Neuronal avalanches organize as nested theta- and beta/gamma-oscillations during development of cortical layer 2/3

During early stages of cerebral cortical development, progenitor cells in the ventricular zone are multipotent, producing neurons of many layers over successive cell divisions. The laminar fate of their progeny depends on environmental cues to which the cells respond prior to mitosis. By the end of neurogenesis, however, progenitors are lineally committed to producing upper-layer neurons. Here we assess the laminar fate potential of progenitors at a middle stage of cortical development. The progenitors of layer 4 neurons were first transplanted into older brains in which layer 2/3 was being generated. The transplanted neurons adopted a laminar fate appropriate for the new environment (layer 2/3), revealing that layer 4 progenitors are multipotent. Mid-stage progenitors were then transplanted into a younger environment, in which layer 6 neurons were being generated. The transplanted neurons bypassed layer 6, revealing that layer 4 progenitors have a restricted fate potential and are incompetent to respond to environmental cues that trigger layer 6 production. Instead, the transplanted cells migrated to layer 4, the position typical of their origin, and also to layer 5, a position appropriate for neither the host nor the donor environment. Because layer 5 neurogenesis is complete by the stage that progenitors were removed for transplantation, restrictions in laminar fate potential must lag behind the final production of a cortical layer. These results suggest that a combination of intrinsic and environmental cues controls the competence of cortical progenitor cells to produce neurons of different layers.

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Simulation of electromyographic recordings following transcranial magnetic stimulation

Journal of Neurophysiology ◽

10.1152/jn.00626.2017 ◽

2018 ◽

Vol 120 (5) ◽

pp. 2532-2541 ◽

Cited By ~ 5

Author(s):

Bahar Moezzi ◽

Natalie Schaworonkow ◽

Lukas Plogmacher ◽

Mitchell R. Goldsworthy ◽

Brenton Hordacre ◽

...

Keyword(s):

Experimental Data ◽

Transcranial Magnetic Stimulation ◽

Magnetic Stimulation ◽

Motor Evoked Potential ◽

Silent Period ◽

Cortical Layer ◽

Detailed Model ◽

Emg Signal ◽

Feed Forward Network ◽

Layer 2

Transcranial magnetic stimulation (TMS) is a technique that enables noninvasive manipulation of neural activity and holds promise in both clinical and basic research settings. The effect of TMS on the motor cortex is often measured by electromyography (EMG) recordings from a small hand muscle. However, the details of how TMS generates responses measured with EMG are not completely understood. We aim to develop a biophysically detailed computational model to study the potential mechanisms underlying the generation of EMG signals following TMS. Our model comprises a feed-forward network of cortical layer 2/3 cells, which drive morphologically detailed layer 5 corticomotoneuronal cells, which in turn project to a pool of motoneurons. EMG signals are modeled as the sum of motor unit action potentials. EMG recordings from the first dorsal interosseous muscle were performed in four subjects and compared with simulated EMG signals. Our model successfully reproduces several characteristics of the experimental data. The simulated EMG signals match experimental EMG recordings in shape and size, and change with stimulus intensity and contraction level as in experimental recordings. They exhibit cortical silent periods that are close to the biological values and reveal an interesting dependence on inhibitory synaptic transmission properties. Our model predicts several characteristics of the firing patterns of neurons along the entire pathway from cortical layer 2/3 cells down to spinal motoneurons and should be considered as a viable tool for explaining and analyzing EMG signals following TMS. NEW & NOTEWORTHY A biophysically detailed model of EMG signal generation following transcranial magnetic stimulation (TMS) is proposed. Simulated EMG signals match experimental EMG recordings in shape and amplitude. Motor-evoked potential and cortical silent period properties match experimental data. The model is a viable tool to analyze, explain, and predict EMG signals following TMS.

