Medial and Lateral Entorhinal Cortex Differentially Excite Deep versus Superficial CA1 Pyramidal Neurons

Although hippocampal CA1 pyramidal neurons (PNs) were thought to comprise a uniform population, recent evidence supports two distinct sublayers along the radial axis, with deep neurons more likely to form place cells than superficial neurons. CA1 PNs also differ along the transverse axis with regard to direct inputs from entorhinal cortex (EC), with medial EC (MEC) providing spatial information to PNs toward CA2 (proximal CA1) and lateral EC (LEC) providing non-spatial information to PNs toward subiculum (distal CA1). We demonstrate that the two inputs differentially activate the radial sublayers and that this difference reverses along the transverse axis, with MEC preferentially targeting deep PNs in proximal CA1 and LEC preferentially exciting superficial PNs in distal CA1. This differential excitation reflects differences in dendritic spine numbers. Our results reveal a heterogeneity in EC-CA1 connectivity that may help explain differential roles of CA1 PNs in spatial and non-spatial learning and memory

Bifurcation analysis of phytoplankton-fish model through parametric control by fish mortality rate and food transfer efficiency

An Algae-zooplankton fish model is studied in this article. First the proposed model is evaluated for positive invariance and boundedness. Then,the Routh-Hurwitz parameters and the Lyapunov function are used to determine the presence of a positive interior steady state and the criteria for plankton model stability (both local and global). Taylor’s sequence is also used to discuss Hopf bifurcation and the stability of bifurcated periodic solutions. The model’s bifurcation analysis reveals that Hopf-bifurcation can occur when mortality rate and food transfer efficiency are used as bifurcation parameters. Finally, we use numerical simulation to validate the analytical results

Surgical versus non-surgical interventions in people with adolescent idiopathic scoliosis

BACKGROUND Adolescent idiopathic scoliosis (AIS) is a three-dimensional deformity of the spine. While AIS can progress during growth and cause a surface deformity, it is usually not symptomatic. However, if the final spinal curvature surpasses a certain critical threshold, the risk of health problems and curve progression is increased. Interventions for the prevention of AIS progression include scoliosis-specific exercises, bracing, and surgery. The main aims of all types of interventions are to correct the deformity and prevent further deterioration of the curve and to restore trunk asymmetry and balance, while minimising morbidity and pain, allowing return to full function. Surgery is normally recommended for curvatures exceeding 40 to 50 degrees to stop curvature progression with a view to achieving better truncal balance and cosmesis. Short-term results of the surgical treatment of people with AIS demonstrate the ability of surgery to improve various outcome measures. However there is a clear paucity of information on long-term follow-up of surgical treatment of people with AIS. OBJECTIVES To examine the impact of surgical versus non-surgical interventions in people with AIS who have severe curves of over 45 degrees, with a focus on trunk balance, progression of scoliosis, cosmetic issues, quality of life, disability, psychological issues, back pain, and adverse effects, at both the short term (a few months) and the long term (over 20 years). SEARCH METHODS We searched the Cochrane Back Review Group Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, four other databases, and three trials registers up to August 2014 with no language limitations. We also checked the reference lists of relevant articles and conducted an extensive handsearch of the grey literature. SELECTION CRITERIA We searched for randomised controlled trials (RCTs) and prospective controlled trials comparing spinal fusion surgery with non-surgical interventions in people with AIS with a Cobb angle greater than 45 degrees. We were interested in all types of instrumented surgical interventions with fusion that aimed to provide curve correction and spine stabilisation. DATA COLLECTION AND ANALYSIS We found no RCTs or prospective controlled trials that met our inclusion criteria. MAIN RESULTS We did not identify any evidence comparing surgical to non-surgical interventions for AIS with severe curves of over 45 degrees. AUTHORS' CONCLUSIONS We cannot draw any conclusions

Epileptiform activity induces distance-dependent alterations of the Ca<SUP>2+</SUP> extrusion mechanism in the apical dendrites of subicular pyramidal neurons

