Localization of auditory cortex neuronal sources using optically pumped magnetometer (OPM) sensor array.
Abstract not provided.
Borna, Amir↗
SEARCH · Engineering Papers
Results for “neuron”
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Biocompatible Graphene Transistors as Artificial Synapses, Neurons, and Dendrites.
Abstract not provided.
Liu, Sam↗
Dynamics of TDP-43 mislocalization and aggregation in motor neuron cytoplasm by Lattice Light Sheet Microscopy
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Biological and medical sciences↗
Developmental regulation of N-methyl-D-aspartate- and kainate-type glutamate receptor expression in the rat spinal cord
Spinal motor neurons undergo experience-dependent development during a critical period in early postnatal life. It has been suggested that the repertoire of glutamate receptor subunits differs between young and mature motor neurons and contributes to this activity-dependent development. In the present study we examined the expression patterns of N-methyl-D-aspartate- and kainate-type glutamate receptor subunits during the postnatal maturation of the spinal cord. Young motor neurons express much higher levels of the N-methyl-D-aspartate receptor subunit NR1 than do adult motor neurons. Although there are eight potential splice variants of NR1, only a subgroup is expressed by motor neurons. With respect to NR2 receptor subunits, young motor neurons express NR2A and C, while adult motor neurons express only NR2A. Young motor neurons express kainate receptor subunits GluR5, 6 and KA2 but we are unable to detect these or any other kainate receptor subunits in the adult spinal cord. Other spinal cord regions display a distinct pattern of developmental regulation of N-methyl-D-aspartate and kainate receptor subunit expression in comparison to motor neurons. Our findings indicate a precise spatio-temporal regulation of individual subunit expression in the developing spinal cord. Specific combinations of subunits in developing neurons influence their excitable properties and could participate in the emergence of adult neuronal form and function.
NASA Discipline Cell Biology↗
Astrocytes in the mouse visual cortex reliably respond to visual stimulation
Highlights: • We performed dual-color in vivo two-photon Ca{sup 2+} imaging of neurons and astrocytes. • α1-adrenoblocker prazosin substantially reduced global astrocytic activities. • Astrocytes showed weak but reliable visual responses in the awake mouse visual cortex. • Astrocytic visual responses were delayed by 5 s relative to the neuronal ones. Astrocytes are known to contact with a great number of synapses and may integrate sensory inputs. In the ferret primary visual cortex, astrocytes respond to a visual stimulus with a delay of several seconds with respect to the surrounding neurons. However, in the mouse visual cortex, it remains unclear whether astrocytes respond to visual stimulations. In this study, using dual-color simultaneous in vivo two-photon calcium imaging of neurons and astrocytes in the awake mouse visual cortex, we examined the visual response of astrocytes and their precise response timing relative to the surrounding neurons. Neurons reliably responded to visual stimulations, whereas astrocytes often showed neuromodulator-mediated global activities, which largely masked small visual responses. Administration of the selective α1-adrenergic receptor antagonist prazosin substantially reduced such global astrocytic activities without affecting the neuronal visual responses. In the presence of prazosin, astrocytes showed weak but consistent visual responses mostly at their somata. Cross-correlation analysis estimated that the astrocytic visual responses were delayed by approximately 5 seconds relative to the surrounding neuronal responses. In conclusion, our research demonstrated that astrocytes in the primary visual cortex of awake mice responded to visual stimuli with a delay of several seconds relative to the surrounding neurons, which may indicate the existence of a common mechanism of neuron–astrocyte communication across species.
