Size Of Neurons Research Articles

Endoplasmic Reticulum Exit Sites scale with somato-dendritic size in neurons.

Nervous systems exhibit dramatic diversity in cell morphology and size. How neurons regulate their biosynthetic and secretory machinery to support such diversity is not well understood. Endoplasmic reticulum exit sites (ERESs) are essential for maintaining secretory flux, and are required for normal dendrite development, but how neurons of different size regulate secretory capacity remains unknown. In Caenorhabditis elegans, we find that the ERES number is strongly correlated with the size of a neuron's dendritic arbor. The elaborately branched sensory neuron, PVD, has especially high ERES numbers. Asymmetric cell division provides PVD with a large initial cell size critical for rapid establishment of PVD's high ERES number before neurite outgrowth, and these ERESs are maintained throughout development. Maintenance of ERES number requires the cell fate transcription factor MEC-3, C. elegans TOR (ceTOR/let-363), and nutrient availability, with mec-3 and ceTOR/let-363 mutant PVDs both displaying reductions in ERES number, soma size, and dendrite size. Notably, mec-3 mutant animals exhibit reduced expression of a ceTOR/let-363 reporter in PVD, and starvation reduces ERES number and somato-dendritic size in a manner genetically redundant with ceTOR/let-363 perturbation. Our data suggest that both asymmetric cell division and nutrient sensing pathways regulate secretory capacities to support elaborate dendritic arbors.

Role of MeCP2 in oligodendrocyte lineage cells in Rett syndrome: review and inference

Rett syndrome (RTT) is a neurodevelopmental disorder primarily caused by mutations in the MECP2 gene. Neuronal damage is the main factor contributing to RTT, and the loss of MeCP2 function can result in reduced neuronal somas size, decreased dendritic abundance, and impaired neuronal function. While specific restoration of MeCP2 expression in neurons has been reported to partially rescue the behavioral phenotype and prolong the lifespan of mice, it cannot provide a complete cure. Therefore, other cells may be involved in the development of RTT. Although imaging and autopsy findings have revealed decreased white matter volume and corpus callosum thickness in RTT patients, the mechanisms underlying the development of white matter abnormalities remain unclear. These abnormalities are predominantly caused by damage to mature oligodendrocytes. This review provides an overview of the proliferation, differentiation, and function of oligodendrocyte lineage cells and elucidates the role of MeCP2 in these cells.

Calcitonin Gene-Related Peptide mRNA Synthesis in Trigeminal Ganglion Neurons after Cortical Spreading Depolarization.

Migraine is a debilitating neurovascular disorder characterized by recurrent headache attacks of moderate to severe intensity. Calcitonin gene-related peptide (GGRP), which is abundantly expressed in trigeminal ganglion (TG) neurons, plays a crucial role in migraine pathogenesis. Cortical spreading depolarization (CSD), the biological correlate of migraine aura, activates the trigeminovascular system. In the present study, we investigated CGRP mRNA expression in TG neurons in a CSD-based mouse migraine model. Our in situ hybridization analysis showed that CGRP mRNA expression was observed in smaller-sized neuronal populations. CSD did not significantly change the density of CGRP mRNA-synthesizing neurons in the ipsilateral TG. However, the cell sizes of CGRP mRNA-synthesizing TG neurons were significantly larger in the 48 h and 72 h post-CSD groups than in the control group. The proportions of CGRP mRNA-synthesizing TG neurons bearing cell diameters less than 14 μm became significantly less at several time points after CSD. In contrast, we found significantly greater proportions of CGRP mRNA-synthesizing TG neurons bearing cell diameters of 14-18 μm at 24 h, 48, and 72 h post-CSD. We deduce that the CSD-induced upward cell size shift in CGRP mRNA-synthesizing TG neurons might be causative of greater disease activity and/or less responsiveness to CGRP-based therapy.