The cellular and molecular mechanisms that underlie acquired changes in Ca<SUP>2+</SUP> dynamics of different neuronal compartments are important in the induction and maintenance of epileptiform activity. Simultaneous electrophysiology and Ca<SUP>2+ </SUP>imaging techniques were used to understand the basic properties of dendritic Ca<SUP>2+</SUP> signaling in rat subicular pyramidal neurons during epileptiform activity. Distance-dependent changes in the Ca<SUP>2+</SUP> decay kinetics locked to spontaneous epileptiform discharges and back-propagating action potentials were observed in the apical dendrites. A decrement in the mean Τ value of Ca<SUP>2+</SUP> decay was observed in distal parts (95-110 μm) of the apical dendrites compared with proximal segments (30-45 μm) in in-vitro epileptic conditions but not in control. Pharmacological agents that block Ca<SUP>2+</SUP> transporters, i.e. Na<SUP>+</SUP>/ Ca<SUP>2+</SUP> exchangers (Benzamil), plasma membrane Ca<SUP>2+</SUP>-ATPase pumps (Calmidazolium) and smooth endoplasmic reticulum Ca<SUP>2+</SUP>-ATPase pumps (Thapsigargin), were applied locally to the proximal and distal part of the apical dendrites in both experimental conditions to understand the molecular aspects of the Ca<SUP>2+</SUP> extrusion mechanisms. The relative contribution of Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchangers in Ca<SUP>2+</SUP> extrusion was higher in the distal apical dendrites in the in-vitro epileptic condition and this property modulated the excitability of the neuron in simulation. The Ca<SUP>2+</SUP> homeostatic mechanisms that restore normal Ca<SUP>2+</SUP> levels could play a major neuroprotective role in the distal dendrites that receive synaptic inputs

Epileptiform activity induces distance-dependent alterations of the Ca2+Ca^{2+} extrusion mechanism in the apical dendrites of subicular pyramidal neurons

The cellular and molecular mechanisms that underlie acquired changes in Ca2+ dynamics of different neuronal compartments are important in the induction and maintenance of epileptiform activity. Simultaneous electrophysiology and Ca2+ imaging techniques were used to understand the basic properties of dendritic Ca2+ signaling in rat subicular pyramidal neurons during epileptiform activity. Distance-dependent changes in the Ca2+ decay kinetics locked to spontaneous epileptiform discharges and back-propagating action potentials were observed in the apical dendrites. A decrement in the mean tau value of Ca2+ decay was observed in distal parts (95-110 mu m) of the apical dendrites compared with proximal segments (30-45 mu m) in in-vitro epileptic conditions but not in control. Pharmacological agents that block Ca2+ transporters, i.e. Na+/ Ca2+ exchangers (Benzamil), plasma membrane Ca2+-ATPase pumps (Calmidazolium) and smooth endoplasmic reticulum Ca2+-ATPase pumps (Thapsigargin), were applied locally to the proximal and distal part of the apical dendrites in both experimental conditions to understand the molecular aspects of the Ca2+ extrusion mechanisms. The relative contribution of Na+/Ca2+ exchangers in Ca2+ extrusion was higher in the distal apical dendrites in the in-vitro epileptic condition and this property modulated the excitability of the neuron in simulation. The Ca2+ homeostatic mechanisms that restore normal Ca2+ levels could play a major neuroprotective role in the distal dendrites that receive synaptic inputs

Mathematical Analysis of a Prey–Predator System: An Adaptive Back-Stepping Control and Stochastic Approach

In this paper, stochastic analysis of a diseased prey&#8315;predator system involving adaptive back-stepping control is studied. The system was investigated for its dynamical behaviours, such as boundedness and local stability analysis. The global stability of the system was derived using the Lyapunov function. The uniform persistence condition for the system is obtained. The proposed system was studied with adaptive back-stepping control, and it is proved that the system stabilizes to its steady state in nonlinear feedback control. The value of the system is described mostly by the environmental stochasticity in the form of Gaussian white noise. We also established some conditions for oscillations of all positive solutions of the delayed system. Numerical simulations are illustrated, and sustained our analytical findings. We concluded that controlled harvesting on the susceptible and infected prey is able to control prey infection