60 APPLIED LIFE SCIENCES↗
Maximized lateral inhibition in paired magnetic domain wall racetracks for neuromorphic computing
Lateral inhibition is an important functionality in neuromorphic computing, modeled after the biological neuron behavior that a firing neuron deactivates its neighbors belonging to the same layer and prevents them from firing. In most neuromorphic hardware platforms lateral inhibition is implemented by external circuitry, thereby decreasing the energy efficiency and increasing the area overhead of such systems. Recently, the domain wall—magnetic tunnel junction (DW-MTJ) artificial neuron is demonstrated in modeling to be intrinsically inhibitory. Without peripheral circuitry, lateral inhibition in DW-MTJ neurons results from magnetostatic interaction between neighboring neuron cells. However, the lateral inhibition mechanism in DW-MTJ neurons has not been studied thoroughly, leading to weak inhibition only in very closely-spaced devices. This work approaches these problems by modeling current- and field- driven DW motion in a pair of adjacent DW-MTJ neurons. We maximize the magnitude of lateral inhibition by tuning the magnetic interaction between the neurons. The results are explained by current-driven DW velocity characteristics in response to an external magnetic field and quantified by an analytical model. Dependence of lateral inhibition strength on device parameters is also studied. Finally, lateral inhibition behavior in an array of 1000 DW-MTJ neurons is demonstrated. Our results provide a guideline for the optimization of lateral inhibition implementation in DW-MTJ neurons. Finally, with strong lateral inhibition achieved, a path towards competitive learning algorithms such as the winner-take-all are made possible on such neuromorphic devices.
77 NANOSCIENCE AND NANOTECHNOLOGY↗
Incomplete segregation of endorgan-specific vestibular ganglion cells in mice and rats
The endorgan-specific distribution of vestibular ganglion cells was studied in neonatal and postnatal rats and mice using indocarbocyanine dye (DiI) and dextran amines for retrograde and anterograde labeling. Retrograde DiI tracing from the anterior vertical canal labeled neurons scattered throughout the whole superior vestibular ganglion, with denser labeling at the dorsal and central regions. Horizontal canal neurons were scattered along the dorsoventral axis with more clustering toward the dorsal and ventral poles of this axis. Utricular ganglion cells occupied predominantly the central region of the superior vestibular ganglion. This utricular population overlapped with both the anterior vertical and horizontal canals' ganglion cells. Posterior vertical canal neurons were clustered in the posterior part of the inferior vestibular ganglion. The saccular neurons were distributed in the two parts of the vestibular ganglion, the superior and inferior ganglia. Within the inferior ganglion, the saccular neurons were clustered in the anterior part. In the superior ganglion, the saccular neurons were widely scattered throughout the whole ganglion with more numerous neurons at the posterior half. Small and large neurons were labeled from all endorgans. Examination of the fiber trajectory within the superior division of the vestibular nerve showed no clear lamination of the fibers innervating the different endorgans. These results demonstrate an overlapping pattern between the different populations within the superior ganglion, while in the inferior ganglion, the posterior canal and saccular neurons show tighter clustering but incomplete segregation. This distribution implies that the ganglion cells are assigned for their target during development in a stochastic rather than topographical fashion.
NASA Discipline Developmental Biology↗
Effect of ghrelin on the motor deficit caused by the ablation of nigrostriatal dopaminergic cells or the inhibition of striatal dopamine receptors
Highlights: • A functional ghrelin receptor GHSR1a is dominantly found in DA neurons in the SNc. • GHSR1a is also located on GABAergic neurons in the SNr. • Activation of GHSRs on SNc-DA neurons improves motor deficits. • GHSRs located on non-DA cells are not associated with motor function. Ghrelin plays roles in a wide range of central functions by activating the growth hormone secretagogue receptor (GHSR). This receptor has recently been found in the substantia nigra (SN) to control dopamine (DA)-related physiological functions. The dysregulation of DA neurons in the SN pars compacta (SNc) and the consequent depletion of striatal DA are known to underlie the motor deficits observed in Parkinson's disease (PD). In the present study, we further investigated the role of the SN-ghrelin system in motor function under the stereotaxic injection of AAV-CMV-FLEX-diphtheria toxin A (DTA) into the SN of dopamine transporter (DAT)-Cre (DAT{sup SN}::DTA) mice to expunge DA neurons of the SNc. First, we confirmed the dominant expression of GHSR1a, which is a functional GHSR, in tyrosine hydroxylase (TH)-positive DA neurons in the SNc of control mice. In DAT{sup SN}::DTA mice, we clearly observed motor dysfunction using several behavioral tests. An immunohistochemical study revealed a dramatic loss of TH-positive DA neurons in the SNc and DAT-labeled axon terminals in the striatum, and an absence of mRNAs for TH and DAT in the SN of DAT{sup SN}::DTA mice. The mRNA level of GHSR1a was drastically decreased in the SN of these mice. In normal mice, we also found the mRNA expression of GHSR1a within GABAergic neurons in the SN pars reticulata (SNr). Under these conditions, a single injection of ghrelin into the SN failed to improve the motor deficits caused by ablation of the nigrostriatal DA network using DAT{sup SN}::DTA mice, whereas intra-SN injection of ghrelin suppressed the motor dysfunction caused by the administration of haloperidol, which is associated with the transient inhibition of DA transmission. These findings suggest that phasic activation of the SNc-ghrelin system could improve the dysregulation of nigrostriatal DA transmission related to the initial stage of PD, but not the motor deficits under the depletion of nigrostriatal DA. Although GHSRs are found in non-DA cells of the SNr, GHSRs on DA neurons in the SNc may play a crucial role in motor function.
