GABAergic Mechanisms Can Redress the Tilted Balance between Excitation and Inhibition in Damaged Spinal Networks

Correct operation of neuronal networks depends on the interplay between synaptic excitation and inhibition processes leading to a dynamic state termed balanced network. In the spinal cord, balanced network activity is fundamental for the expression of locomotor patterns necessary for rhythmic activation of limb extensor and flexor muscles. After spinal cord lesion, paralysis ensues often followed by spasticity. These conditions imply that, below the damaged site, the state of balanced networks has been disrupted and that restoration might be attempted by modulating the excitability of sublesional spinal neurons. Because of the widespread expression of inhibitory GABAergic neurons in the spinal cord, their role in the early and late phases of spinal cord injury deserves full attention. Thus, an early surge in extracellular GABA might be involved in the onset of spinal shock while a relative deficit of GABAergic mechanisms may be a contributor to spasticity. We discuss the role of GABA A receptors at synaptic and extrasynaptic level to modulate network excitability and to offer a pharmacological target for symptom control. In particular, it is proposed that activation of GABA A receptors with synthetic GABA agonists may downregulate motoneuron hyperexcitability (due to enhanced persistent ionic currents) and, therefore, diminish spasticity. This approach might constitute a complementary strategy to regulate network excitability after injury so that reconstruction of damaged spinal networks with new materials or cell transplants might proceed more successfully.

Partially balanced network designs and graph codes generation

<abstract> <p>Partial balanced incomplete block designs have a wide range of applications in many areas. Such designs provide advantages over fully balanced incomplete block designs as they allow for designs with a low number of blocks and different associations. This paper introduces a class of partially balanced incomplete designs. We call it partially balanced network designs (PBNDs). The fundamentals and properties of PBNDs are studied. We are concerned with modeling PBNDs as graph designs. Some direct constructions of small PBNDs and generalized PBNDs are introduced. Besides that, we show that our modeling yields an effective utilization of PNBDs in constructing graph codes. Here, we are interested in constructing graph codes from bipartite graphs. We have proved that these codes have good characteristics for error detection and correction. In the end, the paper introduces a novel technique for generating new codes from already constructed codes. This technique results in increasing the ability to correct errors.</p> </abstract>

Marcksl1 modulates endothelial cell mechanoresponse to haemodynamic forces to control blood vessel shape and size

The formation of vascular tubes is driven by extensive changes in endothelial cell (EC) shape. Here, we have identified a role of the actin-binding protein, Marcksl1, in modulating the mechanical properties of EC cortex to regulate cell shape and vessel structure during angiogenesis. Increasing and depleting Marcksl1 expression level in vivo results in an increase and decrease, respectively, in EC size and the diameter of microvessels. Furthermore, endothelial overexpression of Marcksl1 induces ectopic blebbing on both apical and basal membranes, during and after lumen formation, that is suppressed by reduced blood flow. High resolution imaging reveals that Marcksl1 promotes the formation of linear actin bundles and decreases actin density at the EC cortex. Our findings demonstrate that a balanced network of linear and branched actin at the EC cortex is essential in conferring cortical integrity to resist the deforming forces of blood flow to regulate vessel structure.

Marcksl1 modulates endothelial cell mechanoresponse to haemodynamic forces to control blood vessel shape and size

ABSTRACTThe formation of vascular tubes is driven by extensive changes in endothelial cell (EC) shape. Here, we have identified a novel role of the actin-binding protein, Marcksl1, in modulating the mechanical properties of EC cortex to regulate cell shape and vessel structure during angiogenesis. Increasing and depleting Marcksl1 expression level in vivo resulted in an increase and decrease, respectively, in EC size and the diameter of microvessels. Furthermore, endothelial overexpression of Marcksl1 induced ectopic blebbing on both apical and basal membranes, during and after lumen formation, that is suppressed by reduced blood flow. High resolution imaging revealed that Marcksl1 promotes the formation of linear actin bundles and decreases actin density at the EC cortex. Our findings demonstrate that a balanced network of linear and branched actin at the EC cortex is essential in conferring cortical integrity to resist the deforming forces of blood flow to regulate vessel structure.

Long-range coordination patterns in cortex change with behavioral context

Cortical connectivity mostly stems from local axonal arborizations, suggesting coordination is strongest between nearby neurons in the range of a few hundred micrometers. Yet multi-electrode recordings of resting-state activity in macaque motor cortex show strong positive and negative spike-count covariances between neurons that are millimeters apart. Here we show that such covariance patterns naturally arise in balanced network models operating close to an instability where neurons interact via indirect connections, giving rise to long-range correlations despite short-range connections. A quantitative theory explains the observed shallow exponential decay of the width of the covariance distribution at long distances. Long-range cooperation via this mechanism is not imprinted in specific connectivity structures but rather results dynamically from the network state. As a consequence, neuronal coordination patterns are not static but can change in a state-dependent manner, which we demonstrate by comparing different behavioral epochs of a reach-to-grasp experiment.

Node clone detection using a stable overlay network

Wireless sensor networks consist of number of sensor nodes widely distributed in particular region to communicate and sharing the environmental information and also these data’s are stored in central location for further data prediction. Such nodes are susceptible to cloning attack where the adversary captures a node, replicates with the same identity as that of the captured node and deploys the clone back into the network, causing severe harm to the network. Hence to thwart such attacks, a distributed detection protocol is used with initiator-observer-inspector roles assigned randomly for the nodes to witness the clone and thereby broadcast the evidence through a balanced overlay network. Use of such balanced network provides high security level and reduces the communication cost when compared to other overlay networks with a reasonably less storage consumption.