Novel method for activation of the locomotor circuitry in human

We examine the possibility for activation of the involuntary locomotion of the lower limbs by spinal electromagnetic stimulation (ES). The subject laid on the left side. The legs are supported in a gravity-neutral position by special mounting that to provide horizontal rotation in the hip, knee and ankle. ES (3 Hz and 1.56 Tesla) at the T11,-T12 vertebrae induced involuntary locomotor-like movements in the legs. The latency from the initiation of ES to the first EMG burst compoused 0.68 +/- 1.0 s and it shortened at increasing of the frequency ES from 3 Hz to 20 Hz. Thus, the spinal ES can unduce the activation of the locomotor movements in human.     

Transcutaneous electrical stimulation of the spinal cord: non-invasive tool for activation of locomotor circuitry in human

A new tool for locomotor circuitry activation in the non-injured human by transcutaneous electrical spinal cord stimulation (tSCS) has been described. We show that continuous tSCS over T11-T12 vertebrae at 5-40 Hz induced involuntary locomotor-like stepping movements in subjects with their legs in a gravity-independent position. The increase of frequency of tSCS from 5 to 30 Hz augmented the amplitude of evoked stepping movements. The duration of cycle period did not depend on frequency of tSCS. During tSCS the hip, knee and ankle joints were involved in the stepping performance. It has been suggested that tSCS activates the locomotor circuitry through the dorsal roots. It appears that tSCS can be used as a non-invasive method in rehabilitation of spinal pathology.     

Role of glutamate in locomotor rhythm generating neuronal circuitry

Central pattern generators (CPGs) are defined as neuronal circuits capable of producing a rhythmic and coordinated output without the influence of sensory input. The locomotor and respiratory neuronal circuits are two of the better-characterized CPGs, although much work remains to fully understand how these networks operate. Glutamatergic neurons are involved in most neuronal circuits of the nervous system and considerable efforts have been made to study glutamate receptors in nervous system signaling using a variety of approaches. Because of the complexity of glutamate-mediated signaling and the variety of receptors triggered by glutamate, it has been difficult to pinpoint the role of glutamatergic neurons in neuronal circuits. In addition, glutamate is an amino acid used by every cell, which has hampered identification of glutamatergic neurons. Glutamatergic excitatory neurotransmission is dependent on the release from glutamate-filled presynaptic vesicles loaded by three members of the solute carrier family, Slc17a6-8, which function as vesicular glutamate transporters (VGLUTs). Recent data describe that Vglut2 (Slc17a6) null mutant mice die immediately after birth due to a complete loss of the stable autonomous respiratory rhythm generated by the pre-B?tzinger complex. Surprisingly, we found that basal rhythmic locomotor activity is not affected in Vglut2 null mutant embryos. With this perspective, we discuss data regarding presence of VGLUT1, VGLUT2 and VGLUT3 positive neuronal populations in the spinal cord.     

A new method of evaluation of the masticatory function in humans

A method is proposed to estimate mastication by three indices: chewing effect, chewing performance, chewing efficiency. Definitions are given for these terms. A new chewing test is described, permits studying the influence of the number of chewing strokes, chewing force and volume of test portion on the mastication using a group of 25 dentate persons aged 17-25 years with class I occlusion. A new approach to the estimation of chewing efficiency changes traditional views. A strong positive correlation is first found between chewing effect (A) and integrated bioelectrical activity (J) of chewing muscles with the constant number of chewing strokes. A relation between A and J is established when the number of chewing strokes increases.     

A new interpretation of thalamocortical circuitry

Almost all the information that is needed to specify thalamocortical and neocortical wiring derives from patterned electrical activity induced by the environment. Wiring accuracy must be limited by the anatomical specificity of the cascade of events triggered by neural activity and culminating in synaptogenesis. We present a simple model of learning in the presence of plasticity errors. One way to achieve learning specificity is to build better synapses. We discuss an alternative, circuit-based, approach that only allows plasticity at connections that support highly selective correlations. This circuit resembles some of the more puzzling aspects of thalamocorticothalamic circuitry.     

Oxytocin shapes the neural circuitry of trust and trust adaptation in humans

Trust and betrayal of trust are ubiquitous in human societies. Recent behavioral evidence shows that the neuropeptide oxytocin increases trust among humans, thus offering a unique chance of gaining a deeper understanding of the neural mechanisms underlying trust and the adaptation to breach of trust. We examined the neural circuitry of trusting behavior by combining the intranasal, double-blind, administration of oxytocin with fMRI. We find that subjects in the oxytocin group show no change in their trusting behavior after they learned that their trust had been breached several times while subjects receiving placebo decrease their trust. This difference in trust adaptation is associated with a specific reduction in activation in the amygdala, the midbrain regions, and the dorsal striatum in subjects receiving oxytocin, suggesting that neural systems mediating fear processing (amygdala and midbrain regions) and behavioral adaptations to feedback information (dorsal striatum) modulate oxytocin's effect on trust. These findings may help to develop deeper insights into mental disorders such as social phobia and autism, which are characterized by persistent fear or avoidance of social interactions.     

