Spike initiation properties in the axon support high-fidelity signal transmission

The axon initial segment (AIS) converts graded depolarization into all-or-none spikes that are transmitted by the axon to downstream neurons. Analog-to-digital transduction and digital signal transmission call for distinct spike initiation properties (filters) and those filters should, therefore, differ between the AIS and distal axon. Here we show that unlike the AIS, which spikes repetitively during sustained depolarization, the axon spikes transiently and only if depolarization reaches threshold before KV1 channels activate. Rate of depolarization is critical. This was shown by optogenetically evoking spikes in the distal axon of CA1 pyramidal neurons using different photostimulus waveforms and pharmacological conditions while recording antidromically propagated spikes at the soma, thus circumventing the prohibitive difficulty of patching intact axons. Computational modeling shows that KV1 channels in the axon implement a high-pass filter that is matched to the axial current waveform associated with spike propagation, thus maximizing the signal-to-noise ratio to ensure high-fidelity transmission of spike-based signals.

The Weak Interactions

We present the phenomenology of the weak interactions in a historical perspective, from Fermi’s four-fermion theory to the V−A current×current interaction. The experiments of C.S. Wu, which established parity violation, and M. Goldhaber, which measured the neutrino helicity, are described. We study in turn the leptonic, semi-leptonic and non-leptonic weak interactions. We introduce the concept of the conserved vector current and the partially conserved axial current and show that the latter is the result of spontaneously broken chiral symmetry with the pion the corresponding pseudo-Goldstone boson. We study Gell–Mann’s current algebra and derive the Adler–Weisberger relation. Strangeness changing weak interactions and the Cabibbo theory are described. We present a phenomenological analysis of CP-violation in the neutral kaon system and we end with the intermediate vector boson hypothesis.

Systematic study of the chiral magnetic effect with the AVFD model at LHC energies

We present a systematic study of the correlators used experimentally to probe the Chiral Magnetic Effect (CME) using the Anomalous Viscous Fluid Dynamics (AVFD) model in Pb–Pb and Xe–Xe collisions at LHC energies. We find a parametrization that describes the dependence of these correlators on the value of the axial current density ($$n_5/{\mathrm {s}}$$ n 5 / s ), which dictates the CME signal, and on the parameter that governs the background in these measurements i.e., the percentage of local charge conservation (LCC) within an event. This allows to deduce the values of $$n_5/{\mathrm {s}}$$ n 5 / s and the LCC percentage that provide a quantitative description of the centrality dependence of the experimental measurements. We find that the results in Xe–Xe collisions at $$\sqrt{s_{\mathrm {NN}}} = 5.44$$ s NN = 5.44 TeV are consistent with a background only scenario. On the other hand, the model needs a significant non-zero value of $$n_5/{\mathrm {s}}$$ n 5 / s to match the measurements in Pb–Pb collisions at $$\sqrt{s_{\mathrm {NN}}} = 5.02$$ s NN = 5.02 TeV.

Multifarious Roles of Hidden Chiral-Scale Symmetry: “Quenching” gA in Nuclei

I discuss how the axial current coupling constant gA renormalized in scale symmetric chiral EFT defined at a chiral matching scale impacts on the axial current matrix elements on beta decays in nuclei with and without neutrinos. The “quenched” gA observed in nuclear superallowed Gamow–Teller transitions, a long-standing puzzle in nuclear physics, is shown to encode the emergence of chiral-scale symmetry hidden in QCD in the vacuum. This enables one to explore how trace-anomaly-induced scale symmetry breaking enters in the renormalized gA in nuclei applicable to certain non-unique forbidden processes involved in neutrinoless double beta decays. A parallel is made between the roles of chiral-scale symmetry in quenching gA in highly dense medium and in hadron–quark continuity in the EoS of dense matter in massive compact stars. A systematic chiral-scale EFT, presently lacking in nuclear theory and potentially crucial for the future progress, is suggested as a challenge in the field.

Renormalization of the topological charge density in QCD with dimensional regularization

To all orders of perturbation theory, the renormalization of the topological charge density in dimensionally regularized QCD is shown to require no more than an additive renormalization proportional to the divergence of the flavour-singlet axial current. The proof is based on the standard BRS analysis of the QCD vertex functional in the background gauge and exploits the special algebraic properties of the charge density through the Stora–Zumino chain of descent equations.