Dopamine-mediated striatal activity and function is enhanced in GlyRα2 knockout animals

The glycine receptor alpha 2 (GlyRα2) is a ligand-gated ion channel which upon activation induces a chloride conductance. Here, we investigated the role of GlyRα2 in dopamine-stimulated striatal cell activity and behavior. We show that depletion of GlyRα2 enhances dopamine-induced increases in the activity of putative dopamine D1 receptor-expressing striatal projection neurons, but does not alter midbrain dopamine neuron activity. We next show that the locomotor response to d-amphetamine is enhanced in GlyRα2 knockout animals, and that this increase correlates with c-fos expression in the dorsal striatum. 3-D modeling revealed an increase in the neuronal ensemble size in the striatum in response to D-amphetamine in GlyRα2 KO mice. Finally, we show enhanced appetitive conditioning in GlyRα2 KO animals that is likely due to increased motivation, but not changes in associative learning or hedonic response. Taken together, we show that GlyRα2 is an important regulator of dopamine-stimulated striatal activity and function.

Noise and spike-time-dependent plasticity drive self-organized criticality in spiking neural network: Toward neuromorphic computing

Self-organized criticality (SoC) may optimize information transmission, encoding, and storage in the brain. Therefore, the underlying mechanism of the SoC provides significant insight for large-scale neuromorphic computing. We hypothesized that noise and stochastic spiking plays an essential role in SoC development in spiking neural networks (SNNs). We demonstrated that under appropriate noise levels and spike-time-dependent plasticity (STDP) parameters, an SNN evolves a SoC-like state characterized by a power-law distribution of neuronal avalanche size in a self-organized manner. Consistent with the physiological findings, the development of SNN was characterized by a transition from a subcritical state to a supercritical state and then to a critical state. Excitatory STDP with an asymmetric time window dominated the early phase of development; however, it destabilized the network and transitioned to the supercritical state. Synchronized bursts in the supercritical state enable inhibitory STDP with a symmetric time window, induce the development of inhibitory synapses, and stabilize the network toward the critical state. This sequence of transitions was observed when the appropriate noise level and STDP parameters were set to the initial conditions. Our results suggest that noise or stochastic spiking plays an essential role in SoC development and self-optimizes SNN for computation. Such neural mechanisms of noise harnessing would offer insight into the development of energy-efficient neuromorphic computing.

Machine learning-based segmentation of the rodent hippocampal CA2 area from Nissl-stained sections.

The hippocampus is a center of learning, memory, and spatial navigation. This region is divided into the CA1, CA2, and CA3 areas, which are anatomically different from each other. Among these divisions, the CA2 area is unique in terms of functional relevance to sociality. The CA2 area is often manually detected based on the size, shape, and density of neurons in the hippocampal pyramidal cell layer, but this manual segmentation relying on cytoarchitecture is impractical to apply to a large number of samples and dependent on experimenters' proficiency. Moreover, the CA2 area has been defined based on expression pattern of molecular marker proteins, but it generally takes days to complete immunostaining for such proteins. Thus, we asked whether the CA2 area can be systematically segmented based on cytoarchitecture alone. Since the expression pattern of regulator of G-protein signaling 14 (RGS14) signifies the CA2 area, we visualized the CA2 area in the mouse hippocampus by RGS14-immunostaining and Nissl-counterstaining and manually delineated the CA2 area. We then established "CAseg," a machine learning-based automated algorithm to segment the CA2 area with the F1-score of approximately 0.8 solely from Nissl-counterstained images that visualized cytoarchitecture. CAseg was extended to the segmentation of the prairie vole CA2 area, which raises the possibility that the use of this algorithm can be expanded to other species. Thus, CAseg will be beneficial for investigating unique properties of the hippocampal CA2 area.

Shades of gray in human white matter.