60 APPLIED LIFE SCIENCES↗
Neurofilament protein defines regional patterns of cortical organization in the macaque monkey visual system: a quantitative immunohistochemical analysis
Visual function in monkeys is subserved at the cortical level by a large number of areas defined by their specific physiological properties and connectivity patterns. For most of these cortical fields, a precise index of their degree of anatomical specialization has not yet been defined, although many regional patterns have been described using Nissl or myelin stains. In the present study, an attempt has been made to elucidate the regional characteristics, and to varying degrees boundaries, of several visual cortical areas in the macaque monkey using an antibody to neurofilament protein (SMI32). This antibody labels a subset of pyramidal neurons with highly specific regional and laminar distribution patterns in the cerebral cortex. Based on the staining patterns and regional quantitative analysis, as many as 28 cortical fields were reliably identified. Each field had a homogeneous distribution of labeled neurons, except area V1, where increases in layer IVB cell and in Meynert cell counts paralleled the increase in the degree of eccentricity in the visual field representation. Within the occipitotemporal pathway, areas V3 and V4 and fields in the inferior temporal cortex were characterized by a distinct population of neurofilament-rich neurons in layers II-IIIa, whereas areas located in the parietal cortex and part of the occipitoparietal pathway had a consistent population of large labeled neurons in layer Va. The mediotemporal areas MT and MST displayed a distinct population of densely labeled neurons in layer VI. Quantitative analysis of the laminar distribution of the labeled neurons demonstrated that the visual cortical areas could be grouped in four hierarchical levels based on the ratio of neuron counts between infragranular and supragranular layers, with the first (areas V1, V2, V3, and V3A) and third (temporal and parietal regions) levels characterized by low ratios and the second (areas MT, MST, and V4) and fourth (frontal regions) levels characterized by high to very high ratios. Such density trends may correspond to differential representation of corticocortically (and corticosubcortically) projecting neurons at several functional steps in the integration of the visual stimuli. In this context, it is possible that neurofilament protein is crucial for the unique capacity of certain subsets of neurons to perform the highly precise mapping functions of the monkey visual system.
Non-NASA Center↗
Protective effect of vitreous against hemoglobin neurotoxicity
Highlights: • Bovine vitreous protected cultured neurons from the oxidative toxicity of hemoglobin. • Complete neuroprotection was provided by a 3% vitreous solution. • Ascorbate accounted for most protection in diluted vitreous. • Transferrin and selenium content may contribute in undiluted vitreous. • Vitreous may protect adjacent neurons from hemorrhagic injury. Hemorrhage into the brain parenchyma or subarachnoid space is associated with edema and vascular injury that is likely mediated at least in part by the toxicity of hemoglobin. In contrast, extravascular blood appears to be less neurotoxic when localized to the retina or adjacent vitreous, the gel filling the posterior segment of the eye. In this study, the hypothesis that vitreous protects neurons from hemoglobin toxicity was investigated in a primary cortical cell culture model. Consistent with prior observations, hemoglobin exposure for 24 h resulted in death of most neurons without injury to co-cultured glia. Neuronal loss was reduced in a concentration-dependent fashion by bovine vitreous, with complete protection produced by 3% vitreous solutions. This effect was associated with a reduction in malondialdehyde but an increase in cell iron. At low vitreous concentrations, its ascorbate content was sufficient to account for most neuroprotection, as equivalent concentrations of ascorbate alone had a similar effect. However, other vitreous antioxidants provided significant protection when applied at concentrations present in undiluted vitreous, and prevented all neuronal loss when combined in the absence of ascorbate. These results indicate that vitreous is an antioxidant cocktail that robustly protects neurons from hemoglobin toxicity, and may contribute to the relative resistance of retinal neurons to hemorrhagic injury.