Magneto-vortical effect in strong magnetic field

We develop covariant chiral kinetic theory with Landau level basis. We use it to investigate a magnetized plasma with a transverse electric field and a steady vorticity as perturbations. After taking into account vacuum shift in the latter case, we find the resulting current and stress tensor in both cases can be matched consistently with constitutive equations of magnetohydrodynamics. We find the solution in the vorticity case contains both shifts in temperature and chemical potential as well as excitations of the lowest Landau level states. The solution gives rise to an vector charge density and axial current density. The vacuum parts coming from both shifts and excitations agree with previous studies and the medium parts coming entirely from excitations leads to a new contribution to vector charge and axial current density consistent with standard chiral vortical effect.

Electrical match between initial segment and somatodendritic compartment for action potential backpropagation in retinal ganglion cells

The action potential of most vertebrate neurons initiates in the axon initial segment (AIS), and is then transmitted to the soma where it is regenerated by somatodendritic sodium channels. For successful transmission, the AIS must produce a strong axial current, so as to depolarize the soma to the threshold for somatic regeneration. Theoretically, this axial current depends on AIS geometry and Na+ conductance density. We measured the axial current of mouse retinal ganglion cells using whole-cell recordings with post-hoc AIS labeling. We found that this current is large, implying high Na+ conductance density, and carries a charge that co-varies with capacitance so as to depolarize the soma by ~30 mV. Additionally, we observed that the axial current attenuates strongly with depolarization, consistent with sodium channel inactivation, but temporally broadens so as to preserve the transmitted charge. Thus, the AIS appears to be organized so as to reliably backpropagate the axonal action potential.

Entropy production far from equilibrium in a chiral charged plasma in the presence of external electromagnetic fields

We report on the time evolution of a charged strongly coupled N = 4 SYM plasma with an axial anomaly subjected to strong electromagnetic fields. The evolution of this plasma corresponds to a fully backreacted asymptotically AdS5 solution to the Einstein-Maxwell-Chern-Simons theory. We explore the evolution of the axial current and production of axial charges. As an application we show that after a sufficiently long time both the entropy and the holographic entanglement entropy of a strip-like topology (both parallel to and transverse to the flow of axial current) grow linearly in time.

Ionic Mechanisms of Impulse Propagation Failure in the FHF2-Deficient Heart

Rationale: FHFs (fibroblast growth factor homologous factors) are key regulators of sodium channel (Na V ) inactivation. Mutations in these critical proteins have been implicated in human diseases including Brugada syndrome, idiopathic ventricular arrhythmias, and epileptic encephalopathy. The underlying ionic mechanisms by which reduced Na v availability in Fhf2 knockout ( Fhf2 KO ) mice predisposes to abnormal excitability at the tissue level are not well defined. Objective: Using animal models and theoretical multicellular linear strands, we examined how FHF2 orchestrates the interdependency of sodium, calcium, and gap junctional conductances to safeguard cardiac conduction. Methods and Results: Fhf2 KO mice were challenged by reducing calcium conductance (gCa V ) using verapamil or by reducing gap junctional conductance (Gj) using carbenoxolone or by backcrossing into a cardiomyocyte-specific Cx43 (connexin 43) heterozygous background. All conditions produced conduction block in Fhf2 KO mice, with Fhf2 wild-type ( Fhf2 WT ) mice showing normal impulse propagation. To explore the ionic mechanisms of block in Fhf2 KO hearts, multicellular linear strand models incorporating FHF2-deficient Na v inactivation properties were constructed and faithfully recapitulated conduction abnormalities seen in mutant hearts. The mechanisms of conduction block in mutant strands with reduced gCa V or diminished Gj are very different. Enhanced Na v inactivation due to FHF2 deficiency shifts dependence onto calcium current (I Ca ) to sustain electrotonic driving force, axial current flow, and action potential (AP) generation from cell-to-cell. In the setting of diminished Gj, slower charging time from upstream cells conspires with accelerated Na v inactivation in mutant strands to prevent sufficient downstream cell charging for AP propagation. Conclusions: FHF2-dependent effects on Na v inactivation ensure adequate sodium current (I Na ) reserve to safeguard against numerous threats to reliable cardiac impulse propagation.