Making the T-Type Even Tinier: Corticotropin-Releasing Factor-Mediated Inhibition of Low-Voltage-Activated Calcium Channel Activity: Fig. 1.

2008 ◽  
Vol 73 (6) ◽  
pp. 1589-1591 ◽  
Author(s):  
Diego L. Varela ◽  
Tamara Hermosilla ◽  
Gerald W. Zamponi
Keyword(s):  
Calcium Channel ◽  
Low Voltage ◽  
Corticotropin Releasing Factor ◽  
Channel Activity

Rebound excitation triggered by synaptic inhibition in cerebellar nuclear neurons is suppressed by selective T-type calcium channel block

2011 ◽  
Vol 106 (5) ◽  
pp. 2653-2661 ◽  
Author(s):  
Rebecca Boehme ◽  
Victor N. Uebele ◽  
John J. Renger ◽  
Christine Pedroarena
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Low Voltage ◽  
Chloride Ions ◽  
Synaptic Inhibition ◽  
Channel Activity ◽  
Electrophysiological Properties ◽  
Low Threshold ◽  
Whole Cell Recordings ◽  
Rebound Excitation

Following hyperpolarizing inputs, many neurons respond with an increase in firing rate, a phenomenon known as rebound excitation. Rebound excitation has been proposed as a mechanism to encode and process inhibitory signals and transfer them to target structures. Activation of low-voltage-activated T-type calcium channels and the ensuing low-threshold calcium spikes is one of the mechanisms proposed to support rebound excitation. However, there is still not enough evidence that the hyperpolarization provided by inhibitory inputs, particularly those dependent on chloride ions, is adequate to deinactivate a sufficient number of T-type calcium channels to drive rebound excitation on return to baseline. Here, this issue was investigated in the deep cerebellar nuclear neurons (DCNs), which receive the output of the cerebellar cortex conveyed exclusively by the inhibitory Purkinje cells and are also known to display rebound excitation. Using cerebellar slices and whole cell recordings of large DCNs, we show that a novel piperidine-based compound that selectively antagonizes T-type calcium channel activity, 3,5-dichloro- N-[1-(2,2-dimethyl-tetrahydropyran-4-ylmethyl)-4-fluoro-piperidin-4-ylmethyl]-benzamide (TTA-P2), suppressed rebound excitation elicited by current injection as well as by synaptic inhibition, whereas other electrophysiological properties of large DCNs were unaltered. Furthermore, TTA-P2 suppressed transient high-frequency rebounds found in DCNs with low-threshold spikes as well as the slow rebounds present in DCNs without low-threshold spikes. These findings demonstrate that chloride-dependent synaptic inhibition effectively triggers T-type calcium channel-mediated rebounds and that the latter channels may support slow rebound excitation in neurons without low-threshold spikes.

scholarly journals Glucose-6-Phosphate Dehydrogenase and NADPH Redox Regulates Cardiac Myocyte L-Type Calcium Channel Activity and Myocardial Contractile Function

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e45365 ◽  
Author(s):  
Dhwajbahadur K. Rawat ◽  
Peter Hecker ◽  
Makino Watanabe ◽  
Sukrutha Chettimada ◽  
Richard J. Levy ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Cardiac Myocyte ◽  
Contractile Function ◽  
Channel Activity ◽  
Myocardial Contractile ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Peptide potentiation of calcium channel activity can be seasonally variable

1991 ◽  
Vol 156 (1) ◽  
pp. 607-610
Author(s):  
CA Bishop ◽  
ME Krouse ◽  
JJ Wine
Keyword(s):  
Calcium Channel ◽  
Channel Activity
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