Anatomists have long expressed interest in neurons of the white matter, which is by definition supposed to be free of neurons. Hypotheses regarding their biochemical signature and physiological function are mainly derived from animal models. Here, we investigated 15 whole-brain human postmortem specimens, including cognitively normal cases and those with pathologic Alzheimer's disease (AD). Quantitative and qualitative methods were used to investigate differences in neuronal size and density, and the relationship between neuronal processes and vasculature. Double staining was used to evaluate colocalization of neurochemicals. Two topographically distinct populations of neurons emerged: one appearing to arise from developmental subplate neurons and the other embedded within deep, subcortical white matter. Both populations appeared to be neurochemically heterogeneous, showing positive reactivity to acetylcholinesterase (AChE) [but not choline acetyltransferase (ChAT)], neuronal nuclei (NeuN), nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), microtubule-associated protein 2 (MAP-2), somatostatin (SOM), nonphosphorylated neurofilament protein (SMI-32), and calcium-binding proteins calbindin-D28K (CB), calretinin (CRT), and parvalbumin (PV). PV was more richly expressed in superficial as opposed to deep white matter neurons (WMNs); subplate neurons were also significantly larger than their deeper counterparts. NADPH-d, a surrogate for nitric oxide synthase, allowed for the striking morphological visualization of subcortical WMNs. NADPH-d-positive subcortical neurons tended to embrace the outer walls of microvessels, suggesting a functional role in vasodilation. The presence of AChE positivity in these neurons, but not ChAT, suggests that they are cholinoceptive but noncholinergic. WMNs were also significantly smaller in AD compared to control cases. These observations provide a landscape for future systematic investigations.

Structural plasticity in the entorhinal and perirhinal cortices following hippocampal lesions in rhesus monkeys.

Immature neurons expressing the Bcl2 protein are present in various regions of the mammalian brain, including the amygdala and the entorhinal and perirhinal cortices. Their functional role is unknown but we have previously shown that neonatal and adult hippocampal lesions increase their differentiation in the monkey amygdala. Here, we assessed whether hippocampal lesions similarly affect immature neurons in the entorhinal and perirhinal cortices. Since Bcl2-positive cells were found mainly in areas Eo, Er, and Elr of the entorhinal cortex and in layer II of the perirhinal cortex, we also used Nissl-stained sections to determine the number and soma size of immature and mature neurons in layer III of area Er and layer II of area 36 of the perirhinal cortex. We found different structural changes in these regions following hippocampal lesions, which were influenced by the time of the lesion. In neonate-lesioned monkeys, the number of immature neurons in the entorhinal and perirhinal cortices was generally higher than in controls. The number of mature neurons was also higher in layer III of area Er of neonate-lesioned monkeys but no differences were found in layer II of area 36. In adult-lesioned monkeys, the number of immature neurons in the entorhinal cortex was lower than in controls but did not differ from controls in the perirhinal cortex. The number of mature neurons in layer III of area Er did not differ from controls, but the number of small, mature neurons in layer II of area 36 was lower than in controls. In sum, hippocampal lesions impacted populations of mature and immature neurons in discrete regions and layers of the entorhinal and perirhinal cortices, which are interconnected with the amygdala and provide major cortical inputs to the hippocampus. These structural changes may contribute to some functional recovery following hippocampal injury in an age-dependent manner.

Bayesian optimized multilayer perceptron neural network modelling of biochar and syngas production from pyrolysis of biomass-derived wastes

Biochar and syngas are important products of pyrolysis that can be employed for a wide range of applications such as catalysts for biodiesel production, wastewater treatment, and the production of oxygenated fuel. This study employs Bayesian optimized multilayer perceptron neural network for modelling the prediction of biochar and syngas from pyrolysis of biomass-derived wastes. Sixty neural networks were configured by considering the effect of hyperparameters such as the connecting layers of the network, the size of the network, and the type of neural network algorithms. The feature analysis using F-test algorithms revealed that temperature, biomass composition, N2 flow rates, residence time, and bed height influence the biochar and syngas yield obtained from the pyrolysis process. There is a significant interaction effect between the features as shown by the parametric analysis. The performance of the neural networks was significantly influenced by the number of connecting layers and the size of the hidden neurons. The five-layer neural network with an architecture of 3–2-10–10-1 displayed the best performance in predicting the biochar yield obtained from the pyrolysis process as indicated by R2 of 0.984, and RMSE of 0.34. While the five-layer neural network with an architecture of 3–7-10–3-1 displayed the best performance in predicting the syngas yield from the pyrolysis process as indicated by R2 of 0.999.