A study of epileptogenic network structures in rat hippocampal cultures using first spike latencies during synchronization events

Study of hypersynchronous activity is of prime importance for combating epilepsy. Studies on network structure typically reconstruct the network by measuring various aspects of the interaction between neurons and subsequently measure the properties of the reconstructed network. In sub-sampled networks such methods lead to significant errors in reconstruction. Using rat hippocampal neurons cultured on a multi-electrode array dish and a glutamate injury model of epilepsy in vitro, we studied synchronous activity in neuronal networks. Using the first spike latencies in various neurons during a network burst, we extract various recurring spatio-temporal onset patterns in the networks. Comparing the patterns seen in control and injured networks, we observe that injured networks express a wide diversity in their foci (origin) and activation pattern, while control networks show limited diversity. Furthermore, we note that onset patterns in glutamate injured networks show a positive correlation between synchronization delay and physical distance between neurons, while control networks do not

High level expression of peptides and proteins using cytochrome b5b_5 as a fusion host

A novel fusion protein system based on the highly soluble heme-binding domain of cytochrome $b_5$ has been designed. The ability of cytochrome $b_5$ to increase the levels of expression and solubility of target proteins has been tested by expressing several proteins and peptides, viz., $\alpha$ hemoglobin stabilizing protein, the regulatory subunits of acetohydroxy acid synthase I (ilvM) and II (ilvN), the carboxy terminal domains of mouse neuronal kinesin and pantothenate synthatase, two peptide toxins from cone snails, and the inactivation gate from the brain voltage gated sodium channel, $Na_V1.2$. The fusion protein system has been designed to incorporate protease cleavage sites for commonly used proteases, viz., enterokinase, Factor Xa, and Tobacco etch virus protease. Accumulation of expressed protein as a function of time may be visually ascertained by the fact that the cells take on a bright red color during the course of induction. In all the cases tested so far, the fusion protein accumulates in the soluble fraction to high levels. A novel puriWcation protocol has been designed to purify the fusion proteins using metal aYnity chromatography, without the need of a hexahistidine-tag. Mass spectral analysis has shown that the fusion proteins are of full length. CD studies have shown that the solubilized fusion proteins are structured. The proteins of interest may be cleaved from the parent protein by either chemical or enzymatic means. The results presented here demonstrate the versatility of the cytochrome $b_5$ based fusion system for the production of peptides and small proteins (<15 kDa)

Small-world network topology of hippocampal neuronal network is lost, in an in vitro glutamate injury model of epilepsy

Neuronal network topologies and connectivity patterns were explored in control and glutamate-injured hippocampal neuronal networks, cultured on planar multielectrode arrays. Spontaneous activity was characterized by brief episodes of synchronous firing at many sites in the array (network bursts). During such assembly activity, maximum numbers of neurons are known to interact in the network. After brief glutamate exposure followed by recovery, neuronal networks became hypersynchronous and fired network bursts at higher frequency. Connectivity maps were constructed to understand how neurons communicate during a network burst. These maps were obtained by analysing the spike trains using cross-covariance analysis and graph theory methods. Analysis of degree distribution, which is a measure of direct connections between electrodes in a neuronal network, showed exponential and Gaussian distributions in control and glutamate-injured networks, respectively. Although both the networks showed random features, small-world properties in these networks were different. These results suggest that functional two-dimensional neuronal networks in vitro are not scale-free. After brief exposure to glutamate, normal hippocampal neuronal networks became hyperexcitable and fired a larger number of network bursts with altered network topology. The small-world network property was lost and this was accompanied by a change from an exponential to a Gaussian network

Analysis of connectivity map: Control to glutamate injured and phenobarbital treated neuronal network

We study the responses of a cultured neural network when it is exposed to epileptogenesis glutamate injury causing epilepsy and subsequent treatment with phenobarbital by constructing connectivity map of neurons using correlation matrix. This study is particularly useful in understanding the pharmaceutical drug induced changes in the neuronal network properties with insights into changes at the systems biology level. (C) 2010 American Institute of Physics. [doi:10.1063/1.3398025