Gamma-burst positions - are they reliable?

1995 ◽  
Vol 231 (1-2) ◽  
pp. 217-226 ◽  
Author(s):  
Niels Lund
Keyword(s):  
1981 ◽  
Vol 75 (1) ◽  
pp. 219-224 ◽  
Author(s):  
G. S. Bisnovaty-Kogan ◽  
I. V. Estulin ◽  
N. G. Havenson ◽  
V. G. Kurt ◽  
G. A. Mersov ◽  
...  

1987 ◽  
Vol 125 ◽  
pp. 546-546
Author(s):  
Stirling A. Colgate

The source of the enhanced dissipation or “α” viscosity of Keplerian accretion discs is central in all putative mechanisms for large energy release by matter accreting onto condensed objects and for the basic mechanism of star formation. The circumstances of gamma burst formation on neutron stars suggest convective buoyancy as a necessary condition for the large α. This is because the total mass ≅ 1019 g necessary to supply the energy of a gamma burst derived from infall is a natural limit for the mass stored in a disc without α viscosity. This suggests that buoyancy driven convective turbulence is the source of the enhanced transport in disc evolution models (Shakura and Sunyaev 1973). In support of this conjecture we find that the maximum possible energy released by ideal friction operating on the velocity shear of a disc is twice that required to destabilize the angular momentum distribution of such a disc. The heat energy available from an α viscosity is twice that necessary to create α in the first place. Hence, a nonlinear instability–nonlinear to create convective turbulence and nonlinear to create shear viscosity heating–is sufficient to drive α. One characteristic that would prevent the formation of such an instability is degeneracy of the disc matter as it accumulates near a neutron star (Paczynski and Jaroszynski 1978). Degeneracy inhibits strong convection because a given energy release within degenerate matter results in a large temperature, and hence large energy transport without convection. Convection occurs in an accretion disc whenever the energy which is dissipated in the disc requires a superadiabatic temperature gradient for its radiative or conductive transport to the surface. Some gamma burst mechanisms require exactly such a mechanism as a degenerate disc close to the neutron star in the correct mass (≅ 1019 g), at the correct radius several times the neutron star radius, to supply gravitational energy for a gamma burst. The degenerate disc accumulates mass stably until the density is great enough that degenerate fluid viscosity evolves the disc into contact with the neutron star. The large energy released by velocity shear at contact heats the disc causing rapid evolution and a gamma burst.


1984 ◽  
Author(s):  
Stirling A. Colgate ◽  
Albert G. Petschek ◽  
Robert Sarracino

1982 ◽  
Author(s):  
Stirling A. Colgate
Keyword(s):  

1981 ◽  
Vol 75 (1) ◽  
pp. 35-46 ◽  
Author(s):  
W. D. Evans ◽  
E. E. Fenimore ◽  
R. W. Klebesadel ◽  
J. G. Laros ◽  
N. J. Terrell
Keyword(s):  

1998 ◽  
Author(s):  
Sergey E. Ulin ◽  
K. F. Vlasik ◽  
A. M. Galper ◽  
V. M. Grachev ◽  
Valery V. Dmitrenko ◽  
...  

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Roxanne Lofredi ◽  
Wolf-Julian Neumann ◽  
Antje Bock ◽  
Andreas Horn ◽  
Julius Huebl ◽  
...  

Gamma synchronization increases during movement and scales with kinematic parameters. Here, disease-specific characteristics of this synchronization and the dopamine-dependence of its scaling in Parkinson’s disease are investigated. In 16 patients undergoing deep brain stimulation surgery, movements of different velocities revealed that subthalamic gamma power peaked in the sensorimotor part of the subthalamic nucleus, correlated positively with maximal velocity and negatively with symptom severity. These effects relied on movement-related bursts of transient synchrony in the gamma band. The gamma burst rate highly correlated with averaged power, increased gradually with larger movements and correlated with symptom severity. In the dopamine-depleted state, gamma power and burst rate significantly decreased, particularly when peak velocity was slower than ON medication. Burst amplitude and duration were unaffected by the medication state. We propose that insufficient recruitment of fast gamma bursts during movement may underlie bradykinesia as one of the cardinal symptoms in Parkinson’s disease.


2020 ◽  
Author(s):  
Indie C. Garwood ◽  
Sourish Chakravarty ◽  
Jacob Donoghue ◽  
Pegah Kahali ◽  
Shubham Chamadia ◽  
...  

AbstractKetamine is an NMDA receptor antagonist commonly used to maintain general anesthesia. At anesthetic doses, ketamine causes bursts of 30-50 Hz oscillations alternating with 0.1 to 10 Hz oscillations. These dynamics are readily observed in local field potentials (LFPs) of non-human primates (NHPs) and electroencephalogram (EEG) recordings from human subjects. However, a detailed statistical analysis of these dynamics has not been reported. We characterize ketamine’s neural dynamics using a hidden Markov model (HMM). The HMM observations are sequences of spectral power in 10 Hz frequency bands between 0 to 50 Hz, where power is averaged within each band and scaled between 0 and 1. We model the observations as realizations of multivariate beta probability distributions that depend on a discrete-valued latent state process whose state transitions obey Markov dynamics. Using an expectation-maximization algorithm, we fit this beta-HMM to LFP recordings from 2 NHPs, and separately, to EEG recordings from 9 human subjects who received anesthetic doses of ketamine. Together, the estimated beta-HMM parameters and optimal state trajectory revealed an alternating pattern of states characterized primarily by gamma burst and slow oscillation activity, as well as intermediate states in between. The mean duration of the gamma burst state was 2.5s([1.9,3.4]s) and 1.2s([0.9,1.5]s) for the two NHPs, and 2.7s([1.9,3.8]s) for the human subjects. The mean duration of the slow oscillation state was 1.6s([1.1,2.5]s) and 0.7s([0.6,0.9]s) for the two NHPs, and 2.8s([1.9,4.3]s) for the human subjects. Our beta-HMM framework provides a useful tool for experimental data analysis. Our characterizations of the gamma-burst process offer detailed, quantitative constraints that can inform the development of rhythm-generating neuronal circuit models that give mechanistic insights into this phenomenon and how ketamine produces altered states of arousal.


Sign in / Sign up

Export Citation Format

Share Document