The upper critical magnetic field of holographic superconductor with conformally invariant power-Maxwell electrodynamics

The properties of $(d-1)$-dimensional $s$-wave holographic superconductor in the presence of power-Maxwell field is explored. We study the probe limit in which the scalar and gauge fields do not backreact on the background geometry. Our study is based on the matching of solutions on the boundary and on the horizon at some intermediate point. At first, the case without external magnetic field is considered, and the critical temperature is obtained in terms of the charge density, the dimensionality, and the power-Maxwell exponent. Then, a magnetic field is turned on in the $d$-dimensional bulk which can influence the $(d-1)$-dimensional holographic superconductor at the boundary. The phase behavior of the corresponding holographic superconductor is obtained by computing the upper critical magnetic field in the presence of power-Maxwell electrodynamics, characterized by the power exponent $q$. Interestingly, it is observed that in the presence of magnetic field, the physically acceptable phase behavior of the holographic superconductor is obtained for $q={d}/{4}$, which guaranties the conformal invariance of the power-Maxwell Lagrangian. The case of physical interest in five spacetime dimensions ($d=5$, and $q=5/4$) is considered in detail, and compared with the results obtained for the usual Maxwell electrodynamics $q=1$ in the same dimensions.Comment: 12 pages, 1 table, 5 figure

Identifying specific prefrontal neurons that contribute to autism-associated abnormalities in physiology and social behavior.

Functional imaging and gene expression studies both implicate the medial prefrontal cortex (mPFC), particularly deep-layer projection neurons, as a potential locus for autism pathology. Here, we explored how specific deep-layer prefrontal neurons contribute to abnormal physiology and behavior in mouse models of autism. First, we find that across three etiologically distinct models-in utero valproic acid (VPA) exposure, CNTNAP2 knockout and FMR1 knockout-layer 5 subcortically projecting (SC) neurons consistently exhibit reduced input resistance and action potential firing. To explore how altered SC neuron physiology might impact behavior, we took advantage of the fact that in deep layers of the mPFC, dopamine D2 receptors (D2Rs) are mainly expressed by SC neurons, and used D2-Cre mice to label D2R+ neurons for calcium imaging or optogenetics. We found that social exploration preferentially recruits mPFC D2R+ cells, but that this recruitment is attenuated in VPA-exposed mice. Stimulating mPFC D2R+ neurons disrupts normal social interaction. Conversely, inhibiting these cells enhances social behavior in VPA-exposed mice. Importantly, this effect was not reproduced by nonspecifically inhibiting mPFC neurons in VPA-exposed mice, or by inhibiting D2R+ neurons in wild-type mice. These findings suggest that multiple forms of autism may alter the physiology of specific deep-layer prefrontal neurons that project to subcortical targets. Furthermore, a highly overlapping population-prefrontal D2R+ neurons-plays an important role in both normal and abnormal social behavior, such that targeting these cells can elicit potentially therapeutic effects

Relation between positional specific heat and static relaxation length: Application to supercooled liquids

A general identification of the {\em positional specific heat} as the thermodynamic response function associated with the {\em static relaxation length} is proposed, and a phenomenological description for the thermal dependence of the static relaxation length in supercooled liquids is presented. Accordingly, through a phenomenological determination of positional specific heat of supercooled liquids, we arrive at the thermal variation of the static relaxation length $\xi$, which is found to vary in accordance with $\xi \sim (T-T_0)^{-\nu}$ in the quasi-equilibrium supercooled temperature regime, where $T_0$ is the Vogel-Fulcher temperature and exponent $\nu$ equals unity. This result to a certain degree agrees with that obtained from mean field theory of random-first-order transition, which suggests a power law temperature variation for $\xi$ with an apparent divergence at $T_0$. However, the phenomenological exponent $\nu = 1$, is higher than the corresponding mean field estimate (becoming exact in infinite dimensions), and in perfect agreement with the relaxation length exponent as obtained from the numerical simulations of the same models of structural glass in three spatial dimensions.Comment: Revised version, 7 pages, no figures, submitted to IOP Publishin

The mechanisms shaping CA2 pyramidal neuron action potential bursting induced by muscarinic acetylcholine receptor activation

