Publications by authors named "David L Boothe"

Large cortical and hippocampal pyramidal neurons are elements of neuronal circuitry that have been implicated in cross-frequency coupling (CFC) during cognitive tasks. We investigate potential mechanisms for CFC within these neurons by examining the role that the hyperpolarization-activated mixed cation current (I) plays in modulating CFC characteristics in multicompartment neuronal models. We quantify CFC along the soma-apical dendrite axis and tuft of three models configured to have different spatial distributions of I conductance density: (1) exponential gradient along the soma-apical dendrite axis, (2) uniform distribution, and (3) no I conductance.

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In this paper, we evaluate the computational performance of the GEneral NEural SImulation System (GENESIS) for large scale simulations of neural networks. While many benchmark studies have been performed for large scale simulations with leaky integrate-and-fire neurons or neuronal models with only a few compartments, this work focuses on higher fidelity neuronal models represented by 50-74 compartments per neuron. After making some modifications to the source code for GENESIS and its parallel implementation, PGENESIS, particularly to improve memory usage, we find that PGENESIS is able to efficiently scale on supercomputing resources to network sizes as large as 9 × 10 neurons with 18 × 10 synapses and 2.

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Evidence suggests that layer 5 pyramidal neurons can be divided into functional zones with unique afferent connectivity and membrane characteristics that allow for post-synaptic integration of feedforward and feedback inputs. To assess the existence of these zones and their interaction, we characterized the resonance properties of a biophysically-realistic compartmental model of a neocortical layer 5 pyramidal neuron. Consistent with recently published theoretical and empirical findings, our model was configured to have a "hot zone" in distal apical dendrite and apical tuft where both high- and low-threshold Ca ionic conductances had densities 1-2 orders of magnitude higher than anywhere else in the apical dendrite.

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Within multiscale brain dynamics, the structure-function relationship between cellular changes at a lower scale and coordinated oscillations at a higher scale is not well understood. This relationship may be particularly relevant for understanding functional impairments after a mild traumatic brain injury (mTBI) when current neuroimaging methods do not reveal morphological changes to the brain common in moderate to severe TBI such as diffuse axonal injury or gray matter lesions. Here, we created a physiology-based model of cerebral cortex using a publicly released modeling framework (GEneral NEural SImulation System) to explore the possibility that performance deficits characteristic of blast-induced mTBI may reflect dysfunctional, local network activity influenced by microscale neuronal damage at the cellular level.

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The motor output for walking is produced by a network of neurons termed the spinal central pattern generator (CPG) for locomotion. The basic building block of this CPG is a half-center oscillator composed of two mutually inhibitory sets of interneurons, each controlling one of the two dominant phases of locomotion: flexion and extension. To investigate symmetry between the two components of this oscillator, we analyzed the statistics of natural variation in timing during fictive locomotion induced by stimulation of the midbrain locomotor region in the cat.

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The output of the spinal central pattern generator for locomotion falls into two broad categories: alternation between antagonistic muscles and double bursting within muscles acting on multiple joints. We first model an alternating half-center and then present two different models of double bursting. The first double-bursting model consists of a central clock with an explicit one-to-one mapping between interneuron activity and model output.

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