PB3C-CNN: An integrated PB3C and CNN based approach for plant leaf classification

Plant identification and classification are critical to understand, protect, and conserve biodiversity. Traditional plant classification requires years of intensive training and experience, making it difficult for others to classify plants. Plant leaf classification is a challenging issue as similar features appears in different species of plant. With the development of automated image-based classification, machine learning (ML) is becoming very popular. Deep learning (DL) methods have significantly improved plant image identification and classification. In the last decade, convolutional neural networks (CNN) have entirely dominated the field of computer vision, showing outstanding feature extraction capabilities and significant identification and classification performance. The capability of CNN lies in its network. The primary strategy to continue this trend in the literature relies on further scaling networks in size. However, costs increase rapidly, while performance improvements may be marginal when the number of net-works increases. Hence, there is a need to optimize the CNN network to get the best possible result with the minimum number of networks and other parameters such as the number of epochs, number of layers, batch size and number of neurons. The paper aims to evolve the optimal architecture of CNN using PB3C algorithm for plant leaf classification. For this, we use the nature-inspired computing technique parallel big bang–big crunch to evolve a CNN's optimal architecture automatically. Current study validated the proposed approach for plant leaf classification and compared it with 11 other machine learning-based approaches. From the results obtained it was found that the proposed approach was able to outperforms all 11 existing state-of-the-art techniques.

PLC regulates spontaneous glutamate release triggered by extracellular calcium and readily releasable pool size in neocortical neurons.

Dynamic physiological changes in brain extracellular calcium ([Ca2+]o) occur when high levels of neuronal activity lead to substantial Ca2+ entry via ion channels reducing local [Ca2+]o. Perturbations of the extracellular microenvironment that increase [Ca2+]o are commonly used to study how [Ca2+] regulates neuronal activity. At excitatory synapses, the Ca2+-sensing receptor (CaSR) and other G-protein coupled receptors link [Ca2+]o and spontaneous glutamate release. Phospholipase C (PLC) is activated by G-proteins and is hypothesized to mediate this process. Patch-clamping cultured neocortical neurons, we tested how spontaneous glutamate release was affected by [Ca2+]o and inhibition of PLC activity. We used hypertonic sucrose (HS) to evaluate the readily releasable pool (RRP) and test if it was affected by inhibition of PLC activity. Spontaneous glutamate release substantially increased with [Ca2+]o, and inhibition of PLC activity, with U73122, abolished this effect. PLC-β1 is an abundant isoform in the neocortex, however, [Ca2+]o-dependent spontaneous release was unchanged in PLC-β1 null mutants (PLC-β1-/-). U73122 completely suppressed this response in PLC-β1-/- neurons, indicating that this residual [Ca2+]o-sensitivity may be mediated by other PLC isoforms. The RRP size was substantially reduced after incubation in U73122, but not U73343. Phorbol esters increased RRP size after PLC inhibition. Together these data point to a strong role for PLC in mediating changes in spontaneous release elicited by [Ca2+]o and other extracellular cues, possibly by modifying the size of the RRP.

Effects of sodium oxybate on hypocretin/orexin and locus coeruleus neurons.

Long-term use of sodium oxybate (SXB), (also called gamma-hydroxybutyrate [GHB]) attenuates the cataplexy and sleepiness of human narcolepsy. We had previously found that chronic opiate usage in humans and long-term opiate administration to mice significantly increased the number of detected hypocretin/orexin (Hcrt) neurons, decreased their size, and increased Hcrt level in the hypothalamus. We also found that opiates significantly decreased cataplexy in human narcoleptics as well as in narcoleptic mice and that cessation of locus coeruleus neuronal activity preceded and was tightly linked to cataplectic attacks in narcoleptic dogs. We tested the hypothesis that SXB produces changes similar to opiates and now report that chronic SXB administration significantly increased the size of Hcrt neurons, the reverse of what we had seen with opiates in humans and mice. Levels of Hcrt in the hypothalamus were nonsignificantly lower, in contrast to the significant increase in hypothalamic Hcrt level after opiates. SXB decreased tyrosine hydroxylase levels in the locus coeruleus, the major descending projection of the hypocretin system, also the reverse of what we saw with opioids. Therefore despite some similar effects on narcoleptic symptomatology, SXB does not produce anatomical changes similar to those elicited by opiates. Analysis of changes in other links in the cataplexy pathway might further illuminate SXB's mechanism of action on narcolepsy.

