scholarly journals Dynamically generated inflationary two-field potential via non-Riemannian volume forms

2020 ◽  
Vol 951 ◽  
pp. 114907 ◽  
Author(s):  
D. Benisty ◽  
E.I. Guendelman ◽  
E. Nissimov ◽  
S. Pacheva
Keyword(s):  
Field Potential ◽  
Riemannian Volume ◽  
Volume Forms

scholarly journals Dynamically generated inflation from non-Riemannian volume forms

2019 ◽  
Vol 79 (9) ◽  
Author(s):  
D. Benisty ◽  
E. I. Guendelman ◽  
E. Nissimov ◽  
S. Pacheva
Keyword(s):  
Scalar Field ◽  
Dynamical Systems ◽  
Modified Gravity ◽  
Point Of View ◽  
Riemannian Volume ◽  
Riemannian Spacetime ◽  
Cosmological Solutions ◽  
Volume Forms ◽  
Matter Fields ◽  
Type Potential

Abstract We propose a simple modified gravity model without any initial matter fields in terms of several alternative non-Riemannian spacetime volume elements within the metric (second order) formalism. We show how the non-Riemannian volume-elements, when passing to the physical Einstein frame, create a canonical scalar field and produce dynamically a non-trivial inflationary-type potential for the latter with a large flat region and a stable low-lying minimum. We study the evolution of the cosmological solutions from the point of view of theory of dynamical systems. The theory predicts the spectral index $$n_s \approx 0.96$$ns≈0.96 and the tensor-to-scalar ratio $$r \approx 0.002$$r≈0.002 for 60 e-folds, which is in accordance with the observational data. In the future Euclid and SPHEREx missions or the BICEP3 experiment are expected to provide experimental evidence to test those predictions.

Vagus Nerve Stimulation Induced Synchrony Modulation of Local Field Potential in the Rat Cerebral Cortex

2013 ◽  
Vol 133 (8) ◽  
pp. 1493-1500 ◽  
Author(s):  
Ryuji Kano ◽  
Kenichi Usami ◽  
Takahiro Noda ◽  
Tomoyo I. Shiramatsu ◽  
Ryohei Kanzaki ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Vagus Nerve ◽  
Local Field ◽  
Nerve Stimulation ◽  
Local Field Potential ◽  
Vagus Nerve Stimulation ◽  
Field Potential ◽  
Rat Cerebral Cortex

Aluminum Suppresses Effect of Nicotine on Gamma Oscillations (20-40 Hz) in Mouse Hippocampal Slices

2018 ◽  
Vol 17 (6) ◽  
pp. 404-411 ◽  
Author(s):  
Syeda Mehpara Farhat ◽  
Touqeer Ahmed
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Cholinergic System ◽  
Acetylcholine Receptors ◽  
Peak Power ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Gamma Oscillation ◽  
Facilitatory Effect

Background: Aluminum (Al) causes neurodegeneration and its toxic effects on cholinergic system in the brain is well documented. However, it is unknown whether and how Al changes oscillation patterns, driven by the cholinergic system, in the hippocampus. Objective: We studied acute effects of Al on nicotinic acetylcholine receptors (nAChRs)-mediated modulation of persistent gamma oscillations in the hippocampus. Method: The field potential recording was done in CA3 area of acute hippocampal slices. Results: Carbachol-induced gamma oscillation peak power increased (1.32±0.09mV2/Hz, P<0.01) in control conditions (without Al) by application of 10µM nicotine as compared to baseline value normalized to 1. This nicotine-induced facilitation of gamma oscillation peak power was found to depend on non-α7 nAChRs. In slices with Al pre-incubation for three to four hours, gamma oscillation peak power was reduced (5.4±1.8mV2/Hz, P<0.05) and facilitatory effect of nicotine on gamma oscillation peak power was blocked as compared to the control (18.06±2.1mV2/Hz) or one hour Al pre-incubated slices (11.3±2.5mV2/Hz). Intriguingly wash-out, after three to four hours of Al incubation, failed to restore baseline oscillation power and its facilitation by nicotine as no difference was observed in gamma oscillation peak power between Al wash-out slices (3.4±1.1mV2/Hz) and slices without washout (3.6±0.9mV2/Hz). Conclusion: This study shows that at cellular level, exposure of hippocampal tissue to Al compromised nAChR-mediated facilitation of cholinergic hippocampal gamma oscillations. Longer in vitro Al exposure caused permanent changes in hippocampal oscillogenic circuitry and changed its sensitivity to nAChR-modulation. This study will help to understand the possible mechanism of cognitive decline induced by Al.

Imaging NMDA- and kainate-induced intrinsic optical signals from the hippocampal slice

1996 ◽  
Vol 76 (4) ◽  
pp. 2707-2717 ◽  
Author(s):  
R. D. Andrew ◽  
J. R. Adams ◽  
T. M. Polischuk
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Ampa Receptors ◽  
Hippocampal Slice ◽  
Field Potential ◽  
Nmda Receptor Antagonist ◽  
Light Transmittance ◽  
Stratum Radiatum ◽  
Cell Swelling ◽  
Tissue Resistance

