Rat Somatosensory Cortex Research Articles

Chronic Hyperhomocysteinemia Impairs CSD Propagation and Induces Cortical Damage in a Rat Model of Migraine with Aura

Hyperhomocysteinemia (hHCY) is a metabolic disorder characterized by elevated levels of homocysteine in plasma. hHCY correlates with a high risk of migraine headaches, especially migraine with aura. Cortical spreading depression (CSD) is a wave of depolarization passing through neurons and glial cells of the cortex and is considered an electrophysiological correlate of migraine aura. The aim of the present study was to analyze neuronal activity and CSD in the somatosensory cortex of rats in vivo with prenatal hHCY and to assess cortex viability after 2 h of CSD generation. Female rats were fed a diet high in methionine, and their offspring with high homocysteine levels in plasma were further used in experiments. Recurrent CSD was evoked by local KCl application on the dura surface. Neuronal viability was assessed by measuring the activity of lactate dehydrogenase (LDH) in the brain and 2,3,5-triphenyltetrazolium chloride staining of the somatosensory cortex after two hours of CSD generation. Animals with hHCY exhibited higher neuronal activity, and more CSDs were generated in response to KCl, indicating higher cortical excitability. Propagation of recurrent CSD was impaired in supragranular cortical layers, and the recovery of multiple unit activity and evoked sensory potentials after CSD was delayed in the hHCY group. Finally, in animals with prenatal hHCY, an ischemic focus was identified as a consequence of multiple CSDs, along with elevated levels of LDH activity in brain tissues, suggestive of diminished neuronal viability. These findings imply that prolonged elevated levels of homocysteine may not only predispose to migraine with aura but also potentially elevate the risk of migrainous infarction.

Brain–computer interface for simultaneous dual‐region spatial coding in hippocampal and somatosensory cortex of freely behaving rats

AbstractDecoding of spatial information from place cells is currently limited to individual brain regions, severely constraining the understanding of the brain's spatial navigation mechanisms. In this study, synchronized detection of dual‐brain region spatial encoding was conducted using brain–computer interface (BCI). Therefore, an implantable microelectrode array (MEA) was developed tailored for the simultaneous detection of neuronal activities in the CA1 of the hippocampus and the Barrel Cortex (BC) of the somatosensory cortex in rats as BCI. The MEA was improved by modifying the nanocomposite PtNP/PEDOT:PSS to improve their electrical properties (reducing impedance from 1.82 ± 0.17 MΩ to 3.4 ± 0.3 kΩ), facilitating neural recordings in freely behaving rats. The neural activities were obtained from the CA1 and the BC simultaneously and validated the existence of place cells in both brain regions. This study highlighted the potential of PtNP/PEDOT:PSS‐modified MEA as BCI in concurrently detecting neural activity associated with spatial encoding in two brain regions, offering novel perspectives on the processing of tactile stimuli and the formation of cognitive maps for navigation.

High Spatiotemporal Resolution Radial Encoding Single-Vessel fMRI.

High-field preclinical functional MRI (fMRI) is enabled the high spatial resolution mapping of vessel-specific hemodynamic responses, that is single-vessel fMRI. In contrast to investigating the neuronal sources of the fMRI signal, single-vessel fMRI focuses on elucidating its vascular origin, which can be readily implemented to identify vascular changes relevant to vascular dementia or cognitive impairment. However, the limited spatial and temporal resolution of fMRI is hindered hemodynamic mapping of intracortical microvessels. Here, the radial encoding MRI scheme is implemented to measure BOLD signals of individual vessels penetrating the rat somatosensory cortex. Radial encoding MRI is employed to map cortical activation with a focal field of view (FOV), allowing vessel-specific functional mapping with 50×50 µm2 in-plane resolution at a 1 to 2 Hz sampling rate. Besides detecting refined hemodynamic responses of intracortical micro-venules, the radial encoding-based single-vessel fMRI enables the distinction of fMRI signals from vessel and peri-vessel voxels due to the different contribution of intravascular and extravascular effects.

