Quantitative evaluation of extrinsic factors influencing electrical excitability in neuronal networks： Voltage Threshold Measurement Method(VTMM)

The electrical excitability of neural networks is influenced by different environmental factors. Effective and simple methods are required to objectively and quantitatively evaluate the influence of such factors, including variations in temperature and pharmaceutical dosage. The aim of this paper was to introduce ‘the voltage threshold measurement method＇, which is a new method using microelectrode arrays that can quantitatively evaluate the influence of different factors on the electrical excitability of neural networks. We sought to verify the feasibility and efficacy of the method by studying the effects of acetylcholine, ethanol, and temperature on hippocampal neuronal networks and hippocampal brain slices. First, we determined the voltage of the stimulation pulse signal that elicited action potentials in the two types of neural networks under normal conditions. Second, we obtained the voltage thresholds for the two types of neural networks under different concentrations of acetylcholine, ethanol, and different temperatures. Finally, we obtained the relationship between voltage threshold and the three influential factors. Our results indicated that the normal voltage thresholds of the hippocampal neuronal network and hippocampal slice preparation were 56 and 31 m V, respectively. The voltage thresholds of the two types of neural networks were inversely proportional to acetylcholine concentration, and had an exponential dependency on ethanol concentration. The curves of the voltage threshold and the temperature of the medium for the two types of neural networks were U-shaped. The hippocampal neuronal network and hippocampal slice preparations lost their excitability when the temperature of the medium decreased below 34 and 33°C or increased above 42 and 43°C, respectively. These results demonstrate that the voltage threshold measurement method is effective and simple for examining the performance/excitability of neuronal networks.

How do lateral septum projections to the ventral CA1 influence sociability?

Social dysfunction is a risk factor for several neuropsychiatric illnesses.Previous studies have shown that the lateral septum(LS)-related pathway plays a critical role in mediating social behaviors.Howeve r,the role of the connections between the LS and its downstream brain regions in social behavio rs remains unclea r.In this study,we conducted a three-chamber test using electrophysiological and chemogenetic approaches in mice to determine how LS projections to ventral CA1(vCA1)influence sociability.Our res ults showed that gamma-aminobutyric acid(GABA)-e rgic neuro ns were activated following social experience,and that social behavio rs were enhanced by chemogenetic modulation of these neurons.Moreover,LS GABAergic neurons extended their functional neural connections via vCA1 glutamatergic pyramidal neurons,and regulating LSGABA→vCA1Gluneural projections affected social behaviors,which were impeded by suppressing LSprojecting vCA1 neuronal activity or inhibiting GABAAreceptors in vCA1.These findings support the hypothesis that LS inputs to the vCA1 can control social prefe rences and social novelty behaviors.These findings provide new insights rega rding the neural circuits that regulate sociability.

Soleus arthrogenic muscle inhibition following acute lateral ankle sprain correlates with symptoms and ankle disability but not with postural control

Background:Acute lateral ankle sprains(ALAS)are associated with long-term impairments and instability tied to altered neural excitability.Arthrogenic muscle inhibition(AMI)has been observed in this population;however,relationships with injury-related impairments are unclear,potentially due to the resting,prone position in which AMI is typically measured.Assessing AMI during bipedal stance may provide a better understanding of this relationship.Methods:AMI was assessed in 38 young adults(19 ALAS within 72 h of injury:10 males,21.4±2.7 years;19 healthy controls:10 males,21.9±2.2 years;mean±SD)using the Hoffmann reflex(H-reflex)during bipedal stance.Electrical stimulation was administered to identify the _(max)imal H-reflex(H_(max))and _(max)imal motor response(M_(max))from the soleus,fibularis longus,and tibialis anterior muscles.The primary outcome measure was the H_(max)/M_(max) ratio.Secondary outcomes included acute symptoms(pain and swelling),postural control during bipedal stance,and self-reported function.Results:No significant group-by-limb interactions were observed for any muscle.However,a significant group main effect was observed in the soleus muscle(F(1,35)=6.82,p=0.013),indicating significantly lower H_(max)/M_(max) ratios following ALAS(0.38±0.20)compared to healthy controls(0.53±0.16).Furthermore,lower H_(max)/M_(max) ratios in the soleus significantly correlated with acute symptoms and self-reported function but not with postural control.Conclusion:This study supports previous evidence of AMI in patients with ALAS,providing insight into neurophysiologic impacts of musculoskeletal injury.Our results suggest that assessing AMI in a standing position following acute injury may provide valuable insight into how AMI develops and guide potential therapeutic options to curb and offset the formation of joint instability.

