire dorsal ventral aspect of the OB revealed this rhythm was strongest in ventral areas of the bulb and associated with microcurrent sources about the mitral layer. Pharmacological microinfusion studies revealed HFO was dependent on excitatory-inhibitory synaptic activity, but not gap junctions. Finally, we showed HFO was preserved despite surgical removal of the piriform cortex. We conclude that ketamine-dependent HFO in the OB are driven by nasal airflow and local dendrodendritic interactions. The relevance of our findings to ketamines model of psychosis in awake state are also discussed.

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Spreading depressions and periinfarct spreading depolarizations in the context of cortical plasticity

Studies of cortical function-recovery require a comparison between normal and post-stroke conditions that lead to changes in cortical metaplasticity. Focal cortical stroke impairs experience-dependent plasticity (ExDP) in the neighboring somatosensory cortex and usually evokes periinfarct depolarizations (PiDs) - a spreading depression-like waves. Experimentally induced spreading depressions (SDs) affect gene expression and some of these changes persist for at least 30 days. However, such changes are not stroke-specific: migraine patients had prolonged protein changes after a single SD episode during migraine aura. This study investigates whether non-stroke depolarizations impair cortical ExDP similarly to the stroke. ExDP was induced in rates with SDs or PiDs by a month of contralateral partial whiskers deprivation. Cortical activity was mapped by [14C]-2-deoxy-D-glucose (2DG) incorporation during stimulation of spared and contralateral homotopic whiskers. We found that whiskers deprivation after SDs resulted in normal cortical representation enlargement suggesting that SDs and PiDs depolarization have no influence on ExDP cortical map reorganization. PiDs and the MMP-9, -3, -2 or COX-2 proteins which are assumed to influence metaplasticity in rats after stroke were compared between the SDs induced by high osmolarity KCl solution and the PiDs following cortical photothrombotic stroke (PtS). We found that none of these factors directly caused cortical post-stroke metaplasticity changes. The only significant difference between stoke and induced SD was a greater imbalance in interhemispheric activity equilibrium after stroke. The interhemispheric interactions modified by stroke may therefore be a promising target for future studies of post-stroke ExDP and for convalescence studies. HighlightsO_LIPost-stroke metaplasticity changes in an injured hemisphere are not a consequence of spreading depolarizations C_LIO_LINone of the monitored proteins (MMP-2, -3, -9; COX-2) cause modifications in poststroke cortical plasticity C_LIO_LISpreading depressions have a prolonged, global influence on the functioning of both hemispheres and of the thalamus C_LIO_LIImpaired interhemispheric interactions may underlie the post-stroke metaplasticity changes in the injured hemisphere C_LI

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kCSD-python, a tool for reliable Current Source Density estimation

Interpretation of the extracellular recordings can be difficult due to the long range of electric field but can be facilitated by estimating the density of current sources (CSD). Here we introduce kCSD-python, an open Python package implementing Kernel Current Source Density (kCSD) method, and introduce several new techniques to facilitate CSD analysis of experimental data and interpretation of the results. We investigate the limitations imposed by noise and assumptions in the method itself. kCSD-python allows CSD estimation for arbitrary distribution of electrodes in 1D, 2D, and 3D, assuming distributions of sources in tissue, a slice, or in a single cell, and includes a range of diagnostic aids. We demonstrate its features in a Jupyter notebook tutorial to facilitate uptake by the community.

neuroscience↗