Automatic detection of foot-strike onsets in a rhythmic forelimb movement

Rhythmic movement is the fundamental motion dynamics characterized by repetitive patterns. Precisely defining onsets in rhythmic movement is essential for a comprehensive analysis of motor functions. Our study introduces an automated method for detecting rat's forelimb foot-strike onsets using deep learning tools. This method demonstrates high accuracy of onset detection by combining two techniques using joint coordinates and behavioral confidence scale. The analysis extends to neural oscillatory responses in the rat's somatosensory cortex, validating the effectiveness of our combined approach. Our technique streamlines experimentation, demanding only a camera and GPU-accelerated computer. This approach is applicable across various contexts and promotes our understanding of brain functions during rhythmic movements.

THE INFLUENCE OF MESENCHYMAL STROMAL CELLS OF DIFFERENT GENESIS ON ENERGY METABOLISM IN THE RAT SOMATOSENSORY CORTEX DURING ISCHEMIA-REPERFUSION

Introduction. About 60-80% of cerebral circulation disorders are due to ischemia, that leads to high mortality, disability in working age and economic burden on society in developed countries of the world. Objective: To investigate the effect of ischemia-reperfusion on parameters of carbohydrate and energy exchanges in the rat somatosensory cortex and to determine the cerebroprotective action of mesenchymal stromal cells (MSCs) of various genesis, MSC lysate and the reference drug Citicoline. Methods. The study was performed on 200 male Wistar rats, divided into 9 groups. Group 1 included intact animals; group 2 – sham-operated rats; group 3 – control pathology (rats were subjected to ischemia-reperfusion by occlusion of the internal carotid arteries and injected with a 0.9% saline solution (2 ml/kg) into the femoral vein); group 4 – immediately after ischemia-reperfusion rats were transplanted with 106 MSC cells/animal derived from Wharton’s jelly of the human umbilical cord; group 5 – 106 cells/animal of rat embryonic fibroblasts; group 6 – 106 cells/animal derived from human adipose MSCs; group 7 – 106 cells/animal derived from rat adipose MSCs; group 8 – 0.2 ml/animal of lysate derived from Wharton’s jelly MSCs; group 9 – the reference drug Citicoline (250 mg/kg). Parameters of carbohydrate and energy metabolism in rat somatosensory cortex under the conditions of cerebral IR and on the background of correction studied on the 7th and 14th day. Results. It was found that after cerebral ischemia-reperfusion in the rat somatosensory cortex in research periods an increase in the levels of glucose, lactate, lactate/pyruvate ratio and a decrease in the content of pyruvate and succinate dehydrogenase were revealed. In the groups of experimental animals with intravenous transplantation of MSCs of various origins, MSC lysate and Citicoline, the perturbation in glucose metabolism was reduced, lactate content was decreased and the levels of pyruvate and succinate dehydrogenase were significantly increased (p<0.05), compared to rats with control pathology. A more pronounced positive effect in the recovery of disturbed energy processes and elimination of metabolic acidosis was observed with the use of human Wharton’s jelly-derived MSCs. Conclusions. The study demonstrated that experimental 20-minute model ischemia-reperfusion in rats caused a violation of the carbohydrate and energy balance in the somatosensory cortex. Human umbilical cord blood-derived MSCs contributed to the recovery of disturbed energy processes in the somatosensory cortex and eliminated metabolic acidosis at the level of Citicoline or better than it, which is one of the links of the mechanism of the cerebral protective action of MSCs. Embryonic rat fibroblasts were slightly inferior in efficiency to Citicoline and human umbilical cord Wharton’s jelly MSCs, which indicates a higher cerebroprotective activity of xenotransplantation.

