Calcium conductance of acetylcholine-induced endplate channels

Nature ◽  
1979 ◽  
Vol 279 (5714) ◽  
pp. 638-639 ◽  
Author(s):  
P. D. BREGESTOVSKI ◽  
R. MILEDI ◽  
I. PARKER
Keyword(s):  
Calcium Conductance

scholarly journals Selective increase in T-type calcium conductance of reticular thalamic neurons in a rat model of absence epilepsy

1995 ◽  
Vol 15 (4) ◽  
pp. 3110-3117 ◽  
Author(s):  
E Tsakiridou ◽  
L Bertollini ◽  
M de Curtis ◽  
G Avanzini ◽  
HC Pape
Keyword(s):  
Rat Model ◽  
Absence Epilepsy ◽  
Thalamic Neurons ◽  
Calcium Conductance ◽  
Selective Increase

scholarly journals Potentiation by Endotoxin of Responses Associated with Increases in Calcium Conductance

1973 ◽  
Vol 70 (12) ◽  
pp. 3301-3304 ◽  
Author(s):  
J. Connor ◽  
J. Fine ◽  
K. Kusano ◽  
M. J. Mccrea ◽  
I. Parnas ◽  
...  
Keyword(s):  
Calcium Conductance

Low-Voltage-Activated Calcium Channels in the Lamprey Locomotor Network: Simulation and Experiment

1997 ◽  
Vol 77 (4) ◽  
pp. 1795-1812 ◽  
Author(s):  
Jesper Tegnér ◽  
Jeanette Hellgren-Kotaleski ◽  
Anders Lansner ◽  
Sten Grillner
Keyword(s):  
Calcium Channels ◽  
Simulation Model ◽  
Calcium Current ◽  
Low Voltage ◽  
Network Simulation ◽  
Receptor Activation ◽  
Burst Frequency ◽  
Calcium Conductance ◽  
Simulation And Experiment ◽  
Rebound Firing

Tegnér, Jesper, Jeanette Hellgren-Kotaleski, Anders Lansner, and Sten Grillner. Low-voltage-activated calcium channels in the lamprey locomotor network: simulation and experiment. J. Neurophysiol. 77: 1795–1812, 1997. To evaluate the role of low-voltage-activated (LVA) calcium channels in the lamprey spinal locomotor network, a previous computer simulation model has been extended to include LVA calcium channels. It is also of interest to explore the consequences of a LVA conductance for the electrical behavior of the single neuron. The LVA calcium channel was modeled with voltage-dependent activation and inactivation using the m 3 h form, following a Hodgkin-Huxley paradigm. Experimental data from lamprey neurons was used to provide parameter values of the single cell model. The presence of a LVA calcium conductance in the model could account for the occurrence of a rebound depolarization in the simulation model. The influence of holding potential on the occurrence of a rebound as well the latency at which it is elicited was investigated and compared with previous experiments. The probability of a rebound increased at a more depolarized holding potential and the latency was also reduced under these conditions. Furthermore, the effect of changing the holding potential and the reversal potential of the calcium dependent potassium conductance were tested to determine under which conditions several rebound spikes could be elicited after a single inhibitory pulse in the simulation model. A reduction of the slow afterhyperpolarization (sAHP) after the action potential reduced the tendency for a train of rebound spikes. The experimental effects of γ-aminobutyric acid-B(GABAB) receptor activation were simulated by reducing the maximal LVA calcium conductance. A reduced tendency for rebound firing and a slower rising phase with sinusoidal current stimulation was observed, in accordance with earlier experiments. The effect of reducing the slow afterhyperpolarization and reducing the LVA calcium current was tested experimentally in the lamprey spinal cord, during N-methyl-d-aspartate (NMDA)-induced fictive locomotion. The reduction of burst frequency was more pronounced with GABAB agonists than with apamin (inhibitor of K(Ca) current) when using high NMDA concentration (high burst frequency). The burst frequency increased after the addition of a LVA calcium current to the simulated segmental network, due to a faster recovery during the inhibitory phase as the activity switches between the sides. This result is consistent with earlier experimental findings because GABAB receptor agonists reduce the locomotor frequency. These results taken together suggest that the LVA calcium channels contribute to a larger degree with respect to the burst frequency regulation than the sAHP mechanism at higher burst frequencies. The range in which a regular burst pattern can be simulated is extended in the lower range by the addition of LVA calcium channels, which leads to more stable activity at low locomotor frequencies. We conclude that the present model can account for rebound firing and trains of rebound spikes in lamprey neurons. The effects of GABAB receptor activation on the network level is consistent with a reduction of the calcium current through LVA calcium channels even though GABAB receptor activation will affect the sAHP indirectly and also presynaptic inhibition.

Increased Synchrony with Increase of a Low-Threshold Calcium Conductance in a Model Thalamic Network: A Phase-Shift Mechanism

2000 ◽  
Vol 12 (7) ◽  
pp. 1553-1571 ◽  
Author(s):  
Elizabeth Thomas ◽  
Thierry Grisar
Keyword(s):  
Phase Shift ◽  
Computer Model ◽  
Calcium Current ◽  
Epileptic Activity ◽  
Absence Epilepsy ◽  
Similar Increase ◽  
Calcium Conductance ◽  
Synchronous Firing ◽  
Low Threshold Spike ◽  
Low Threshold

A computer model of a thalamic network was used in order to examine the effects of an isolated augmentation in a low-threshold calcium current. Such an isolated augmentation has been observed in the reticular thalamic (RE) nucleus of the genetic absence epilepsy rat from the Strasbourg (GAERS) model of absence epilepsy. An augmentation of the low-threshold calcium conductance in the RE neurons (gTs) of the model thalamic network was found to lead to an increase in the synchronized firing of the network. This supports the hypothesis that the isolated increase in gTs may be responsible for epileptic activity in the GAERS rat. The increase of gTs in the RE neurons led to a slight increase in the period of the isolated RE neuron firing. In contrast, the low-threshold spike of the RE neuron remained relatively unchanged by the increase of gTs. This suggests that the enhanced synchrony in the network was primarily due to a phase shift in the firing of the RE neurons with respect to the thalamocortical neurons. The ability of this phase-shift mechanism to lead to changes in synchrony was further examined using the model thalamic network. A similar increase in the period of RE neuron oscillations was obtained through an increase in the conductance of the calcium-mediated potassium channel. This change was once again found to increase synchronous firing in the network.

Sign in / Sign up

Export Citation Format

Share Document