84 research outputs found
Frequency dependence of signal power and spatial reach of the local field potential
The first recording of electrical potential from brain activity was reported
already in 1875, but still the interpretation of the signal is debated. To take
full advantage of the new generation of microelectrodes with hundreds or even
thousands of electrode contacts, an accurate quantitative link between what is
measured and the underlying neural circuit activity is needed. Here we address
the question of how the observed frequency dependence of recorded local field
potentials (LFPs) should be interpreted. By use of a well-established
biophysical modeling scheme, combined with detailed reconstructed neuronal
morphologies, we find that correlations in the synaptic inputs onto a
population of pyramidal cells may significantly boost the low-frequency
components of the generated LFP. We further find that these low-frequency
components may be less `local' than the high-frequency LFP components in the
sense that (1) the size of signal-generation region of the LFP recorded at an
electrode is larger and (2) that the LFP generated by a synaptically activated
population spreads further outside the population edge due to volume
conduction
Electrodiffusive model for astrocytic and neuronal ion concentration dynamics
Electrical neural signalling typically takes place at the time-scale of
milliseconds, and is typically modeled using the cable equation. This is a good
approximation for processes when ionic concentrations vary little during the
time course of a simulation. During periods of intense neural signalling,
however, the local extracellular K+ concentration may increase by several
millimolars. Clearance of excess K+ likely depends partly on diffusion in the
extracellular space, partly on local uptake by- and intracellular transport
within astrocytes. This process takes place at the time scale of seconds, and
can not be modeled accurately without accounting for the spatiotemporal
variations in ion concentrations. The work presented here consists of two main
parts: First, we developed a general electrodiffusive formalism for modeling
ion concentration dynamics in a one-dimensional geometry, including both an
intra- and extracellular domain. The formalism was based on the Nernst-Planck
equations. It ensures (i) consistency between the membrane potential and ion
concentrations, (ii) global particle/charge conservation, and (iii) accounts
for diffusion and concentration dependent variations in resistivities. Second,
we applied the formalism to model how astrocytes exchange ions with the ECS,
and identified the key astrocytic mechanisms involved in K+ removal from high
concentration regions. We found that a local increase in extracellular
K\textsuperscript{+} evoked a local depolarization of the astrocyte membrane,
which at the same time (i) increased the local astrocytic uptake of
K\textsuperscript{+}, (ii) suppressed extracellular transport of K+, (iii)
increased transport of K+ within astrocytes, and (iv) facilitated astrocytic
relase of K+ in extracellular low concentration regions. In summary, these
mechanisms seem optimal for shielding the extracellular space from excess K+.Comment: 19 pages, 5 figures, 1 table (Equations 37 & 38 and the two first
equations in Figure 2 were corrected May 30th 2013
A computational analysis of the long-term regulation of arterial pressure
The asserted dominant role of the kidneys in the chronic regulation of blood pressure and in the etiology of hypertension has been debated since the 1970s. At the center of the theory is the observation that the acute relationships between arterial pressure and urine production—the acute pressure-diuresis and pressure-natriuresis curves—physiologically adapt to perturbations in pressure and/or changes in the rate of salt and volume intake. These adaptations, modulated by various interacting neurohumoral mechanisms, result in chronic relationships between water and salt excretion and pressure that are much steeper than the acute relationships. While the view that renal function is the dominant controller of arterial pressure has been supported by computer models of the cardiovascular system known as the “Guyton-Coleman model”, no unambiguous description of a computer model capturing chronic adaptation of acute renal function in blood pressure control has been presented. Here, such a model is developed with the goals of: 1. representing the relevant mechanisms in an identifiable mathematical model; 2. identifying model parameters using appropriate data; 3. validating model predictions in comparison to data; and 4. probing hypotheses regarding the long-term control of arterial pressure and the etiology of primary hypertension. The developed model reveals: long-term control of arterial blood pressure is primarily through the baroreflex arc and the renin-angiotensin system; and arterial stiffening provides a sufficient explanation for the etiology of primary hypertension associated with ageing. Furthermore, the model provides the first consistent explanation of the physiological response to chronic stimulation of the baroreflex
- …