A universal workflow for creation, validation, and generalization of detailed neuronal models

Detailed single-neuron modeling is widely used to study neuronal functions. While cellular and functional diversity across the mammalian cortex is vast, most of the available computational tools focus on a limited set of specific features characteristic of a single neuron. Here, we present a generalized automated workflow for the creation of robust electrical models and illustrate its performance by building cell models for the rat somatosensory cortex. Each model is based on a 3D morphological reconstruction and a set of ionic mechanisms. We use an evolutionary algorithm to optimize neuronal parameters to match the electrophysiological features extracted from experimental data. Then we validate the optimized models against additional stimuli and assess their generalizability on a population of similar morphologies. Compared to the state-of-the-art canonical models, our models show 5-fold improved generalizability. This versatile approach can be used to build robust models of any neuronal type.

Comparative Study of Terminal Cortical Potentials Using Iridium and Ag/AgCl Electrodes.

Brain ischemia induces slow voltage shifts in the cerebral cortex, including waves of spreading depolarization (SD) and negative ultraslow potentials (NUPs), which are considered as brain injury markers. However, different electrode materials and locations yield variable SD and NUP features. Here, we compared terminal cortical events during isoflurane or sevoflurane euthanasia using intracortical linear iridium electrode arrays and Ag/AgCl-based electrodes in the rat somatosensory cortex. Inhalation of anesthetics caused respiratory arrest, associated with hyperpolarization and followed by SD and NUP on both Ir and Ag electrodes. Ag-NUPs were bell shaped and waned within half an hour after death. Ir-NUPs were biphasic, with the early fast phase corresponding to Ag-NUP, and the late absent on Ag electrodes, phase of a progressive depolarizing voltage shift reaching -100 mV by two hours after death. In addition, late Ir-NUPs were more ample in the deep layers than at the cortical surface. Thus, intracortical Ag and Ir electrodes reliably assess early manifestations of terminal brain injury including hyperpolarization, SD and the early phase of NUP, while the late, giant amplitude phase of NUP, which is present only on Ir electrodes, is probably related to the sensitivity of Ir electrodes to a yet unidentified factor related to brain death.

The effect of mesenchymal stromal cells of different origin on morphological parameters in the somatosensory cortex of rats with acute cerebral ischemia

Ischemic stroke is the second leading cause of death and the leading cause of disability worldwide. So far, promising experimental data have been obtained regarding the elimination of neurological dysfunction and the reduction of the area of ischemic damage when using mesenchymal stromal cells (MSCs). Purpose: to characterize the influence of MSCs of different origin, MSC lysate of human Wharton cells and citicoline on the dynamics of destructive changes in the somatosensory cortex of rats with acute cerebrovascular accident according to light microscopy and micromorphometry data. Materials and methods. An experiment was performed using 190 -4-month-old male Wistar rats weighing 160-190 g, which were subjected to transient bilateral 20-minute ischemia-reperfusion (IR) of the internal carotid arteries. After modeling the pathology, the animals were injected into the femoral vein with obtained from human umbilical cord Wharton’s jelly-derived MSCs, human and rat adipose tissue-derived MSCs at a dose of 106 cells/animal. Other groups of experimental animals were intravenously injected with fetal rat fibroblasts at a dose of 106 cells/animal in 0.2 ml of physiological solution and lysate of human umbilical cord Wharton’s jelly-derived MSCs at a dose of 0.2 ml/animal. Control animals were injected IV with 0.2 ml of physiological solution. The last group of rats received a single dose of the reference drug citicoline at a dose of 250 mg/kg. The studies were conducted on the 7th and 14th day. In the somatosensory cortex, the total number of neuron nuclei per 1 mm2 was counted, and the ratio of the number of intact neuron nuclei and nuclei with pathological changes (karyorrhexis and karyopyknosis) was also determined. Results: The transplantation of stem cells, lysate of human umbilical cord Wharton’s jelly-derived MSCs, or citicoline contributed to an increase in the number of neurons with nuclei in the somatosensory cortex, as well as an increase in the number of nuclei that did not undergo pathological changes. The transplantation of human umbilical cord Wharton’s jelly-derived MSCs had the most positive effect. The number of neuron nuclei in 1 mm2 that did not undergo pathological changes in the somatosensory cortex in this group of animals approached the number of nuclei in the group of pseudo-operated animals, while the number of nuclei that did not undergo pathological changes significantly exceeded the number of nuclei with signs of destruction. Conclusion: A significant increase in the number of neurons without signs of pathological changes was observed in all experimental groups of rats during the simulation of ischemic brain damage after the introduction of various types of studied mesenchymal stromal cells, lysate or citicoline. The most positive result in the somatosensory cortex was achieved after the introduction of human umbilical cord Wharton’s jelly-derived MSCs.