Comparative analysis of structural modifications induced by monocular retinal inactivation and monocular deprivation in the developing cat lateral geniculate nucleus.

During a critical period of postnatal life, monocular deprivation (MD) by eyelid closure reduces the size of neurons in layers of the dorsal lateral geniculate nucleus (dLGN) connected to the deprived eye and shifts cortical ocular dominance in favor of the non-deprived eye. Temporary inactivation of the non-deprived eye can promote superior recovery from the effects of long-term MD compared to conventional occlusion therapy. In the current study, we assessed the modification of neuron size in the dLGN as a means of measuring the impact of a brief period of monocular inactivation (MI) imposed at different postnatal ages. The biggest impact of MI was observed when it occurred at the peak of the critical period. Unlike the effect of MD, structural plasticity following MI was observed in both the binocular and monocular segments of the dLGN. With increasing age, the capacity for inactivation to alter postsynaptic cell size diminished but was still significant beyond the critical period. In comparison to MD, inactivation produced effects that were about double in magnitude and exhibited efficacy at older ages. Notwithstanding the large neural alterations precipitated by MI, its effects were remediated with a short period of binocular experience, and vision through the previously inactivated eye fully recovered. These results demonstrate that MI is a potent means of modifying the visual pathway and does so at ages when occlusion is ineffective. The efficacy and longevity of inactivation to elicit plasticity highlight its potential to ameliorate disorders of the visual system such as amblyopia.

Activation of mTOR signaling in the paraventricular nucleus of the hypothalamus (PVN) contributes to stress- and BDNF-induced hypertensive responses

The paraventricular nucleus of the hypothalamus (PVN) integrates afferent inputs from limbic, medullary and hypothalamic regions to orchestrate cardiovascular stress responses via its medullary and spinal projections. Brain-derived neurotrophic factor (BDNF) is an important pro-hypertensive regulator in the PVN upregulated during stress that transforms the PVN neurocircuitry to facilitate responsiveness to hypertensive stimuli by shifting the balance of excitatory/inhibitory synaptic mechanisms. Mechanistic target of rapamycin (mTOR), as part of mTOR complex-1 (mTORC1), is stimulated by trophic factors, such as BDNF, in other brain regions to induce changes in neuronal morphology and increases in neuronal excitability. We tested the hypothesis that activation of mTORC1 in the PVN by BDNF and acute stress plays a key role in stimulating hypertensive responses. Male Sprague Dawley (SD) rats (n=4/group) received bilateral PVN injections of AAV2 viral vectors expressing myc-tagged BDNF (BDNFmyc), shRNA against TSC1 (a repressor of mTORC1) to stimulate mTORC1, shRNA against Raptor (a key component of the mTORC1) to inhibit mTORC1 or GFP for control. Blood pressure and heart rate were monitored by telemetry for 4 wks, and cardiovascular responses to restraint (60min) and water stress (15 minutes, 1-cm deep, 25°C water) were recorded 4-5 wks after vector injections. Vector injections were confirmed and neuronal morphology as well as pS6 levels (a marker of mTOR activity) were analyzed with immunofluorescence. Activation mTORC1 with TSC1 knock-down significantly increased resting blood pressure compared with control, but inhibition of mTORC1 with Raptor knock-down had no effect. BDNF overexpression significantly elevated blood pressure, as we have shown previously, and these increases were completely abolished by Raptor knock-down (daytime mean arterial pressure: shTSC1: 108.0±1.4*; BDNFmyc: 131.4±2.5*; shRaptor: 101.8±0.9; BDNF+shRaptor: 102.7±2.8#, GFP: 96.5±1.8 mmHg at week 4, *p<0.05 vs GFP; #p<0.05 vs. BDNFmyc). In addition, mTORC1 inhibition with Raptor knock-down also significantly diminished stress-induced hypertensive responses. Maximum blood pressure increase in shRaptor rats was 30.3±1.3 mmHg during restraint and 26.0±3.4 mmHg during water stress vs 43.8±2.2 and 37.4±2.5 mmHg in control rats (p<0.05). Immunofluorescence of pS6, an indicator of mTOR activity, and neuronal soma size were significantly elevated by both TSC1 knock-down and BDNF overexpression in the PVN, whereas Raptor knock-down reduced pS6 intensity and soma size and completely abolished the effects of BDNF. In summary, we demonstrated that mTOR activation in the PVN significantly increased blood pressure both during baseline conditions and during acute stress, and mediated hypertensive responses and neuronal morphological changes elicited by BDNF. Supported by R01 HL133211. R01 HL133211 (BE), R03 AG072016 (BE) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Sensitivity of Hypocretin System to Chronic Alcohol Exposure: A Human and Animal Study