Recurrent circuitry dynamically shapes the activation of piriform cortex

In the piriform cortex, individual odorants activate a unique ensemble of neurons that are distributed without discernable spatial order. Piriform neurons receive convergent excitatory inputs from random collections of olfactory bulb glomeruli. Pyramidal cells also make extensive recurrent connections with other excitatory and inhibitory neurons. We introduced channelrhodopsin into the piriform cortex to characterize these intrinsic circuits and to examine their contribution to activity driven by afferent bulbar inputs. We demonstrated that individual pyramidal cells are sparsely interconnected by thousands of excitatory synaptic connections that extend, largely undiminished, across the piriform cortex, forming a large excitatory network that can dominate the bulbar input. Pyramidal cells also activate inhibitory interneurons that mediate strong, local feedback inhibition that scales with excitation. This recurrent network can enhance or suppress bulbar input, depending on whether the input arrives before or after the cortex is activated. This circuitry may shape the ensembles of piriform cells that encode odorant identity.     

A new approach for anthelmintic discovery for humans

Natural product-based drug discovery has been deemphasized by the pharmaceutical industry. This situation is discordant with the fact that most people in developing countries rely on traditional medicines derived from local biodiversity for healthcare. Despite economic growth in the past 10 years, Africa remains plagued by parasitic infections, out of reach of eradication. Limited regional funding for drug discovery complicates the situation. Novel models are needed to bring sustainability to local drug discovery programs. This Opinion describes an innovative partnership that promotes local leadership to harness a recombinant yeast-based assay to screen for novel anthelmintic candidates in collections of African natural products. Implementation of this strategy in biodiversity-rich but resource-constrained settings can help build sustainable local capacity for drug discovery.     

A new method to determine optimum temperature and activation energies for enzymatic reactions

A new method for determination of the optimum temperature and activation energies based on an idea of the average rate of enzymatic reaction has been developed. A mathematical model describing the effect of temperature on a dimensionless activity for enzyme deactivation following the first-order kinetics has been derived. The necessary condition for existence of the function extreme of the optimal temperature has been applied in the model. The developed method has been verified using the experimental data for inulinase from Kluyveromyces marxianus.     

Music notation: a new method for visualizing social interaction in animals and humans

Background

Researchers have developed a variety of techniques for the visual presentation of quantitative data. These techniques can help to reveal trends and regularities that would be difficult to see if the data were left in raw form. Such techniques can be of great help in exploratory data analysis, making apparent the organization of data sets, developing new hypotheses, and in selecting effects to be tested by statistical analysis. Researchers studying social interaction in groups of animals and humans, however, have few tools to present their raw data visually, and it can be especially difficult to perceive patterns in these data. In this paper I introduce a new graphical method for the visual display of interaction records in human and animal groups, and I illustrate this method using data taken on chickens forming dominance hierarchies.

Results

This new method presents data in a way that can help researchers immediately to see patterns and connections in long, detailed records of interaction. I show a variety of ways in which this new technique can be used: (1) to explore trends in the formation of both group social structures and individual relationships; (2) to compare interaction records across groups of real animals and between real animals and computer-simulated animal interactions; (3) to search for and discover new types of small-scale interaction sequences; and (4) to examine how interaction patterns in larger groups might emerge from those in component subgroups. In addition, I discuss how this method can be modified and extended for visualizing a variety of different kinds of social interaction in both humans and animals.

Conclusion

This method can help researchers develop new insights into the structure and organization of social interaction. Such insights can make it easier for researchers to explain behavioural processes, to select aspects of data for statistical analysis, to design further studies, and to formulate appropriate mathematical models and computer simulations.     

A rat model for neural circuitry abnormalities in schizophrenia

Animal models for complex brain disorders, such as schizophrenia, are essential for the interpretation of postmortem findings. These models allow empirical testing of hypotheses regarding the role of genetic and environmental factors, the pathophysiological mechanisms and brain circuits that are responsible for specific neural abnormalities and their associated behavioral impairment, and the effectiveness of therapeutic treatments relative to these diseases. Recently, we developed a rodent model for neural circuitry abnormalities in discrete corticolimbic subregions of subjects with major psychoses. According to our protocol, the GABA-A receptor antagonist picrotoxin is stereotaxically infused in the basolateral amygdala to mimic a GABA defect in this region that is postulated to occur in these disorders. This protocol has been tested with a number of acute and chronic time schedules. Following picrotoxin administration in the basolateral amygdala, changes in GABAergic neurons and/or terminals in hippocampal regions CA2/3 are observed, similar to those seen in major psychoses, as well as a marked reduction in GABA-receptor-mediated currents in pyramidal neurons of this region. This has established the construct and predictive validity of this model for studying limbic-lobe circuitry abnormalities. We propose that this modeling strategy may provide a valid alternative to isomorphic models of these diseases.     

A new method for determining the Michaelis constant

A new method is described for evaluating the parameters K(m) and V in the Michaelis-Menten equation, and is illustrated with experimental data from the literature.