Repetitive transcranial magnetic stimulation improves consciousness disturbance in stroke patients A quantitative electroencephalography spectral power analysis

Repetitive transcranial magnetic stimulation is a noninvasive treatment technique that can directly alter cortical excitability and improve cerebral functional activity in unconscious patients. To investigate the effects and the electrophysiological changes of repetitive transcranial magnetic stimulation cortical treatment, 10 stroke patients with non-severe brainstem lesions and with disturbance of consciousness were treated with repetitive transcranial magnetic stimulation. A quantitative electroencephalography spectral power analysis was also performed. The absolute power in the alpha band was increased immediately after the first repetitive transcranial magnetic stimulation treatment, and the energy was reduced in the delta band. The alpha band relative power values slightly decreased at 1 day post-treatment, then increased and reached a stable level at 2 weeks post-treatment. Glasgow Coma Score and JFK Coma Recovery Scale-Revised score were improved. Relative power value in the alpha band was positively related to Glasgow Coma Score and JFK Coma Recovery Scale-Revised score. These data suggest that repetitive transcranial magnetic stimulation is a noninvasive, safe, and effective treatment technology for improving brain functional activity and promoting awakening in unconscious stroke patients.

Biomimetic Control of Mechanical Systems Equipped with Musculotendon Actuators

This paper addresses the problem of modelling, control, and simulation of a mechanical system actuated by an agonist-antagonist musculotendon subsystem. Contraction dynamics is given by case 1 of Zajac＇s model. Saturated semi positive proportional-derivative-type controllers with switching as neural excitation inputs are proposed. Stability theory of switched system and SOSTOOLS, which is a sum of squares optimization toolbox of Matlab, are used to determine the stability of the obtained closed-loop system. To corroborate the obtained theoretical results numerical simulations are carried out. As additional contribution, the discussed ideas are applied to the biomimetic control of a DC motor, i.e., the position control is addressed assuming the presence of musculotendon actuators. Real-experiments corroborate the expected results.

Inhibition of intracellular proton-sensitive Ca^(2+)-permeable TRPV3 channels protects against ischemic brain injury

Ischemic brain stroke is pathologically characterized by tissue acidosis, sustained calcium entry and progressive cell death. Previous studies focusing on antagonizing N-methyl-D-aspartate(NMDA) receptors have failed to translate any clinical benefits, suggesting a non-NMDA mechanism involved in the sustained injury after stroke. Here, we report that inhibition of intracellular proton-sensitive Ca^(2+)-permeable transient receptor potential vanilloid 3(TRPV3) channel protects against cerebral ischemia/reperfusion(I/R) injury. TRPV3 expression is upregulated in mice subjected to cerebral I/R injury. Silencing of TRPV3 reduces intrinsic neuronal excitability, excitatory synaptic transmissions, and also attenuates cerebral I/R injury in mouse model of transient middle cerebral artery occlusion(tMCAO). Conversely, overexpressing or re-expressing TRPV3 increases neuronal excitability, excitatory synaptic transmissions and aggravates cerebral I/R injury. Furthermore, specific inhibition of TRPV3 by natural forsythoside B decreases neural excitability and attenuates cerebral I/R injury. Taken together, our findings for the first time reveal a causative role of neuronal TRPV3 channel in progressive cell death after stroke, and blocking overactive TRPV3 channel may provide therapeutic potential for ischemic brain injury.