A code to unfold scintillation spectrometer polyenergetic gamma photon experimental distributions

FORTRAN code to unfold sodium iodide scintillation spectrometer polyenergetic gamma photon experimental distribution

A continuum model for the dynamics of the phase transition from slow-wave sleep to REM sleep

Previous studies have shown that activated cortical states (awake and rapid eye-movement (REM) sleep), are associated with increased cholinergic input into the cerebral cortex. However, the mechanisms that underlie the detailed dynamics of the cortical transition from slow-wave to REM sleep have not been quantitatively modeled. How does the sequence of abrupt changes in the cortical dynamics (as detected in the electrocorticogram) result from the more gradual change in subcortical cholinergic input? We compare the output from a continuum model of cortical neuronal dynamics with experimentally-derived rat electrocorticogram data. The output from the computer model was consistent with experimental observations. In slow-wave sleep, 0.5–2-Hz oscillations arise from the cortex jumping between “up” and “down” states on the stationary-state manifold. As cholinergic input increases, the upper state undergoes a bifurcation to an 8-Hz oscillation. The coexistence of both oscillations is similar to that found in the intermediate stage of sleep of the rat. Further cholinergic input moves the trajectory to a point where the lower part of the manifold in not available, and thus the slow oscillation abruptly ceases (REM sleep). The model provides a natural basis to explain neuromodulator-induced changes in cortical activity, and indicates that a cortical phase change, rather than a brainstem “flip-flop”, may describe the transition from slow-wave sleep to REM

What can a mean-field model tell us about the dynamics of the cortex?

In this chapter we examine the dynamical behavior of a spatially homogeneous two-dimensional model of the cortex that incorporates membrane potential, synaptic flux rates and long- and short-range synaptic input, in two spatial dimensions, using parameter sets broadly realistic of humans and rats. When synaptic dynamics are included, the steady states may not be stable. The bifurcation structure for the spatially symmetric case is explored, identifying the positions of saddle–node and sub- and supercritical Hopf instabilities. We go beyond consideration of small-amplitude perturbations to look at nonlinear dynamics. Spatially-symmetric (breathing mode) limit cycles are described, as well as the response to spatially-localized impulses. When close to Hopf and saddle–node bifurcations, such impulses can cause traveling waves with similarities to the slow oscillation of slow-wave sleep. Spiral waves can also be induced. We compare model dynamics with the known behavior of the cortex during natural and anesthetic-induced sleep, commenting on the physiological significance of the limit cycles and impulse responses

Connexin36 knockout mice display increased sensitivity to pentylenetetrazol-induced seizure-like behaviors

Large-scale synchronous firing of neurons during seizures is modulated by electrotonic coupling between neurons via gap junctions. To explore roles for connexin36 (Cx36) gap junctions in seizures, we examined the seizure threshold of connexin36 knockout (Cx36KO) mice using a pentylenetetrazol (PTZ) model

Measuring the electrical impedance of mouse brain tissue

We report on an experimental method to measure conductivity of cortical tissue. We use a pair of 5mm diameter Ag/AgCl electrodes in a Perspex sandwich device that can be brought to a distance of 400 microns apart. The apparatus is brought to uniform temperature before use. Electrical impedance of a sample is measured across the frequency range 20 Hz-2.0 MHz with an Agilent 4980A four-point impedance monitor in a shielded room. The equipment has been used to measure the conductivity of mature mouse brain cortex in vitro. Slices 400 microns in thickness are prepared on a vibratome. Slices are bathed in artificial cerebrospinal fluid (ACSF) to keep them alive. Slices are removed from the ACSF and sections of cortical tissue approximately 2 mm times 2 mm are cut with a razor blade. The sections are photographed through a calibrated microscope to allow identification of their cross-sectional areas. Excess ACSF is removed from the sample and the sections places between the electrodes. The impedance is measured across the frequency range and electrical conductivity calculated. Results show two regions of dispersion. A low frequency region is evident below approximately 10 kHz, and a high frequency dispersion above this. Results at the higher frequencies show a good fit to the Cole-Cole model of impedance of biological tissue; this model consists of resistive and non-linear capacitive elements. Physically, these elements are likely to arise due to membrane polarization and migration of ions both intra- and extra-cellularly.http://www.iupab2014.org/assets/IUPAB/NewFolder/iupab-abstracts.pd