Activation of inflammasomes and their effects on neuroinflammation at the microelectrode-tissue interface in intracortical implants

Invasive neuroprosthetics rely on microelectrodes (MEs) to record or stimulate the activity of large neuron assemblies. However, MEs are subjected to tissue reactivity in the central nervous system (CNS) due to the foreign body response (FBR) that contribute to chronic neuroinflammation and ultimately result in ME failure. An endogenous, acute set of mechanisms responsible for the recognition and targeting of foreign objects, called the innate immune response, immediately follows the ME implant-induced trauma. Inflammasomes are multiprotein structures that play a critical role in the initiation of an innate immune response following CNS injuries. The activation of inflammasomes facilitates a range of innate immune response cascades and results in neuroinflammation and programmed cell death. Despite our current understanding of inflammasomes, their roles in the context of neural device implantation remain unknown. In this study, we implanted a non-functional Utah electrode array (UEA) into the rat somatosensory cortex and studied the inflammasome signaling and the corresponding downstream effects on inflammatory cytokine expression and the inflammasome-mediated cell death mechanism of pyroptosis. Our results not only demonstrate the continuous activation of inflammasomes and their contribution to neuroinflammation at the electrode-tissue interface but also reveal the therapeutic potential of targeting inflammasomes to attenuate the FBR in invasive neuroprosthetics.

Anoxic spreading depolarization in the neonatal rat cortex in vitro.

Anoxic spreading depolarization (aSD) is a hallmark of ischemic injury in the cerebral cortex. In adults, aSD is associated with rapid and nearly complete neuronal depolarization and loss of neuronal functions. While ischemia also evokes aSD in the immature cortex, developmental aspects of neuronal behavior during aSD remain largely unknown. Here, using oxygen-glucose deprivation (OGD) ischemia model in slices of the postnatal rat somatosensory cortex, we found that immature neurons displayed much more complex behaviors: they initially moderately depolarized during aSD, then transiently repolarised (for up to tens of minutes), and only then passed to terminal depolarization. The ability to fire action potentials was maintained in neurons mildly depolarized during aSD without reaching the level of depolarization block, and these functions were regained in the majority of immature neurons during post-aSD transient repolarization. The amplitude of depolarization and the probability of depolarization block during aSD increased, whereas transient post-SD repolarization levels and duration, and associated recovery in neuronal firing decreased with age. By the end of the first postnatal month, aSD acquired an adult-like phenotype, where depolarization during aSD merged with terminal depolarization and the phase of transient recovery was lost. Thus, changes in neuronal function during aSD undergo remarkable developmental changes that may contribute to lower susceptibility of the immature neurons to ischemia.

Spherical harmonics representation of the steady-state membrane potential shift induced by tDCS in realistic neuron models

Objective. We provide a systematic framework for quantifying the effect of externally applied weak electric fields on realistic neuron compartment models as captured by physiologically relevant quantities such as the membrane potential or transmembrane current as a function of the orientation of the field. Approach. We define a response function as the steady-state change of the membrane potential induced by a canonical external field of 1 V m−1 as a function of its orientation. We estimate the function values through simulations employing reconstructions of the rat somatosensory cortex from the Blue Brain Project. The response of different cell types is simulated using the NEURON simulation environment. We represent and analyze the angular response as an expansion in spherical harmonics. Main results. We report membrane perturbation values comparable to those in the literature, extend them to different cell types, and provide their profiles as spherical harmonic coefficients. We show that at rest, responses are dominated by their dipole terms (), in agreement with experimental findings and compartment theory. Indeed, we show analytically that for a passive cell, only the dipole term is nonzero. However, while minor, other terms are relevant for states different from resting. In particular, we show how and terms can modify the function to induce asymmetries in the response. Significance. This work provides a practical framework for the representation of the effects of weak electric fields on different neuron types and their main regions—an important milestone for developing micro- and mesoscale models and optimizing brain stimulation solutions.

