scholarly journals The dendritic location of the L-type current and its deactivation by the somatic AHP current both contribute to firing bistability in motoneurons

Author(s):  
Marin Manuel ◽  
Daniel Zytnicki ◽  
Claude Meunier
Keyword(s):  
1999 ◽  
Vol 81 (2) ◽  
pp. 535-543 ◽  
Author(s):  
Erik P. Cook ◽  
Daniel Johnston

Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both αamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid– and N-methyl-d-aspartate–like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials.


2006 ◽  
Vol 95 (3) ◽  
pp. 1295-1297 ◽  
Author(s):  
Idan Segev

This essay looks at the historical significance of four APS classic papers that are freely available online: Rall W. Distinguishing theoretical synaptic potentials computed for different soma-dendritic distributions of synaptic input. J Neurophysiol 30: 1138–1168, 1967 ( http://jn.physiology.org/cgi/reprint/30/5/1138 ). Rall W, Burke RE, Smith TG, Nelson PG, and Frank K. Dendritic location of synapses and possible mechanisms for the monosynaptic EPSP in motoneurons. J Neurophysiol 30: 1169–1193, 1967 ( http://jn.physiology.org/cgi/reprint/30/5/1169 ). Rall W and Shepherd GM. Theoretical reconstruction of field potentials and dendrodendritic synaptic interactions in olfactory bulb. J Neurophysiol 31: 884–915, 1968 ( http://jn.physiology.org/cgi/reprint/31/6/884 ). Segev I and Rall W. Computational study of an excitable dendritic spine. J Neurophysiol 60: 499–523, 1988 ( http://jn.physiology.org/cgi/reprint/60/2/499 ).


2003 ◽  
Vol 90 (3) ◽  
pp. 1807-1816 ◽  
Author(s):  
C. Bernard ◽  
D. Johnston

In hippocampal CA1 pyramidal neurons, action potentials generated in the axon back-propagate in a decremental fashion into the dendritic tree where they affect synaptic integration and synaptic plasticity. The amplitude of back-propagating action potentials (b-APs) is controlled by various biological factors, including membrane potential ( Vm). We report that, at any dendritic location ( x), the transition from weak (small-amplitude b-APs) to strong (large-amplitude b-APs) back-propagation occurs when Vm crosses a threshold potential, θ x. When Vm > θ x, back-propagation is strong (mostly active). Conversely, when Vm < θ x, back-propagation is weak (mostly passive). θ x varies linearly with the distance ( x) from the soma. Close to the soma, θ x ≪ resting membrane potential (RMP) and a strong hyperpolarization of the membrane is necessary to switch back-propagation from strong to weak. In the distal dendrites, θ x ≫ RMP and a strong depolarization is necessary to switch back-propagation from weak to strong. At ∼260 μm from the soma, θ260 ≈ RMP, suggesting that in this dendritic region back-propagation starts to switch from strong to weak. θ x depends on the availability or state of Na+ and K+ channels. Partial blockade or phosphorylation of K+ channels decreases θ x and thereby increases the portion of the dendritic tree experiencing strong back-propagation. Partial blockade or inactivation of Na+ channels has the opposite effect. We conclude that θ x is a parameter that captures the onset of the transition from weak to strong back-propagation. Its modification may alter dendritic function under physiological and pathological conditions by changing how far large action potentials back-propagate in the dendritic tree.


1991 ◽  
Vol 88 (6) ◽  
pp. 2093-2097 ◽  
Author(s):  
H. Tiedge ◽  
R. T. Fremeau ◽  
P. H. Weinstock ◽  
O. Arancio ◽  
J. Brosius
Keyword(s):  

Neuroreport ◽  
2001 ◽  
Vol 12 (16) ◽  
pp. 3503-3507 ◽  
Author(s):  
Illya Kruglikov ◽  
Leonid Shutov ◽  
Evgeniy Potapenko ◽  
Nana Voitenko ◽  
Platon Kostyuk

2008 ◽  
Vol 20 (7) ◽  
pp. 1717-1731 ◽  
Author(s):  
Xiaoshen Li ◽  
Giorgio A. Ascoli

The firing rate of individual neurons depends on the firing frequency of their distributed synaptic inputs, with linear and nonlinear relations subserving different computational functions. This letter explores the relationship between the degree of synchrony among excitatory synapses and the linearity of the response using detailed compartmental models of cortical pyramidal cells. Synchronous input resulted in a linear input-output relationship, while asynchronous stimulation yielded sub- and supraproportional outputs at low and high frequencies, respectively. The dependence of input-output linearity on synchrony was sigmoidal and considerably robust with respect to dendritic location, stimulus irregularity, and alteration of active and synaptic properties. Moreover, synchrony affected firing rate differently at lower and higher input frequencies. A reduced integrate-and-fire model suggested a mechanism explaining these results based on spatiotemporal integration, with fundamental implications relating synchrony to memory encoding.


2021 ◽  
Author(s):  
Julie Haas ◽  
Austin Mendoza

Electrical synapses couple inhibitory neurons across the brain, underlying a variety of functions that are modifiable by activity. Despite recent advances, many basic functions and contributions of electrical synapses within neural circuitry remain underappreciated. Among these is the source and impact of electrical synapse asymmetry. Using multi-compartmental models of neurons coupled through dendritic electrical synapses, we investigated intrinsic factors that contribute to synaptic asymmetry and that result in modulation of spike time between coupled cells. We show that electrical synapse location along a dendrite, input resistance, internal dendritic resistance, or directional conduction of the electrical synapse itself each alter asymmetry as measured by coupling between cell somas. Conversely, true synapse asymmetry can be masked by each of these properties. Furthermore, we show that asymmetry alters the spiking timing and latency of coupled cells by up to tens of milliseconds, depending on direction of conduction or dendritic location of the electrical synapse. These simulations illustrate that causes of asymmetry are multifactorial, may not be apparent in somatic measurements of electrical coupling, influence dendritic processing, and produce a variety of outcomes on spike timing of coupled cells. Our findings highlight aspects of electrical synapses that should be considered in experimental demonstrations of coupling, and when assembling networks containing electrical synapses.


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