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A computational model of neuro-glio-vascular loop interactions.
No full textWe present a computational, biophysical model of neuron-astrocyte-vessel interaction. Unlike other cells, neurons convey "hunger" signals to the vascular network via an intervening layer of glial cells (astrocytes); vessels dilate and release glucose which fuels neuronal firing. Existing computational models focus on only parts of this loop (neuron→astrocyte→vessel→neuron), whereas the proposed model describes the entire loop. Neuronal firing causes release of a neurotransmitter like glutamate which triggers release of vasodilator by astrocytes via a cascade of biochemical events. Vasodilators released from astrocytic endfeet cause blood vessels to dilate and release glucose into the interstitium, part of which is taken up by the astrocyticendfeet. Glucose is converted into lactate in the astrocyte and transported into the neuron. Glucose from the interstitium and lactate (produced from glucose) influx from astrocyte are converted into ATP in the neuron. Neuronal ATP is used to drive the Na(+)/K(+)ATPase pumps, which maintain ionic gradients necessary for neuronal firing. When placed in the metabolic loop, the neuron exhibits sustained firing only when the stimulation current is more than a minimum threshold. For various combinations of initial neuronal [ATP] and external current, the neuron exhibits a variety of firing patterns including sustained firing, firing after an initial pause, burst firing etc. Neurovascular interactions under conditions of constricted vessels are also studied. Most models of cerebral circulation describe neurovascular interactions exclusively in the "forward" neuron→vessel direction. The proposed model indicates possibility of "reverse" influence also, with vasomotion rhythms influencing neural firing patterns. Another idea that emerges out of the proposed work is that brain's computations may be more comprehensively understood in terms of neuro-glial-vascular dynamics and not in terms of neural firing alone
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Simulation results depicting variation of (a) Neuronal <i>Ca<sup>2</sup></i>
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<sup><b>+</b></sup><b> concentration along with (b) as reported in </b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0048802#pone.0048802-Lee1" target="_blank">[<b>25</b>]</a><b>.</b></p
Schematic representation of induced vessel oscillations.
No full text<p>Vessel dynamics are externally supplied and vessel activation due to astrocyte is blocked.</p
Dorsal Root Ganglion Stimulation Relieves Chronic Neuropathic Pain Along With a Decrease in Cortical γ Power
No full text(a) Induced vessel oscillation at 0.2 Hz with vessel dilation for 0.5 s and corresponding (b) change in neuronal membrane potential bound by reversal potential of sodium and potassium channel.
No full text<p>(a) Induced vessel oscillation at 0.2 Hz with vessel dilation for 0.5 s and corresponding (b) change in neuronal membrane potential bound by reversal potential of sodium and potassium channel.</p
(a) Neuronal membrane potential bound by reversal potential of sodium and potassium channel along with (b) corresponding change in extracellular [EET] and subsequently the vessel radius.
No full text<p>(a) Neuronal membrane potential bound by reversal potential of sodium and potassium channel along with (b) corresponding change in extracellular [EET] and subsequently the vessel radius.</p
(A) Neuronal membrane potential bound by reversal potential of sodium and potassium channel, (B) <i>Na</i><sup>+</sup>/<i>K</i><sup>+</sup> ATPase pump current, <i>Na</i><sup>+</sup> (+ve) pump current and <i>K</i><sup>+</sup> (−ve) pump current. (C) astrocytic<i>IP<sub>3</sub></i> and <i>Ca<sup>2</sup></i>
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<sup><b>+</b></sup><b> concentration and the corresponding (D) </b><b><i>EET</i></b><b> released. (E) vessel radius, (F) glucose (</b><b><i>Glc</i></b><b>) and lactate (</b><b><i>Lac</i></b><b>) concentration in astrocyte. (G) glucose (</b><b><i>Glc</i></b><b>) and lactate (</b><b><i>Lac</i></b><b>) concentration in neuron along with (H) cytosolic </b><b><i>ATP</i></b><b> concentration in neuron.</b></p
Regimes obtained for various combinations of stimulation current (I<sub>S</sub>) and initial [ATP].
No full text<p>(1) Bursting, (2)Transition phase from bursting to firing with initial pause, (3) Firing with initial pause and (4) Continuous firing.</p
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