Mapping of morpho-electric features to molecular identity of cortical inhibitory neurons.

Knowledge of the cell-type-specific composition of the brain is useful in order to understand the role of each cell type as part of the network. Here, we estimated the composition of the whole cortex in terms of well characterized morphological and electrophysiological inhibitory neuron types (me-types). We derived probabilistic me-type densities from an existing atlas of molecularly defined cell-type densities in the mouse cortex. We used a well-established me-type classification from rat somatosensory cortex to populate the cortex. These me-types were well characterized morphologically and electrophysiologically but they lacked molecular marker identity labels. To extrapolate this missing information, we employed an additional dataset from the Allen Institute for Brain Science containing molecular identity as well as morphological and electrophysiological data for mouse cortical neurons. We first built a latent space based on a number of comparable morphological and electrical features common to both data sources. We then identified 19 morpho-electrical clusters that merged neurons from both datasets while being molecularly homogeneous. The resulting clusters best mirror the molecular identity classification solely using available morpho-electrical features. Finally, we stochastically assigned a molecular identity to a me-type neuron based on the latent space cluster it was assigned to. The resulting mapping was used to derive inhibitory me-types densities in the cortex.

Tickle contagion in the rat somatosensory cortex.

The cellular mechanisms of emotional contagion are unknown. We investigated tickle contagion and the underlying neuronal representations in playful rats. We recorded trunk somatosensory cortex activity of observer rats while they received tickling and audiovisual playback of tickling footage and while they witnessed tickling of demonstrator rats. Observers vocalized and showed "Freudensprünge" ("joy jumps") during witnessing live tickling, while they showed little behavioral responses to playbacks. Deep layers in the trunk somatosensory neurons showed a larger correlation between direct and witnessed tickling responses compared to superficial layers. Trunk somatosensory neurons discharged upon emission of own and demonstrator's vocalizations and might drive contagious "laughter". We conclude that trunk somatosensory cortex might represent ticklishness contagion.

Subthreshold repetitive transcranial magnetic stimulation suppresses ketamine-induced poly population spikes in rat sensorimotor cortex.

Cortical oscillations within or across brain regions play fundamental roles in sensory, motor, and memory functions. It can be altered by neuromodulations such as repetitive transcranial magnetic stimulation (rTMS) and pharmacological manipulations such as ketamine. However, the neurobiological basis of the effects of rTMS and ketamine, as well as their interactions, on cortical oscillations is not understood. In this study, we developed and applied a rodent model that enabled simultaneous rTMS treatment, pharmacological manipulations, and invasive electrophysiological recordings, which is difficult in humans. Specifically, a miniaturized C-shaped coil was designed and fabricated to deliver focal subthreshold rTMS above the primary somatosensory (S1) and motor (M1) cortex in rats. Multi-electrode arrays (MEA) were implanted to record local field potentials (LFPs) and single unit activities. A novel form of synchronized activities, poly population spikes (PPS), was discovered as the biomarker of ketamine in LFPs. Brief subthreshold rTMS effectively and reversibly suppressed PPS while increasing the firing rates of single unit activities. These results suggest that ketamine and rTMS have convergent but opposing effects on cortical oscillations and circuits. This highly robust phenomenon has important implications to understanding the neurobiological mechanisms of rTMS and ketamine as well as developing new therapeutic strategies involving both neuromodulation and pharmacological agents.

