Supervised Learning in Spiking Neural Networks with Synaptic Delay Plasticity: An Overview

Throughout the central nervous system (CNS), the information communicated between neurons is mainly implemented by the action potentials (or spikes). Although the spike-timing based neuronal codes have significant computational advantages over rate encoding scheme, the exact spike timing-based learning mechanism in the brain remains an open question. To close this gap, many weight-based supervised learning algorithms have been proposed for spiking neural networks. However, it is insufficient to consider only synaptic weight plasticity, and biological evidence suggest that the synaptic delay plasticity also plays an important role in the learning progress in biological neural networks. Recently, many learning algorithms have been proposed to consider both the synaptic weight plasticity and synaptic delay plasticity. The goal of this paper is to give an overview of the existing synaptic delay-based learning algorithms in spiking neural networks. We described the typical learning algorithms and reported the experimental results. Finally, we discussed the properties and limitations of each algorithm and made a comparison among them.

Structure and function of the nervous system in nectophores of the siphonophore Nanomia bijuga

SummaryAlthough Nanomia nectophores are specialized for locomotion, their cellular elements and complex nerve structures suggest they have multiple subsidiary functions.The main nerve complex is a nerve ring, an adjacent columnar-shaped matrix plus two associated nerve projections. An upper nerve tract appears to provide a sensory input while a lower nerve tract connects with the rest of the colony.The nerve cell cluster that gives rise to the lower nerve tract may relay information from the colony stem.The structure of the extensively innervated “flask cells” located around the bell margin suggests a secretory function. They are ideally placed to release chemical messengers or toxins into the jet of water that leaves the nectophore during each swim.The numerous nematocytes present on exposed nectophore ridges appear to have an entangling rather than a penetrating role.Movements of the velum, produced by contraction of the Claus’ muscle system during backwards swimming, can be elicited by electrical stimulation of the surface epithelium even when the major nerve tracts serving the nerve ring have been destroyed (confirming Mackie, 1964).Epithelial impulses generated by electrical stimulation elicit synaptic potentials in Claus’ muscle fibres. Their amplitude suggests a neural input in the vicinity of the Claus’ muscle system. The synaptic delay is <1.3 ms (Temperature 11.5 to 15° C).During backward swimming radial muscle fibres in the endoderm contract isometrically providing the Claus’ fibres with a firm foundation.Summary StatementNanomia colonies have specialized swimming bells capable of backwards swimming; thrust is redirected by an epithelial signal that leads to muscle contraction via a synaptic rather than an electrotonic event.

Understanding the Role of Diffusion in Synaptic Transmission through Inquiry-Based Learning & Quantitative Reasoning

The elucidation of the principal features of chemical synaptic transmission has been one of the great achievements in the history of neuroscience, yet students have significant difficulties developing a deeper understanding of the underlying concept. This is particularly true for the role that diffusion of neurotransmitters across the synaptic cleft plays in this process. At least part of the learning problem is due to an erroneous view of diffusion as a slow process, and to an inability to apply the concepts of size and scale to the synapse and its structural components. To overcome these difficulties, a structured/guided inquiry activity, combined with quantitative reasoning tasks, is described for teaching chemical synaptic transmission as part of undergraduate biology or neuroscience courses. Through this activity, students familiarize themselves with the absolute and relative dimensions of the structural components of synapses; use data from morphometric and schematic models of synapses to estimate the time it takes a neurotransmitter to diffuse across the synaptic cleft; and evaluate how this process relates to synaptic delay and generation of a sufficiently high concentration of transmitter molecules for activation of postsynaptic receptors.

Effect of severity of hypertension on brain stem auditory evoked potentials

Background: Hypertension is one of the most important public health problems among worldwide. Central nervous system dysfunctions are common in these patients due to micro-infarctions caused by arteriolar spasm of cerebral blood vessels. This will lead to hypoperfusion, subcortical white matter demyelination, and cognitive decline. The Brainstem auditory evoked potentials (BAEP) are far field subcortical electrical potentials which provide an objective electrophysiological method for assessing the auditory pathway from auditory nerve to the brainstem. Aim and objective of the study was to assess the effect of increasing severity of hypertension on the brainstem auditory pathway, among the patients of essential hypertension.Methods: A total of 75 subjects of age group 30 to 60 years were included in the study. Among them 25 were healthy age and sex matched controls (Group I), 25 were stage 1 hypertensives (Group IIa) and 25 were stage 2 hypertensives (Group IIb) as per JNC 7 criteria. The absolute latencies I, III, V and interpeak latencies (IPL) I-III, III-V, I-V were recorded by using Neuroperfect EMG 2000 system with installed BAER and data were statistically analyzed using Student unpaired t test.Results: All the hypertensive (Group IIa and IIb) patients were found to have significantly prolonged absolute latency of wave III, V and IPL III-V, I-V as compared to that of normal healthy controls. The wave V latency was prolonged as the severity of hypertension increased. Intergroup comparison among hypertensive patients (Group IIa and IIb) revealed a significant prolongation of absolute latency of Wave III, V and IPL III-V, I-V.Conclusions: The results show that there exists a sensory deficit along with synaptic delay across the auditory pathway in the hypertensive patients and the sensory deficit progresses with the severity of the disease.

Impact of spatiotemporal calcium dynamics within presynaptic active zones on synaptic delay at the frog neuromuscular junction

The spatiotemporal calcium dynamics within presynaptic neurotransmitter release sites (active zones, AZs) at the time of synaptic vesicle fusion is critical for shaping the dynamics of neurotransmitter release. Specifically, the relative arrangement and density of voltage-gated calcium channels (VGCCs) as well as the concentration of calcium buffering proteins can play a large role in the timing, magnitude, and plasticity of release by shaping the AZ calcium profile. However, a high-resolution understanding of the role of AZ structure in spatiotemporal calcium dynamics and how it may contribute to functional heterogeneity at an adult synapse is currently lacking. We demonstrate that synaptic delay varies considerably across, but not within, individual synapses at the frog neuromuscular junction (NMJ). To determine how elements of the AZ could contribute to this variability, we performed a parameter search using a spatially realistic diffusion reaction-based computational model of a frog NMJ AZ (Dittrich M, Pattillo JM, King JD, Cho S, Stiles JR, Meriney SD. Biophys J 104: 2751–2763, 2013; Ma J, Kelly L, Ingram J, Price TJ, Meriney SD, Dittrich M. J Neurophysiol 113: 71–87, 2015). We demonstrate with our model that synaptic delay is sensitive to significant alterations in the spatiotemporal calcium dynamics within an AZ at the time of release caused by manipulations of the density and organization of VGCCs or by the concentration of calcium buffering proteins. Furthermore, our data provide a framework for understanding how AZ organization and structure are important for understanding presynaptic function and plasticity. NEW & NOTEWORTHY The structure of presynaptic active zones (AZs) can play a large role in determining the dynamics of neurotransmitter release across many model preparations by influencing the spatiotemporal calcium dynamics within the AZ at the time of vesicle fusion. However, less is known about how different AZ structural schemes may influence the timing of neurotransmitter release. We demonstrate that variations in AZ structure create different spatiotemporal calcium profiles that, in turn, lead to differences in synaptic delay.