60 APPLIED LIFE SCIENCES↗
Berberine regulates neurite outgrowth through AMPK-dependent pathways by lowering energy status
As a widely used anti-bacterial agent and a metabolic inhibitor as well as AMP-activated protein kinase (AMPK) activator, berberine (BBR) has been shown to cross the blood–brain barrier. Its efficacy has been investigated in various disease models of the central nervous system. Neurite outgrowth is critical for nervous system development and is a highly energy-dependent process regulated by AMPK-related pathways. In the present study, we aimed to investigate the effects of BBR on AMPK activation and neurite outgrowth in neurons. The neurite outgrowth of primary rat cortical neurons at different stages of polarization was monitored after exposure of BBR. Intracellular energy level, AMPK activation and polarity-related pathways were also inspected. The results showed that BBR suppressed neurite outgrowth and affected cytoskeleton stability in the early stages of neuronal polarization, which was mediated by lowered energy status and AMPK activation. Liver kinase B1 and PI3K–Akt–GSK3β signaling pathways were also involved. In addition, mitochondrial dysfunction and endoplasmic reticulum stress contributed to the lowered energy status induced by BBR. This study highlighted the knowledge of the complex activities of BBR in neurons and corroborated the significance of energy status during the neuronal polarization. - Highlights: • BBR inhibited neurite outgrowth in early stages of neuronal development. • Lowered neuronal energy status was induced by BBR treatment. • Neuronal energy stress induced by BBR activated AMPK-related pathways. • BBR induced mitochondrial dysfunction and endoplasmic reticulum stress.
60 APPLIED LIFE SCIENCES↗
Comparative study of the effects of prenatal sevoflurane exposure at different cortical stages on forebrain development and maturation in offspring
Introduction Brain development involves several critical stages, such as proliferation, neuronal migration, axonal pathfinding, and connection formation. Sevoflurane, a γ -aminobutyric acid (GABA) receptor agonist, is widely used as an inhaled general anesthetic. However, its impact on brain development has raised increasing concerns, particularly regarding prenatal exposure. This study aims to investigate the effects of prenatal sevoflurane exposure (PSE) at different cortical stages, focusing on its impact on the migration of glutamatergic and GABAergic neurons and neuronal behavior in offspring. Methods PSE was administered at two critical prenatal stages: embryonic day (E) 12.5 and E18.5. Double in situ hybridization was used to identify the coexpression of GABA receptors in Pax6- and Mash1-positive cells in the forebrain. The radial migration of glutamatergic neurons and the tangential migration of GABAergic neurons were analyzed. Behavioral tests, including the open-field test, elevated plus-maze test, forced swim test, tail suspension test, sucrose preference test, and Morris water maze, were performed on offspring to assess anxiety-like behaviors, depression, and learning and memory impairments. Results PSE inhibits the radial migration of glutamatergic neurons and promotes the tangential migration of GABAergic neurons. Specifically, early exposure (E12.5) inhibited the expression of the Pax6–Tbr2–Tbr1 cascade and the radial migration of Tbr1 in the ventral prefrontal cortex (PFC), whereas late exposure (E18.5) inhibited this process on the dorsal side. In addition, offspring mice with PSE exhibited increased anxiety-like behaviors, rather than depression, as demonstrated by reduced time spent in the center of the open-field test and in the open arms of the elevated plus-maze test. No significant differences were observed in the forced swim test, tail suspension test, or sucrose preference test. Furthermore, learning and memory impairments were observed in the Morris water maze. Conclusion Our results indicate that PSE at E12.5 and E18.5 leads to abnormalities in the migration of glutamatergic and GABAergic neurons, affecting long-term anxiety-like behaviors and causing learning and memory impairments in offspring mice.
