Comparison of Activation Methods for 3D-Printed Electrodes for Microbial Electrochemical Technologies

Three-dimensional printing could provide flexibility in the design of a new generation of electrodes to be used in microbial electrochemical technologies (MET). In this work, we demonstrate the feasibility of using polylactic acid (PLA)/graphene—a common 3D-printing material—to build custom bioelectrodes. We also show that a suitable activation procedure is crucial to achieve an acceptable electrochemical performance (plain PLA/graphene bioanodes produce negligible amounts of current). Activation with acetone and dimethylformamide resulted in current densities similar to those typically observed in bioanodes built with more conventional materials (about 5A m−2). In addition, the electrodes thus activated favored the proliferation of electroactive bacteria.

Dynamic divisive normalization circuits explain and predict change detection in monkey area MT

Sudden changes in visual scenes often indicate important events for behavior. For their quick and reliable detection, the brain must be capable to process these changes as independently as possible from its current activation state. In motion-selective area MT, neurons respond to instantaneous speed changes with pronounced transients, often far exceeding the expected response as derived from their speed tuning profile. We here show that this complex, non-linear behavior emerges from the combined temporal dynamics of excitation and divisive inhibition, and provide a comprehensive mathematical analysis. A central prediction derived from this investigation is that attention increases the steepness of the transient response irrespective of the activation state prior to a stimulus change, and irrespective of the sign of the change (i.e. irrespective of whether the stimulus is accelerating or decelerating). Extracellular recordings of attention-dependent representation of both speed increments and decrements confirmed this prediction and suggest that improved change detection derives from basic computations in a canonical cortical circuitry.

Contributions of CaV1.3 Channels to Ca2+ Current and Ca2+-Activated BK Current in the Suprachiasmatic Nucleus

Daily regulation of Ca2+– and voltage-activated BK K+ channel activity is required for action potential rhythmicity in the suprachiasmatic nucleus (SCN) of the hypothalamus, the brain's circadian clock. In SCN neurons, BK activation is dependent upon multiple types of Ca2+ channels in a circadian manner. Daytime BK current predominantly requires Ca2+ influx through L-type Ca2+ channels (LTCCs), a time when BK channels are closely coupled with their Ca2+ source. Here we show that daytime BK current is resistant to the Ca2+ chelator BAPTA. However, at night when LTCCs contribute little to BK activation, BK current decreases by a third in BAPTA compared to control EGTA conditions. In phase with this time-of-day specific effect on BK current activation, LTCC current is larger during the day. The specific Ca2+ channel subtypes underlying the LTCC current in SCN, as well as the subtypes contributing the Ca2+ influx relevant for BK current activation, have not been identified. SCN neurons express two LTCC subtypes, CaV1.2 and CaV1.3. While a role for CaV1.2 channels has been identified during the night, CaV1.3 channel modulation has also been suggested to contribute to daytime SCN action potential activity, as well as subthreshold Ca2+ oscillations. Here we characterize the role of CaV1.3 channels in LTCC and BK current activation in SCN neurons using a global deletion of CACNA1D in mouse (CaV1.3 KO). CaV1.3 KO SCN neurons had a 50% reduction in the daytime LTCC current, but not total Ca2+ current, with no difference in Ca2+ current levels at night. During the day, CaV1.3 KO neurons exhibited oscillations in membrane potential, and most neurons, although not all, also had BK currents. Changes in BK current activation were only detectable at the highest voltage tested. These data show that while CaV1.3 channels contribute to the daytime Ca2+ current, this does not translate into a major effect on the daytime BK current. These data suggest that BK current activation does not absolutely require CaV1.3 channels and may therefore also depend on other LTCC subtypes, such as CaV1.2.

BK channel activation by L-type Ca2+ channels CaV1.2 and CaV1.3 during the subthreshold phase of an action potential

Mammalian circadian (24-hour) rhythms are timed by the pattern of spontaneous action potential firing in the suprachiasmatic nucleus (SCN). This oscillation in firing is produced through circadian regulation of several membrane currents, including large-conductance Ca2+- and voltage-activated K+ (BK) and L-type Ca2+ channel (LTCC) currents. During the day, steady-state BK currents depend mostly on LTCCs for activation, while at night, they depend predominantly on RyRs. However, the contribution of these Ca2+ channels to BK channel activation during action potential firing has not been thoroughly investigated. In this study, we used a pharmacological approach to determine that both LTCCs and RyRs contribute to the baseline membrane potential of SCN action potential waveforms, as well as action potential-evoked BK current, during the day and night, respectively. Since the baseline membrane potential is a major determinant of circadian firing rate, we focused on the LTCCs contributing to low voltage activation of BK channels during the subthreshold phase. For these experiments, two LTCC subtypes found in SCN (CaV1.2 and CaV1.3) were co-expressed with BK channels in heterologous cells, where their differential contributions could be separately measured. CaV1.3 channels produced currents that were shifted to more hyperpolarized potentials compared to CaV1.2, resulting in increased subthreshold Ca2+ and BK currents during an action potential command. These results show that while multiple Ca2+ sources in SCN can contribute to the activation of BK current during an action potential, specific BK-CaV1.3 partnerships may optimize the subthreshold BK current activation that is critical for firing rate regulation.

The relative balance between languages predicts the magnitude of whole-language inhibition.