Transcranial ultrasound neuromodulation induces neuronal correlation change in the rat somatosensory cortex

Objective. Transcranial focused ultrasound (tFUS) is a neuromodulation technique which has been the focus of increasing interest for noninvasive brain stimulation with high spatial specificity. Its ability to excite and inhibit neural circuits as well as to modulate perception and behavior has been demonstrated, however, we currently lack understanding of how tFUS modulates the ways neurons interact with each other. This understanding would help elucidate tFUS’s mechanism of systemic neuromodulation and allow future development of therapies for treating neurological disorders. Approach. In this study, we investigate how tFUS modulates neural interaction and response to peripheral electrical limb stimulation through intracranial multi-electrode recordings in the rat somatosensory cortex. We deliver ultrasound in a pulsed pattern to induce frequency dependent plasticity in a manner similar to what is found following electrical stimulation. Main Results. We show that neural firing in response to peripheral electrical stimulation is increased after ultrasound stimulation at all frequencies, showing tFUS induced changes in excitability of individual neurons in vivo. We demonstrate tFUS sonication repetition frequency dependent pairwise correlation changes between neurons, with both increases and decreases observed at different frequencies. Significance. These results extend previous research showing tFUS to be capable of inducing synaptic depression and demonstrate its ability to modulate network dynamics as a whole.

In vivo low-intensity magnetic pulses durably alter neocortical neuron excitability and spontaneous activity.

Magnetic brain stimulation is a promising treatment for neurological and psychiatric disorders. However, a better understanding of its effects at the individual neuron level is essential to improve its clinical application. We combined focal low-intensity repetitive transcranial magnetic stimulation (LI-rTMS) to the rat somatosensory cortex with intracellular recordings of subjacent pyramidal neurons in vivo. Continuous 10Hz LI-rTMS reliably evoked firing at ∼4-5Hz during the stimulation period and induced durable attenuation of synaptic activity and spontaneous firing in cortical neurons, through membrane hyperpolarization and a reduced intrinsic excitability. However, inducing firing in individual neurons by repeated intracellular current injection did not reproduce the effects of LI-rTMS on neuronal properties. These data provide a novel understanding of mechanisms underlying magnetic brain stimulation showing that, in addition to inducing biochemical plasticity, even weak magnetic fields can activate neurons and enduringly modulate their excitability. KEY POINTS: Repetitive transcranial magnetic stimulation (rTMS) is a promising technique to alleviate neurological and psychiatric disorders caused by alterations in cortical activity. Our knowledge of the cellular mechanisms underlying rTMS-based therapies remains limited. We combined in vivo focal application of low-intensity rTMS (LI-rTMS) to the rat somatosensory cortex with intracellular recordings of subjacent pyramidal neurons to characterize the effects of weak magnetic fields at single cell level. Ten minutes of LI-rTMS delivered at 10Hz reliably evoked action potentials in cortical neurons during the stimulation period, and induced durable attenuation of their intrinsic excitability, synaptic activity and spontaneous firing. These results help us better understand the mechanisms of weak magnetic stimulation and should allow optimizing the effectiveness of stimulation protocols for clinical use.

Histological and electrophysiological evidence on the safe operation of a sharp-tip multimodal optrode during infrared neuromodulation of the rat cortex

Infrared neuromodulation is an emerging technology in neuroscience that exploits the inherent thermal sensitivity of neurons to excite or inhibit cellular activity. Since there is limited information on the physiological response of intracortical cell population in vivo including evidence on cell damage, we aimed to create and to validate the safe operation of a microscale sharp-tip implantable optrode that can be used to suppress the activity of neuronal population with low optical power continuous wave irradiation. Effective thermal cross-section and electric properties of the multimodal microdevice was characterized in bench-top tests. The evoked multi-unit activity was monitored in the rat somatosensory cortex, and using NeuN immunocytochemistry method, quantitative analysis of neuronal density changes due to the stimulation trials was evaluated. The sharp tip implant was effectively used to suppress the firing rate of neuronal populations. Histological staining showed that neither the probe insertion nor the heating protocols alone lead to significant changes in cell density in the close vicinity of the implant with respect to the intact control region. Our study shows that intracortical stimulation with continuous-wave infrared light at 1550 nm using a sharp tip implantable optical microdevice is a safe approach to modulate the firing rate of neurons.