1. Brain ischemia causes excess release and accumulation of glutamate that binds to postsynaptic receptors. This opens ionotropic channels that mediate neuronal depolarization and ionic fluxes that can lead to neuronal death. 2. The CA1 pyramidal cell region of the hippocampus is particularly susceptible to this neurotoxic process. Brain cell swelling is considered an early excitotoxic event, but remains poorly under stood and documented. As cells swell, light transmittance (LT) increases through brain tissue, so we hypothesized that brief exposure to glutamate agonists would elicit cell swelling that could be imaged in real time in the hippocampal slice. 3. A 1-min bath application of 100 microM N-methyl-D-aspartate (NMDA) or 100 microM kainate at 22 degrees C greatly increased LT, particularly in the dendritic regions of CA1. The response peaked by 2-3 min and slowly reversed over the subsequent 20 min following exposure. Peak LT increases were > 50% in CA1 stratum radiatum and > 20% in both CA1 stratum oriens and the dendritic region of the dentate gyrus, all areas with a high concentration of NMDA and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors. The CA3 stratum radiatum, which contains fewer of these receptors, showed a comparatively small LT increase. 4. The NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP-5) [but not 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)] blocked the CA1 response to NMDA, whereas the non-NMDA receptor antagonist CNQX (but not AP-5) blocked the response to kainate. The relative tissue resistance measured across CA1 stratum radiatum increased after NMDA or kainate exposure with a time course similar to the LT change described above. The increase in relative tissue resistance was blocked by kynurenate, a nonspecific glutamate antagonist. Increases in both LT and tissue resistance provide two independent lines of evidence that cell swelling rapidly developed in CA1 dendritic areas after activation of NMDA or AMPA receptors. 5. This swelling at 22 degrees C was accompanied by a temporary loss of the evoked CA1 field potential. However, at 37 degrees C the dendritic swelling rapidly progressed to an irreversible LT increase (swelling) of the CA1 cell bodies accompanied by a permanent loss of the evoked field. 6. We propose that dendritic swelling mediated by NMDA and AMPA receptors is an early excitotoxic event that can herald permanent damage to CA1 neurons, those cells most vulnerable to ischemic insult.

scholarly journals CHAOTIC INFLATION ON THE RANDALL–SUNDRUM TWO-BRANE MODEL

2010 ◽  
Vol 25 (31) ◽  
pp. 2697-2713
Author(s):  
KOUROSH NOZARI ◽  
SIAMAK AKHSHABI
Keyword(s):  
Scalar Field ◽  
Field Potential ◽  
Friedmann Equation ◽  
Warp Factor ◽  
Model Parameters ◽  
Stabilization Mechanism ◽  
Brane Model ◽  
Inflation Model ◽  
Bulk Scalar Field ◽  
Chaotic Inflation

We construct an inflation model on the Randall–Sundrum I (RSI) brane where a bulk scalar field stabilizes the inter-brane separation. We study impact of the bulk scalar field on the inflationary dynamics on the brane. We proceed in two different approaches: in the first approach, the stabilizing field potential is directly appeared in the Friedmann equation and the resulting scenario is effectively a two-field inflation. In the second approach, the stabilization mechanism is considered in the context of a warp factor so that there is just one field present that plays the roles of both inflaton and stabilizer. We study constraints imposed on the model parameters from recent observations.

scholarly journals Comparative analysis of spreading depolarizations in brain slices exposed to osmotic or metabolic stress

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Rita Frank ◽  
Ferenc Bari ◽  
Ákos Menyhárt ◽  
Eszter Farkas
Keyword(s):  
Osmotic Stress ◽  
Tissue Injury ◽  
Brain Slices ◽  
Field Potential ◽  
Metabolic Stress ◽  
Glucose Deprivation ◽  
Optical Signal ◽  
Light Illumination ◽  
Glass Capillary ◽  
Experimental Conditions

Abstract Background Recurrent spreading depolarizations (SDs) occur in stroke and traumatic brain injury and are considered as a hallmark of injury progression. The complexity of conditions associated with SD in the living brain encouraged researchers to study SD in live brain slice preparations, yet methodological differences among laboratories complicate integrative data interpretation. Here we provide a comparative evaluation of SD evolution in live brain slices, in response to selected SD triggers and in various media, under otherwise standardized experimental conditions. Methods Rat live coronal brain slices (350 μm) were prepared (n = 51). Hypo-osmotic medium (Na+ content reduced from 130 to 60 mM, HM) or oxygen-glucose deprivation (OGD) were applied to cause osmotic or ischemic challenge. Brain slices superfused with artificial cerebrospinal fluid (aCSF) served as control. SDs were evoked in the control condition with pressure injection of KCl or electric stimulation. Local field potential (LFP) was recorded via an intracortical glass capillary electrode, or intrinsic optical signal imaging was conducted at white light illumination to characterize SDs. TTC and hematoxylin-eosin staining were used to assess tissue damage. Results Severe osmotic stress or OGD provoked a spontaneous SD. In contrast with SDs triggered in aCSF, these spontaneous depolarizations were characterized by incomplete repolarization and prolonged duration. Further, cortical SDs under HM or OGD propagated over the entire cortex and occassionally invaded the striatum, while SDs in aCSF covered a significantly smaller cortical area before coming to a halt, and never spread to the striatum. SDs in HM displayed the greatest amplitude and the most rapid propagation velocity. Finally, spontaneous SD in HM and especially under OGD was followed by tissue injury. Conclusions While the failure of Na+/K+ ATP-ase is thought to impair tissue recovery from OGD-related SD, the tissue swelling-related hyper excitability and the exhaustion of astrocyte buffering capacity are suggested to promote SD evolution under osmotic stress. In contrast with OGD, SD propagating under hypo-osmotic condition is not terminal, yet it is associated with irreversible tissue injury. Further investigation is required to understand the mechanistic similarities or differences between the evolution of SDs spontaneously occurring in HM and under OGD.

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