After naming pictures in their second language (L2), bilinguals experience difficulty in naming pictures in their native language (L1). The “L2 after-effect” is a lingering consequence of inhibition applied to L1 to facilitate L2 production. We proposed that the amount of L1 inhibition depends on the relative balance between current activation of L1 and L2. In two experiments, bilinguals performed a blocked picture-naming task which provided a measure of the relative balance between the two languages and indexed whole-language inhibition via the magnitude of the L2 after-effect. The higher the activation level of L1 and the lower the activation level of L2, the bigger the L2 after-effect. The results also reveal an enduring down-regulation of L1 activation level in more language-balanced speakers. The outcomes support the main tenets of the inhibitory account of bilingual language production and indicate a high level of dynamics in the language system.

Insight into Electrical and Dielectric Relaxation of Doped Tellurite Lithium-Silicate Glasses with Regard to Ionic Charge Carrier Number Density Estimation

We investigate the role of tellurite on a lithium-silicate glass 0.1 TeO2 − 0.9 (Li2O-2SiO2) (LSTO) system proposed for the use in solid electrolyte for lithium ion batteries. The measurements of electrical impedance are performed in the frequency 100 Hz–30 MHz and temperature from 50 to 150 °C. The electrical conductivity of LSTO glass increases compared with that of Li2O-2SiO2 (LSO) glass due to an increase in the number of Li+ ions. The ionic hopping and relaxation processes in disordered solids are generally explained using Cole–Cole, power law and modulus representations. The power law conductivity analysis, which is driven by the modified Rayleigh equation, presents the estimation of the number of ionic charge carriers explicitly. The estimation counts for direct contribution of about a 14% increase in direct current conductivity in the case of TeO2 doping. The relaxation process by modulus analysis confirms that the cations are trapped strongly in the potential wells. Both the direct current and alternating current activation energies (0.62–0.67 eV) for conduction in the LSO glass are the same as those in the LSTO glass.

Firing patterns of the CA1 pyramidal neuron with geometric singular perturbation: a model study

An investigation of CA1 pyramidal model is an important issue for applications, which is intimately related to the composition of ions in the extracellular environment and external stimulation. In this paper, it is demonstrated that the effects of different electrophysiological parameters such as muscarinic-sensitive potassium current activation variable and sustained sodium current inactivation variable on the firing sequence of model by numerical simulations. Furthermore, the paper also discusses that the temperature affects the firing of the CA1 model from direct current (DC) and alternating current (AC) stimuli. It is found that the model exhibits excellent spiking and bursting patterns, even chaotic patterns occur. Meanwhile, generalized mixed oscillations emerge in the model. Additionally, the firing modes are depicted by providing the response curve (RC), inter-spike interval curve (ISI), phase diagram curve (PDC) and the number of spikes per burst curve (NC). Mathematically, the paper elaborates the results which are presented to obtain two lower dimensional subsystems, which govern the fast and slow dynamics for giving insight into the dynamic behaviors of the full 5D system based on the geometric singular perturbation theory (GSPT). Particularly, we analyse the phase diagrams of the CA1 model to understand the properties better. The present results may contribute to further understand the information processing of the CA1 pyramidal neurons.

A simple canonical circuitry for non-stationary normalization by inhibition to explain and predict change detection in monkey area MT

Sudden changes in visual scenes often indicate important events for behavior. For their quick and reliable detection, the brain must be capable to process these changes as independent as possible from its current activation state. In motion-selective area MT, neurons respond to instantaneous speed changes with pronounced transients, often far exceeding the expected response as derived from their speed tuning profile. We here show that this complex, non-linear behavior emerges from the combined temporal dynamics of excitation and divisive inhibition, and provide a comprehensive formal analysis. A central prediction derived from this investigation is that attention increases the steepness of the transient response irrespective of the activation state prior to a stimulus change, and irrespective of the sign of the change. Extracellular recordings of attention-dependent representation of both speed increments and decrements confirmed this prediction and suggest that improved change detection derives from basic computations in a canonical cortical circuitry.

Neuronal kinase SGK1.1 protects against brain damage after status epilepticus

ABSTRACTEpilepsy is a neurological condition associated to significant brain damage produced by status epilepticus (SE) including neurodegeneration, gliosis and ectopic neurogenesis. Reduction of these processes constitutes a useful strategy to improve recovery and ameliorate negative outcomes after an initial insult. SGK1.1, the neuronal isoform of the serum and glucocorticoids-regulated kinase 1 (SGK1), has been shown to increase M-current density in neurons, leading to reduced excitability and protection against seizures. We now show that SGK1.1 activation potently reduces levels of neuronal death and gliosis after SE induced by kainate, even in the context of high seizure activity. This neuroprotective effect is not exclusively a secondary effect of M-current activation but is also directly linked to decreased apoptosis levels through regulation of Bim and Bcl-xL cellular levels. Our results demonstrate that this newly described antiapoptotic role of SGK1.1 activation acts synergistically with the regulation of cellular excitability, resulting in a significant reduction of SE-induced brain damage. The protective role of SGK1.1 occurs without altering basal neurogenesis in brain areas relevant to epileptogenesis.SIGNIFICANCE STATEMENTApproaches to control neuronal death and inflammation are of increasing interest in managing epilepsy, one of the most important idiopathic brain diseases. We have previously shown that activation of SGK1.1 reduces neuronal excitability by increasing M-current levels, significantly reducing seizure severity. We now describe a potent neuroprotective role of SGK1.1, which dramatically reduces neuronal death and gliosis after status epilepticus. This effect is partially dependent on M-current activation and includes an additional anti-apoptotic role of SGK1.1. Our data strongly support the relevance of this kinase as a potential target for epilepsy treatment.