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Comparison of the Upper Marginal Neurons of Cortical Layer 2 with Layer 2/3 Pyramidal Neurons in Mouse Temporal Cortex

Frontiers in Neuroanatomy ◽

10.3389/fnana.2017.00115 ◽

2017 ◽

Vol 11 ◽

Cited By ~ 9

Author(s):

Huan Luo ◽

Kayoko Hasegawa ◽

Mingsheng Liu ◽

Wen-Jie Song

Keyword(s):

Pyramidal Neurons ◽

Temporal Cortex ◽

Cortical Layer ◽

Layer 2

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Cortical layer-specific modulation of neuronal activity after sensory deprivation due to spinal cord injury

10.1101/2020.12.28.424612 ◽

2020 ◽

Author(s):

Marta Zaforas ◽

Juliana M Rosa ◽

Elena Alonso-Calviño ◽

Elena Fernández-López ◽

Claudia Miguel-Quesada ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Neuronal Activity ◽

Large Scale ◽

Sensory Deprivation ◽

Sensory Stimulation ◽

Gamma Oscillations ◽

Cortical Layer ◽

Cord Injury

SummaryCortical areas have the capacity of large-scale reorganization following sensory deprivation. However, it remains unclear whether this is a unique process that homogenously affects the entire deprived region or it is suitable to changes depending on local circuitries across layers. By using in vivo electrophysiology to record neuronal activity simultaneously across cortical depth, we showed that sensory deprivation due to spinal cord injury induces layer-specific changes in both spontaneous and evoked-activity. While supragranular layers specifically increased gamma oscillations and the ability to initiate up-states during spontaneous activity, infragranular layers displayed increased, faster and delayed evoked-responses to sensory stimulation. Therefore, sensory deprivation immediately modifies local circuitries allowing supragranular layers to better integrate spontaneous corticocortical information to maintain column excitability, and infragranular layers to better integrate evoked-sensory inputs to preserve subcortical outputs. These layer-specific changes may guide long-term alterations in excitability and plasticity associated to network rearrangements and the appearance of sensory pathologies associated with spinal cord injury.

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The influence of cortical depth on neuronal responses in mouse visual cortex

10.1101/241661 ◽

2018 ◽

Cited By ~ 1

Author(s):

Philip O’Herron ◽

John Woodward ◽

Prakash Kara

Keyword(s):

Visual Cortex ◽

Neuronal Response ◽

Superficial Layer ◽

Cortical Layer ◽

Contrast Imaging ◽

Response Properties ◽

Layer 2 ◽

Layer 4 ◽

Thalamic Projections ◽

Mouse Visual Cortex

AbstractWith the advent of two-photon imaging as a tool for systems neuroscience, the mouse has become a preeminent model system for studying sensory processing. One notable difference that has been found however, between mice and traditional model species like cats and primates is the responsiveness of the cortex. In the primary visual cortex of cats and primates, nearly all neurons respond to simple visual stimuli like drifting gratings. In contrast, imaging studies in mice consistently find that only around half of the neurons respond to such stimuli. Here we show that visual responsiveness is strongly dependent on the cortical depth of neurons. Moving from superficial layer 2 down to layer 4, the percentage of responsive neurons increases dramatically, ultimately reaching levels similar to what is seen in other species. Over this span of cortical depth, neuronal response amplitude also increases and orientation selectivity moderately decreases. These depth dependent response properties may be explained by the distribution of thalamic inputs in mouse V1. Unlike in cats and primates where thalamic projections to the granular layer are constrained to layer 4, in mice they spread up into layer 2/3, qualitatively matching the distribution of response properties we see. These results show that the analysis of neural response properties must take into consideration not only the overall cortical lamina boundaries but also the depth of recorded neurons within each cortical layer. Furthermore, the inability to drive the majority of neurons in superficial layer 2/3 of mouse V1 with grating stimuli indicates that there may be fundamental differences in the role of V1 between rodents and other mammals.

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Abstract 14: Synaptic Remodeling after Stroke Enhanced by Transplanted Human Neural Stem Cells is Coincident with Functional Recovery

Stroke ◽

10.1161/str.45.suppl_1.14 ◽

2014 ◽

Vol 45 (suppl_1) ◽

Author(s):

Takeshi Hiu ◽

Tonya Bliss ◽

Nathan Manley ◽

Eric Wang ◽

Yasuhiro Nishiyama ◽

...