Tetra­kis(picolinato-κ2 N,O)zirconium(IV) dihydrate

In the title compound, [Zr(C6H4NO2)4]·2H2O, the ZrIV atom is located on a crystallographic fourfold rotoinversion axis () and is coordinated by four picolinate anions with Zr—O and Zr—N distances of 2.120 (2) and 2.393 (2) Å, respectively. An approximate square-anti­prismatic coordination polyhedron of the N,O-coordination ligand atoms is formed, with a distortion towards dodeca­hedral geometry. The crystal packing is stabilized by inter­molecular π–π inter­actions between adjacent picolinate rings [centroid–centroid distances = 3.271 (1) and 3.640 (2) Å], as well as O—H⋯O hydrogen bonds between the solvent mol­ecules and the coordinated ligands, thereby linking the mol­ecules into a supra­molecular three-dimensional network

Biomarkers of Metabolism in Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the deterioration of motor neurons. However, this complex disease extends beyond the boundaries of the central nervous system, with metabolic alterations being observed at the systemic and cellular level. While the number of studies that assess the role and impact of metabolic perturbations in ALS is rapidly increasing, the use of metabolism biomarkers in ALS remains largely underinvestigated. In this review, we discuss current and potential metabolism biomarkers in the context of ALS. Of those for which data does exist, there is limited insight provided by individual markers, with specificity for disease, and lack of reproducibility and efficacy in informing prognosis being the largest drawbacks. However, given the array of metabolic markers available, the potential exists for a panel of metabolism biomarkers, which may complement other current biomarkers (including neurophysiology, imaging, as well as CSF, blood and urine markers) to overturn these limitations and give rise to new diagnostic and prognostic indicators

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle

Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with associated β adrenergic receptor (ADRβ) desensitization. Our objectives were to measure insulin-sensitive glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADRβ2 agonist and ADRβ1/β3 antagonists for 1 month normalizes their glucose metabolism. Growth, glucose-stimulated insulin secretion (GSIS) and glucose utilization rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: clenbuterol atenolol and SR59230A (IUGR-AR). In IUGR lambs, islet insulin content and GSIS were less than in controls; however, insulin sensitivity and whole-bodyGUR were not different from controls.Of importance, ADRβ2 stimulation with β1/β3 inhibition increases both insulin sensitivity and whole-body glucose utilization in IUGR lambs. In IUGR and IUGR-AR lambs, hindlimb GURs were greater but fractional glucose oxidation rates and ex vivo skeletal muscle glucose oxidation rates were lower than controls. Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR-AR skeletal muscle than in controls but GLUT1 was greater in IUGR-AR. ADRβ2, insulin receptor, glycogen content and citrate synthase activity were similar among groups. In IUGR and IUGR-AR lambs heart rates were greater, which was independent of cardiac ADRβ1 activation. We conclude that targeted ADRβ2 stimulation improved whole-body insulin sensitivity but minimally affected defects in GSIS and skeletal muscle glucose oxidation. We show that risk factors for developing diabetes are independent of postnatal catch-up growth in IUGR lambs as early as 1 month of age and are inherent to the islets and myocytes

No evidence of an 11.16 MeV 2+ state in 12C

An experiment using the 11B(3He,d)12C reaction was performed at iThemba LABS at an incident energy of 44 MeV and analyzed with a high energy-resolution magnetic spectrometer, to re-investigate states in 12C published in 1971. The original investigation reported the existence of an 11.16 MeV state in 12C that displays a 2+ nature. In the present experiment data were acquired at laboratory angles of 25-, 30- and 35- degrees, to be as close to the c.m. angles of the original measurements where the clearest signature of such a state was observed. These new low background measurements revealed no evidence of the previously reported state at 11.16 MeV in 12C