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The hardware‐level construction of artificial synapses, mimicking the functionality of biological synapses, is widely acknowledged as a pivotal stride in artificial intelligence systems. Particularly, establishing all‐optical artificial synapses for neuromorphic computing, leveraging on‐chip optical interconnects instead of conventional wired connections, has garnered widespread attention. Here, high‐quality CsPbBr3 single crystals are synthesized, and intriguing relaxation processes associated with reversible photo‐induced phase transition (PIPT) are observed, leading to a corresponding change in the birefringence effect. The birefringence change is systematically analyzed by an optical system. The relaxation time of reversible PIPT is similar to the behavior patterns of biological synapses, enabling the device to mimic synaptic features. The device successfully mimics excitatory/inhibitory synaptic behaviors such as EPSP/IPSP, PPF, SDDP, SFDP, and SIDP by using 1310 nm signal. Furthermore, the device continues to exhibit excitatory/inhibitory synaptic functionality when 940 and 1550 nm signals are applied, achieving multi‐wavelength synaptic behaviors. The all‐optical devices have the advantages of low crosstalk, fast signaling, and wide optical bandwidth, which lays the foundation of all‐optical hardware for neuromorphic computing systems. [ABSTRACT FROM AUTHOR]

Time-delay-induced synchronous behaviors and synchronization transitions have been widely investigated for coupled neurons, and they play important roles for physiological functions. In the present study, time-delay-induced synchronized subthreshold oscillations were simulated, and the bifurcations underlying the synchronized behaviors were identified for a pair of coupled FitzHugh–Nagumo neurons. Multiple transitions between in-phase and anti-phase synchronizations induced by the time delay were simulated for the inhibitory and excitatory couplings. Subcritical or supercritical Hopf bifurcations and the stability of the Hopf-bifurcating periodic subthreshold oscillations were acquired using center manifold reduction and normal form theory. The in-phase or anti-phase synchronizations of the stable periodic subthreshold oscillations, which appear for multiple values of the time delay, were interpreted with the related eigenspace. The distributions of the different dynamical behaviors, including the synchronizations and bifurcations in the two-parameter plane of the time delay and coupling strength, were acquired for both types of synapses, and the different roles of the inhibitory and excitatory couplings on the synchronization transitions were compared. [ABSTRACT FROM AUTHOR]

To generate rhythmic motor behaviors, both single neurons and neural circuits require a balance between excitatory inputs that trigger action potentials and inhibitory inputs that promote a stable resting potential (E/I balance). Previous studies have focused on individual neurons and have shown that, over a short spatial scale, excitatory and inhibitory (E/I) synapses tend to form structured territories with inhibitory inputs enriched on cell bodies and proximal dendrites and excitatory inputs on distal dendrites. However, systems-level E/I patterns, at spatial scales larger than single neurons, are largely uncharted. We used immunostaining for PSD-95 and gephyrin postsynaptic scaffolding proteins as proxies for excitatory and inhibitory synapses, respectively, to quantify the numbers and map the distributions of E/I synapses in zebrafish spinal cord at both an embryonic stage and a larval stage. At the embryonic stage, we found that PSD-95 puncta outnumber gephyrin puncta, with the number of gephyrin puncta increasing to match that of PSD-95 puncta at the larval stage. At both stages, PSD-95 puncta are enriched in the most lateral neuropil corresponding to distal dendrites while gephyrin puncta are enriched on neuronal somata and in the medial neuropil. Significantly, similar to synaptic puncta, neuronal processes also exhibit medial-lateral territories at both developmental stages with enrichment of glutamatergic (excitatory) processes laterally and glycinergic (inhibitory) processes medially. This establishment of neuropil excitatory-inhibitory structure largely precedes dendritic arborization of primary motor neurons, suggesting that the structured neuropil could provide a framework for the development of E/I balance at the cellular level. J. Comp. Neurol. 525:1649-1667, 2017. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

The immune system plays important functional roles in regeneration after injury to the mammalian central and peripheral nervous systems. After damage to the peripheral nerve several types of immune cells, invade the nerve within hours after the injury. To gain insights into the contribution of T- and B-lymphocytes to recovery from injury we used the mouse femoral nerve injury paradigm. RAG2 −/− mice lacking mature T- and B-lymphocytes due to deletion of the recombination activating gene 2 were subjected to resection and surgical reconstruction of the femoral nerve, with the wild-type mice of the same inbred genetic background serving as controls. According to single frame motion analyses, RAG2 −/− mice showed better motor recovery in comparison to control mice at four and eight weeks after injury. Retrograde tracing of regrown/sprouted axons of spinal motoneurons showed increased numbers of correctly projecting motoneurons in the lumbar spinal cord of RAG2 −/− mice compared with controls. Whereas there was no difference in the motoneuron soma size between genotypes, RAG2 −/− mice displayed fewer cholinergic and inhibitory synaptic terminals around somata of spinal motoneurons both prior to and after injury, compared with wild-type mice. Extent of myelination of regrown axons in the motor branch of the femoral nerve measured as g-ratio was more extensive in RAG2 −/− than in control mice eight weeks after injury. We conclude that activated T- and B-lymphocytes restrict motor recovery after femoral nerve injury, associated with the increased survival of motoneurons and improved remyelination. [ABSTRACT FROM AUTHOR]