Human heroin addicts and mice administered morphine for a 2 week period show a greatly increased number of hypothalamic hypocretin (Hcrt or orexin) producing neurons with a concomitant reduction in Hcrt cell size. Male rats addicted to cocaine similarly show an increased number of detectable Hcrt neurons. These findings led us to hypothesize that humans with alcohol use disorder (AUD) would show similar changes. We now report that humans with AUD have a decreased number and size of detectable Hcrt neurons. In addition, the intermingled melanin concentrating hormone (MCH) neurons are reduced in size. We saw no change in the size and number of tuberomammillary histamine neurons in AUD. Within the Hcrt/MCH neuronal field we found that microglia cell size was increased in AUD brains. In contrast, male rats with 2 week alcohol exposure, sufficient to elicit withdrawal symptoms, show no change in the number or size of Hcrt, MCH and histamine neurons, and no change in the size of microglia. The present study indicates major differences between the response of Hcrt neurons to opioids and that to alcohol in human subjects with a history of substance abuse.

Follicle-innervating Aδ-low threshold mechanoreceptive neurons form receptive fields through homotypic competition

The mammalian somatosensory system is comprised of multiple neuronal populations that form specialized, highly organized sensory endings in the skin. The organization of somatosensory endings is essential to their functions, yet the mechanisms which regulate this organization remain unclear. Using a combination of genetic and molecular labeling approaches, we examined the development of mouse hair follicle-innervating low-threshold mechanoreceptors (LTMRs) and explored competition for innervation targets as a mechanism involved in the patterning of their receptive fields. We show that follicle innervating neurons are present in the skin at birth and that LTMR receptive fields gradually add follicle-innervating endings during the first two postnatal weeks. Using a constitutive Bax knockout to increase the number of neurons in adult animals, we show that two LTMR subtypes have differential responses to an increase in neuronal population size: Aδ-LTMR neurons shrink their receptive fields to accommodate the increased number of neurons innervating the skin, while C-LTMR neurons do not. Our findings suggest that competition for hair follicles to innervate plays a role in the patterning and organization of follicle-innervating LTMR neurons.

Quantitative optical coherence microscopy of neuron morphology in human entorhinal cortex.

The size and shape of neurons are important features indicating aging and the pathology of neurodegenerative diseases. Despite the significant advances of optical microscopy, quantitative analysis of the neuronal features in the human brain remains largely incomplete. Traditional histology on thin slices bears tremendous distortions in three-dimensional reconstruction, the magnitude of which are often greater than the structure of interest. Recently development of tissue clearing techniques enable the whole brain to be analyzed in small animals; however, the application in the human remains challenging. In this study, we present a label-free quantitative optical coherence microscopy (OCM) technique to obtain the morphological parameters of neurons in human entorhinal cortex (EC). OCM uses the intrinsic back-scattering property of tissue to identify individual neurons in 3D. The area, length, width, and orientation of individual neurons are quantified and compared between layer II and III in EC. The high-resolution mapping of neuron size, shape, and orientation shows significant differences between layer II and III neurons in EC. The results are validated by standard Nissl staining of the same samples. The quantitative OCM technique in our study offers a new solution to analyze variety of neurons and their organizations in the human brain, which opens new insights in advancing our understanding of neurodegenerative diseases.