Keyword(s):

Stem Cells ◽

Stem Cell ◽

Cell Therapy ◽

Stem Cell Therapy ◽

Functional Recovery ◽

Cortical Layer ◽

Synaptic Remodeling ◽

Array Tomography ◽

Layer 2 ◽

Glutamate Synapses

Background: Stem cell transplantation (Tx) has emerged as a promising new experimental treatment for stroke; understanding its mechanism of action will facilitate the translation of stem cell therapy to the clinic. The ultimate change in brain plasticity is manifested at the synaptic level, however, the synaptic remodeling after stem cell therapy remains unknown. Here we evaluate the effect of transplanted human neural progenitor cells (hNPCs) on the peri-infarct synaptic remodeling in the post-ischemic brain. Materials and Methods: We use array tomography, a high-resolution proteomic imaging method, to determine how hNPCs affect the number and subtype of glutamate and GABA synapses after stroke. Vehicle or hNPCs were transplanted into the ischemic cortex of Nude rats 7 days after distal middle cerebral artery occlusion. Neurological recovery was assessed weekly using a battery of behavioral tests. The arrays of serial ultrathin sections (70 nm), removed from the peri-infarct cortex at 1 and 4 weeks post-Tx, were stained using multiple synaptic markers and imaged in cortical layer 2/3 and 5. Computational analysis of the resultant staining pattern was used to identify and quantify subtypes of glutamate and GABA synapses. Results: Tx of hNPCs significantly improved behavioral recovery after stroke compared to vehicle-treated rats (4 weeks post-transplantation; p<0.01) without altering the infarct size. hNPC-treated rats had a higher density of VGluT1-containing glutamate synapses (0.223 vs 0.185 synapses/μm3, p<0.05), and GluA2-containing glutamate synapses (0.091 vs 0.069 synapses/μm3, p<0.05) in layer 5 at 4 weeks post-Tx, compared to vehicle-treated rats. However, hNPCs had did not alter total number of glutamate synapses. This synaptic increase was cortical layer-specific observed in layer 5 but not .in layer 2/3. hNPCs had no detectable effect on the density of GABA synapses in either layer 5 or 2/3 at 1 week or 4 weeks post-Tx. Conclusions: These results provide novel new information about the organization of synaptic circuitry and its plasticity after stem cell therapy. These data suggest that stem cells alter the subunit composition of glutamate synapses after stroke and this is coincident with stem cell-induced functional recovery.

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Ipsi- and contralateral corticocortical projection-dependent subcircuits in layer 2 of the rat frontal cortex

Journal of Neurophysiology ◽

10.1152/jn.00333.2019 ◽

2019 ◽

Vol 122 (4) ◽

pp. 1461-1472 ◽

Cited By ~ 1

Author(s):

Yoshifumi Ueta ◽

Jaerin Sohn ◽

Fransiscus Adrian Agahari ◽

Sanghun Im ◽

Yasuharu Hirai ◽

...

Keyword(s):

Motor Cortex ◽

Frontal Cortex ◽

Pyramidal Cell ◽

Pyramidal Tract ◽

Pyramidal Cells ◽

Cortical Layer ◽

Electrophysiological Properties ◽

Monosynaptic Connection ◽

Layer 2 ◽

Rat Frontal Cortex

In the neocortex, both layer 2/3 and layer 5 contain corticocortical pyramidal cells projecting to other cortices. We previously found that among L5 pyramidal cells of the secondary motor cortex (M2), not only intratelencephalic projection cells but also pyramidal tract cells innervate ipsilateral cortices and that the two subtypes are different in corticocortical projection diversity and axonal laminar distributions. Layer 2/3 houses intratelencephalically projecting pyramidal cells that also innervate multiple ipsilateral and contralateral cortices. However, it remained unclear whether layer 2/3 pyramidal cells can be divided into projection subtypes each with distinct innervation to specific targets. In the present study we show that layer 2 pyramidal cells are organized into subcircuits on the basis of corticocortical projection targets. Layer 2 corticocortical cells of the same projection subtype were monosynaptically connected. Between the contralaterally and ipsilaterally projecting corticocortical cells, the monosynaptic connection was more common from the former to the latter. We also found that ipsilaterally and contralaterally projecting corticocortical cell subtypes differed in their morphological and physiological characteristics. Our results suggest that layer 2 transfers separate outputs from M2 to individual cortices and that its subcircuits are hierarchically organized to form the discrete corticocortical outputs. NEW & NOTEWORTHY Pyramidal cell subtypes and their dependent subcircuits are well characterized in cortical layer 5, but much less is understood for layer 2/3. We demonstrate that in layer 2 of the rat secondary motor cortex, ipsilaterally and contralaterally projecting corticocortical cells are largely segregated. These layer 2 cell subtypes differ in dendrite morphological and intrinsic electrophysiological properties, and form subtype-dependent connections. Our results suggest that layer 2 pyramidal cells form distinct subcircuits to provide discrete corticocortical outputs.

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