Wang, Tianyuan↗
Improved Autoassociative Neural Networks
Improved autoassociative neural networks, denoted nexi, have been proposed for use in controlling autonomous robots, including mobile exploratory robots of the biomorphic type. In comparison with conventional autoassociative neural networks, nexi would be more complex but more capable in that they could be trained to do more complex tasks. A nexus would use bit weights and simple arithmetic in a manner that would enable training and operation without a central processing unit, programs, weight registers, or large amounts of memory. Only a relatively small amount of memory (to hold the bit weights) and a simple logic application- specific integrated circuit would be needed. A description of autoassociative neural networks is prerequisite to a meaningful description of a nexus. An autoassociative network is a set of neurons that are completely connected in the sense that each neuron receives input from, and sends output to, all the other neurons. (In some instantiations, a neuron could also send output back to its own input terminal.) The state of a neuron is completely determined by the inner product of its inputs with weights associated with its input channel. Setting the weights sets the behavior of the network. The neurons of an autoassociative network are usually regarded as comprising a row or vector. Time is a quantized phenomenon for most autoassociative networks in the sense that time proceeds in discrete steps. At each time step, the row of neurons forms a pattern: some neurons are firing, some are not. Hence, the current state of an autoassociative network can be described with a single binary vector. As time goes by, the network changes the vector. Autoassociative networks move vectors over hyperspace landscapes of possibilities.
Hand, Charles↗
Nanoporous Gold as a Neural Interface Coating: Effects of Topography, Surface Chemistry, and Feature Size
We report that designing neural interfaces that maintain close physical coupling of neurons to an electrode surface remains a major challenge for both implantable and in vitro neural recording electrode arrays. Typically, low-impedance nanostructured electrode coatings rely on chemical cues from pharmaceuticals or surface-immobilized peptides to suppress glial scar tissue formation over the electrode surface (astrogliosis), which is an obstacle to reliable neuron–electrode coupling. Nanoporous gold (np-Au), produced by an alloy corrosion process, is a promising candidate to reduce astrogliosis solely through topography by taking advantage of its tunable length scale. In the present in vitro study on np-Au’s interaction with cortical neuron–glia co-cultures, we demonstrate that the nanostructure of np-Au achieves close physical coupling of neurons by maintaining a high neuron-to-astrocyte surface coverage ratio. Atomic layer deposition-based surface modification was employed to decouple the effect of morphology from surface chemistry. Additionally, length scale effects were systematically studied by controlling the characteristic feature size of np-Au through variations in the dealloying conditions. In conclusion, our results show that np-Au nanotopography, not surface chemistry, reduces astrocyte surface coverage while maintaining high neuronal coverage and may enhance neuron–electrode coupling through nanostructure-mediated suppression of scar tissue formation.
36 MATERIALS SCIENCE↗
Monitoring of glutamate‐induced excitotoxicity by mitochondrial oxygen consumption
Abstract Dysfunction of mitochondrial activity is often associated with the onset and progress of neurodegenerative diseases. Membrane depolarization induced by Na + influx increases intracellular Ca 2+ levels in neurons, which upregulates mitochondrial activity. However, overlimit of Na + influx and its prolonged retention ultimately cause excitotoxicity leading to neuronal cell death. To return the membrane potential to the normal level, Na + /K + ‐ATPase exchanges intracellular Na + with extracellular K + by consuming a large amount of ATP. This is a reason why mitochondria are important for maintaining neurons. In addition, astrocytes are thought to be important for supporting neighboring neurons by acting as energy providers and eliminators of excessive neurotransmitters. In this study, we examined the meaning of changes in the mitochondrial oxygen consumption rate (OCR) in primary mouse neuronal populations. By varying the medium constituents and using channel modulators, we found that pyruvate rather than lactate supported OCR levels and conferred on neurons resistance to glutamate‐mediated excitotoxicity. Under a pyruvate‐restricted condition, our OCR monitoring could detect excitotoxicity induced by glutamate at only 10 μM. The OCR monitoring also revealed the contribution of the N‐methyl‐D‐aspartate receptor and Na + /K + ‐ATPase to the toxicity, which allowed evaluating spontaneous excitation. In addition, the OCR monitoring showed that astrocytes preferentially used glutamate, not glutamine, for a substrate of the tricarboxylic acid cycle. This mechanism may be coupled with astrocyte‐dependent protection of neurons from glutamate‐mediated excitotoxicity. These results suggest that OCR monitoring would provide a new powerful tool to analyze the mechanisms underlying neurotoxicity and protection against it.
Kumagai, Ayako↗