scholarly journals Somatic modulation of ectopic action potential initiation in distal axons

2018 ◽  
Vol 596 (21) ◽  
pp. 5067-5068
Author(s):  
Aurélie Fékété ◽  
Dominique Debanne
Keyword(s):  
Action Potential ◽  
Action Potential Initiation ◽  
Potential Initiation

scholarly journals Differential Effects of Axon Initial Segment and Somatodendritic GABAA Receptors on Excitability Measures in Rat Dentate Granule Neurons

2011 ◽  
Vol 105 (1) ◽  
pp. 366-379 ◽  
Author(s):  
Patricio Rojas ◽  
Alejandro Akrouh ◽  
Lawrence N. Eisenman ◽  
Steven Mennerick
Keyword(s):  
Action Potential ◽  
Initial Segment ◽  
Input Resistance ◽  
Receptor Activation ◽  
Axon Initial Segment ◽  
Granule Neurons ◽  
Voltage Threshold ◽  
Granule Neuron ◽  
Action Potential Initiation ◽  
Potential Initiation

GABAA receptors are found on the somatodendritic compartment and on the axon initial segment of many principal neurons. The function of axonal receptors remains obscure, although it is widely assumed that axonal receptors must have a strong effect on excitability. We found that activation of GABAA receptors on the dentate granule neuron axon initial segment altered excitability by depolarizing the voltage threshold for action potential initiation under conditions that minimally affected overall cell input resistance. In contrast, activation of somatic GABAA receptors strongly depressed the input resistance of granule neurons without affecting the voltage threshold of action potential initiation. Although these effects were observed over a range of intracellular chloride concentrations, average voltage threshold was unaffected when ECl rendered GABAA axon initial segment responses explicitly excitatory. A compartment model of a granule neuron confirmed these experimental observations. Low ambient agonist concentrations designed to activate granule neuron tonic currents did not stimulate axonal receptors sufficiently to raise voltage threshold. Using excitatory postsynaptic current (EPSC)-like depolarizations, we show physiological consequences of axonal versus somatic GABAA receptor activation. With axonal inhibition, individual excitatory postsynaptic potentials (EPSPs) largely retained their amplitude and time course, but EPSPs that were suprathreshold under basal conditions failed to reach threshold with GABAA activation. By contrast, somatic inhibition depressed individual EPSPs because of strong shunting. Our results suggest that axonal GABAA receptors have a privileged effect on voltage threshold and that two major measures of neuronal excitability, voltage threshold and rheobase, are differentially affected by axonal and somatic GABAA receptor activation.

Determinants of action potential initiation in isolated rabbit atrial and ventricular myocytes

1998 ◽  
Vol 274 (6) ◽  
pp. H1902-H1913 ◽  
Author(s):  
David A. Golod ◽  
Rajiv Kumar ◽  
Ronald W. Joyner
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Cell Types ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Isolated Cells ◽  
Atrial Cells ◽  
Ventricular Cells ◽  
Action Potential Initiation ◽  
Potential Initiation

Action potential conduction through the atrium and the ventricle of the heart depends on the membrane properties of the atrial and ventricular cells, particularly with respect to the determinants of the initiation of action potentials in each cell type. We have utilized both current- and voltage-clamp techniques on isolated cells to examine biophysical properties of the two cell types at physiological temperature. The resting membrane potential, action potential amplitude, current threshold, voltage threshold, and maximum rate of rise measured from atrial cells (−80 ± 1 mV, 109 ± 3 mV, 0.69 ± 0.05 nA, −59 ± 1 mV, and 206 ± 17 V/s, respectively; means ± SE) differed significantly ( P < 0.05) from those values measured from ventricular cells (−82.7 ± 0.4 mV, 127 ± 1 mV, 2.45 ± 0.13 nA, −46 ± 2 mV, and 395 ± 21 V/s, respectively). Input impedance, capacitance, time constant, and critical depolarization for activation also were significantly different between atrial (341 ± 41 MΩ, 70 ± 4 pF, 23.8 ± 2.3 ms, and 19 ± 1 mV, respectively) and ventricular (16.5 ± 5.4 MΩ, 99 ± 4.3 pF, 1.56 ± 0.32 ms, and 36 ± 1 mV, respectively) cells. The major mechanism of these differences is the much greater magnitude of the inward rectifying potassium current in ventricular cells compared with that in atrial cells, with an additional difference of an apparently lower availability of inward Na current in atrial cells. These differences in the two cell types may be important in allowing the atrial cells to be driven successfully by normal regions of automaticity (e.g., the sinoatrial node), whereas ventricular cells would suppress action potential initiation from a region of automaticity (e.g., an ectopic focus).

Transduction mechanisms in airway sensory nerves

2006 ◽  
Vol 101 (3) ◽  
pp. 950-959 ◽  
Author(s):  
Thomas Taylor-Clark ◽  
Bradley J. Undem
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Membrane Depolarization ◽  
Sensory Nerves ◽  
Metabotropic Receptors ◽  
Metabotropic Receptor ◽  
Transduction Mechanisms ◽  
The Central Nervous System ◽  
Action Potential Initiation ◽  
Potential Initiation

The induction of action potentials in airway sensory nerves relies on events leading to the opening of cation channels in the nerve terminal membrane and subsequent membrane depolarization. If the membrane depolarization is of sufficient rate and amplitude, action potential initiation will occur. The action potentials are then conducted to the central nervous system, leading to the initiation of various sensations and cardiorespiratory reflexes. Triggering events in airway sensory nerves include mechanical perturbation, inflammatory mediators, pH, temperature, and osmolarity acting through a variety of ionotropic and metabotropic receptors. Action potential initiation can be modulated (positively or negatively) through independent mechanisms caused mainly by autacoids and other metabotropic receptor ligands. Finally, gene expression of sensory nerves can be altered in adult mammals. This neuroplasticity can change the function of sensory nerves and likely involve both neurotrophin and use-dependent mechanisms. Here we provide a brief overview of some of the transduction mechanisms underlying these events.

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