Layer-specific distribution and expression pattern of AMPA- and NMDA-type glutamate receptors in the barrel field of the adult rat somatosensory cortex: a quantitative electron microscopic analysis.

AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and NMDA (N-methyl-d-aspartate) glutamate receptors are driving forces for synaptic transmission and plasticity at neocortical synapses. However, their distribution pattern in the adult rat neocortex is largely unknown and was quantified using freeze fracture replication combined with postimmunogold-labeling. Both receptors were co-localized at layer (L)4 and L5 postsynaptic densities (PSDs). At L4 dendritic shaft and spine PSDs, the number of gold grains detecting AMPA was similar, whereas at L5 shaft PSDs AMPA-receptors outnumbered those on spine PSDs. Their number was significantly higher at L5 vs. L4 PSDs. At L4 and L5 dendritic shaft PSDs, the number of gold grains detecting GluN1 was ~2-fold higher than at spine PSDs. The number of gold grains detecting the GluN1-subunit was higher for both shaft and spine PSDs in L5 vs. L4. Both receptors showed a large variability in L4 and L5. A high correlation between the number of gold grains and PSD size for both receptors and targets was observed. Both receptors were distributed over the entire PSD but showed a layer- and target-specific distribution pattern. The layer- and target-specific distribution of AMPA and GluN1 glutamate receptors partially contribute to the observed functional differences in synaptic transmission and plasticity in the neocortex.

Classification of Whisker Deflections From Evoked Responses in the Somatosensory Barrel Cortex With Spiking Neural Networks.

Spike-based neuromorphic hardware has great potential for low-energy brain-machine interfaces, leading to a novel paradigm for neuroprosthetics where spiking neurons in silicon read out and control activity of brain circuits. Neuromorphic processors can receive rich information about brain activity from both spikes and local field potentials (LFPs) recorded by implanted neural probes. However, it was unclear whether spiking neural networks (SNNs) implemented on such devices can effectively process that information. Here, we demonstrate that SNNs can be trained to classify whisker deflections of different amplitudes from evoked responses in a single barrel of the rat somatosensory cortex. We show that the classification performance is comparable or even superior to state-of-the-art machine learning approaches. We find that SNNs are rather insensitive to recorded signal type: both multi-unit spiking activity and LFPs yield similar results, where LFPs from cortical layers III and IV seem better suited than those of deep layers. In addition, no hand-crafted features need to be extracted from the data—multi-unit activity can directly be fed into these networks and a simple event-encoding of LFPs is sufficient for good performance. Furthermore, we find that the performance of SNNs is insensitive to the network state—their performance is similar during UP and DOWN states.

GACSON software for automated segmentation and morphology analyses of myelinated axons in 3D electron microscopy

Background and ObjectiveAdvances in electron microscopy (EM) now allow three-dimensional (3D) imaging of hundreds of micrometers of tissue with nanometer-scale resolution, providing new opportunities to study the ultrastructure of the brain. In this work, we introduce a freely available Matlab-based gACSON software for visualization, segmentation, assessment, and morphology analysis of myelinated axons in 3D-EM volumes of brain tissue samples. MethodsThe software is equipped with a graphical user interface (GUI). It automatically segments the intra-axonal space of myelinated axons and their corresponding myelin sheaths and allows manual segmentation, proofreading, and interactive correction of the segmented components. gACSON analyzes the morphology of myelinated axons, such as axonal diameter, axonal eccentricity, myelin thickness, or g-ratio. ResultsWe illustrate the use of the software by segmenting and analyzing myelinated axons in six 3D-EM volumes of rat somatosensory cortex after sham surgery or traumatic brain injury (TBI). Our results suggest that the equivalent diameter of myelinated axons in somatosensory cortex was decreased in TBI animals five months after the injury. ConclusionOur results indicate that gACSON is a valuable tool for visualization, segmentation, assessment, and morphology analysis of myelinated axons in 3D-EM volumes. It is freely available at https://github.com/AndreaBehan/g-ACSON under the MIT license.