International audienceRecent studies have revealed that hippocampal area CA2 plays an important role in hippocampal network function. Disruption of this region has been implicated in neuropsychiatric disorders. It is well appreciated that cholinergic input to the hippocampus plays an important role in learning and memory. While the effect of elevated cholinergic tone has been well studied in areas CA1 and CA3, it remains unclear how changes in cholinergic tone impact synaptic transmission and the intrinsic properties of neurons in area CA2. In this study, we applied the cholinergic agonist carbachol and performed on-cell, whole-cell, and extracellular recordings in area CA2. We observed that under conditions of high cholinergic tone, CA2 pyramidal neurons depolarized and rhythmically fired bursts of action potentials. This depolarization depended on the activation of M1 and M3 cholinergic receptors. Furthermore, we examined how the intrinsic properties and action-potential firing were altered in CA2 pyramidal neurons treated with 10 µM carbachol. While this intrinsic burst firing persisted in the absence of synaptic transmission, bursts were shaped by synaptic inputs in the intact network. We found that both excitatory and inhibitory synaptic transmission were reduced upon carbachol treatment. Finally, we examined the contribution of different channels to the cholinergic-induced changes in neuronal properties. We found that a conductance from Kv7 channels partially contributed to carbachol-induced changes in resting membrane potential and membrane resistance. We also found that D-type potassium currents contributed to controlling several properties of the bursts, including firing rate and burst kinetics. Furthermore, we determined that T-type calcium channels and small conductance calcium-activated potassium channels play a role in regulating bursting activity

Identifying specific prefrontal neurons that contribute to autism-associated abnormalities in physiology and social behavior.

Functional imaging and gene expression studies both implicate the medial prefrontal cortex (mPFC), particularly deep-layer projection neurons, as a potential locus for autism pathology. Here, we explored how specific deep-layer prefrontal neurons contribute to abnormal physiology and behavior in mouse models of autism. First, we find that across three etiologically distinct models-in utero valproic acid (VPA) exposure, CNTNAP2 knockout and FMR1 knockout-layer 5 subcortically projecting (SC) neurons consistently exhibit reduced input resistance and action potential firing. To explore how altered SC neuron physiology might impact behavior, we took advantage of the fact that in deep layers of the mPFC, dopamine D2 receptors (D2Rs) are mainly expressed by SC neurons, and used D2-Cre mice to label D2R+ neurons for calcium imaging or optogenetics. We found that social exploration preferentially recruits mPFC D2R+ cells, but that this recruitment is attenuated in VPA-exposed mice. Stimulating mPFC D2R+ neurons disrupts normal social interaction. Conversely, inhibiting these cells enhances social behavior in VPA-exposed mice. Importantly, this effect was not reproduced by nonspecifically inhibiting mPFC neurons in VPA-exposed mice, or by inhibiting D2R+ neurons in wild-type mice. These findings suggest that multiple forms of autism may alter the physiology of specific deep-layer prefrontal neurons that project to subcortical targets. Furthermore, a highly overlapping population-prefrontal D2R+ neurons-plays an important role in both normal and abnormal social behavior, such that targeting these cells can elicit potentially therapeutic effects

Reproducibility of in-vivo electrophysiological measurements in mice

Understanding whole-brain-scale electrophysiological recordings will rely on the collective work of multiple labs. Because two labs recording from the same brain area often reach different conclusions, it is critical to quantify and control for features that decrease reproducibility. To address these issues, we formed a multi-lab collaboration using a shared, open-source behavioral task and experimental apparatus. We repeatedly inserted Neuropixels multi-electrode probes targeting the same brain locations (including posterior parietal cortex, hippocampus, and thalamus) in mice performing the behavioral task. We gathered data across 9 labs and developed a common histological and data processing pipeline to analyze the resulting large datasets. After applying stringent behavioral, histological, and electrophysiological quality-control criteria, we found that neuronal yield, firing rates, spike amplitudes, and task-modulated neuronal activity were reproducible across laboratories. To quantify variance in neural activity explained by task variables (e.g., stimulus onset time), behavioral variables (timing of licks/paw movements), and other variables (e.g., spatial location in the brain or the lab ID), we developed a multi-task neural network encoding model that extends common, simpler regression approaches by allowing nonlinear interactions between variables. We found that within-lab random effects captured by this model were comparable to between-lab random effects. Taken together, these results demonstrate that across-lab standardization of electrophysiological procedures can lead to reproducible results across labs. Moreover, our protocols to achieve reproducibility, along with our analyses to evaluate it are openly accessible to the scientific community, along with our extensive electrophysiological dataset with corresponding behavior and open-source analysis code