BigNeuron: a resource to benchmark and predict performance of algorithms for automated tracing of neurons in light microscopy datasets.

BigNeuron is an open community bench-testing platform with the goal of setting open standards for accurate and fast automatic neuron tracing. We gathered a diverse set of image volumes across several species that is representative of the data obtained in many neuroscience laboratories interested in neuron tracing. Here, we report generated gold standard manual annotations for a subset of the available imaging datasets and quantified tracing quality for 35 automatic tracing algorithms. The goal of generating such a hand-curated diverse dataset is to advance the development of tracing algorithms and enable generalizable benchmarking. Together with image quality features, we pooled the data in an interactive web application that enables users and developers to perform principal component analysis, t-distributed stochastic neighbor embedding, correlation and clustering, visualization of imaging and tracing data, and benchmarking of automatic tracing algorithms in user-defined data subsets. The image quality metrics explain most of the variance in the data, followed by neuromorphological features related to neuron size. We observed that diverse algorithms can provide complementary information to obtain accurate results and developed a method to iteratively combine methods and generate consensus reconstructions. The consensus trees obtained provide estimates of the neuron structure ground truth that typically outperform single algorithms in noisy datasets. However, specific algorithms may outperform the consensus tree strategy in specific imaging conditions. Finally, to aid users in predicting the most accurate automatic tracing results without manual annotations for comparison, we used support vector machine regression to predict reconstruction quality given an image volume and a set of automatic tracings.

Post-Morther Changes in Rat Paretial Cortic and Hippocampus Neurons. Morphological Characteristics

Target. Analysis of changes in the morphological characteristics of neurons in such phylogenetically different parts of the rat cerebral cortex in different periods after total cerebral ischemia. Methodology. Experiments were performed on 42 male outbred white rats with an initial weight of 240±20 g. Total cerebral ischemia in outbred white rats was modeled by decapitation. The material was taken at the 1st, 5th, 15th, 30th, and 60th minutes, as well as 5 and 24 hours after decapitation. Results. With total cerebral ischemia, a significant decrease in the size of neurons and deformation of the perikarya were observed. Normochromic neurons completely disappeared at the 60th minute. The number of hyperchromic neurons increased and then progressively decreased. Shriveled neurons accounted for the majority of cells in the studied areas of the cortex at 30-60 minutes, and then, after 5 and 24 hours, cells with pericellular edema predominated in the neuron population. Conclusion. The obtained data on histological changes in neurons of phylogenetically different parts of the cerebral cortex in the dynamics of total cerebral ischemia provide the basis for further detailed study of post-mortem changes in the brain, determining the time of death, creating a fundamental basis for studying the properties of neurons, including their transition from one functional state to other.

A 5.3 pJ/Spike CMOS Neural Array Employing Time-Modulated Axon-Sharing and Background Mismatch Calibration Techniques

Inspired by the human brain, spiking neuron networks are promising to realize energy-efficient and low-latency neuromorphic computing. However, even state-of-the-art silicon neurons are orders of magnitude worse than biological neurons in terms of area and power consumption due to the limitations. Moreover, limited routing in typical CMOS processes is another challenge for realizing the fully-parallel high-throughput synapse connections compared to biological synapses. This paper presents an SNN circuit that utilizes resource-sharing techniques to address the two challenges. Firstly, a comparator sharing neuron circuit with a background calibration technique is proposed to shrink the size of a single neuron without performance degradation. Secondly, a time-modulated axon-sharing synapse system is proposed to realize a fully-parallel connection with limited hardware overhead. To validate the proposed approaches, a CMOS neuron array is designed and fabricated under a 55-nm process. It consists of 48 LIF neurons with 3125 neurons/mm 2 area density, power consumption of 5.3 pJ/spike, and equivalent 2304 fully parallel synapses providing a unit throughput of 5500 events/s/neuron. It proves the proposed approaches are promising to realize a high-throughput high-efficiency SNN with CMOS technology.