In previous work, we found that the protein messenger Jacob is involved in N-methyl- d-aspartate receptor (NMDAR) signaling to the nucleus and cAMP response element-binding protein (CREB) mediated gene expression in hippocampal primary neurons. Particularly, extrasynaptic NMDAR activation drives Jacob efficiently into the nucleus where it then induces gene expression that promotes neurodegeneration. However, the protein also translocates to the nucleus in CA1 neurons after Schaffer collateral long-term potentiation (LTP) but not long-term depression (LTD), suggesting that Jacob might be involved in hippocampal and LTP-dependent learning and memory processes. Not much is known about the cellular and subcellular distribution of the protein in brain. In this paper, we provide an overview of the expression of Jacob in rat brain with special emphasis on the hippocampus. We show that Jacob is abundant in hippocampal pyramidal neurons and interneurons but absent from astrocytes and microglia. Interestingly, we found that Jacob is also present in mossy fiber axons. Double immunofluorescence confocal laser scans with presynaptic markers demonstrate that Jacob is indeed found at excitatory but not inhibitory presynaptic sites. Accordingly, we found no substantial co-localization of Jacob with a postsynaptic marker of inhibitory synapses, gephyrin. In contrast, almost all postsynaptic density protein 95 (PSD-95) positive excitatory postsynaptic sites also exhibited strong Jacob-immunofluorescence. Taken together, these data support a synaptic and nuclear role of Jacob that implicates long-distance NMDAR signaling to the nucleus in excitatory neurons. [ABSTRACT FROM AUTHOR]

Abstract: An electron microscopic analysis has been carried out on the effects of age on the numerical density of both excitatory (asymmetric) and inhibitory (symmetric) synapses in the neuropil of layers 2/3 and of layer 5 in area 46 from the frontal cortex of behaviorally tested rhesus monkeys. There is no change in the lengths of synaptic junctions with age or in the percentage distribution of synapses relative to the postsynaptic spines and dendritic shafts. However, in layers 2/3 there is an overall loss of about 30% of synapses from 5 to 30 years of age, and both asymmetric and symmetric synapses are lost at the same rate. In layer 5 the situation is different; the overall loss of synapses is only 20% and this is almost entirely due to a loss of asymmetric synapses, since there is no significant loss of symmetric synapses from this layer with age. When the synapse data are correlated with the overall cognitive impairment shown by the monkeys, it is found that there is a strong correlation between the numerical density of asymmetric synapses in layers 2/3 and cognitive impairment, with a weaker correlation between symmetric synapse loss and cognitive impairment. In layer 5 on the other hand there is no correlation between synapse loss and cognitive impairment. However synapse loss is not the only factor causing cognitive impairment, since in previous studies of area 46 we have found that age-related alteration in myelin in this frontal area also significantly contributes to cognitive decline. The synapse loss is also considered in light of earlier studies, which show that the frequency of spontaneous excitatory synaptic responses is reduced with age in layers 2/3 neurons. [Copyright &y& Elsevier]

Propagation of brain rhythms among cortical regions is a relevant aspect of cognitive neuroscience, which is often investigated using functional connectivity (FC) estimation techniques. The aim of this work is to assess the relationship between rhythm propagation, FC and brain functioning using data generated from neural mass models of connected Regions of Interest (ROIs). We simulated networks of four interconnected ROIs, each with a different intrinsic rhythm (in θ, α, β and γ ranges). Connectivity was estimated using eight estimators and the relationship between structural connectivity and FC was assessed as a function of the connectivity strength and of the inputs to the ROIs. Results show that the Granger estimation provides the best accuracy, with a good capacity to evaluate the connectivity strength. However, the estimated values strongly depend on the input to the ROIs and hence on nonlinear phenomena. When a population works in the linear region, its capacity to transmit a rhythm increases drastically. Conversely, when it saturates, oscillatory activity becomes strongly affected by rhythms incoming from other regions. Changes in functional connectivity do not always reflect a physical change in the synapses. A unique connectivity network can propagate rhythms in very different ways depending on the specific working conditions. [ABSTRACT FROM AUTHOR]