scholarly journals Ca v 3.2 T‐type calcium channel mutation influences kindling‐induced thalamic neuronal firing patterns in Genetic Absence Epilepsy Rats From Strasbourg

Epilepsia ◽  
2019 ◽  
Vol 60 (7) ◽  
pp. 1378-1386 ◽  
Author(s):  
Nihan Çarçak ◽  
Idrish Ali ◽  
Kim Powell ◽  
Thomas Zheng ◽  
Filiz Onat ◽  
...  
Epilepsia ◽  
2014 ◽  
Vol 55 (5) ◽  
pp. 654-665 ◽  
Author(s):  
Nihan Çarçak ◽  
Thomas Zheng ◽  
Idrish Ali ◽  
Ahmad Abdullah ◽  
Chris French ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Fernando R. Fernandez ◽  
Mircea C. Iftinca ◽  
Gerald W. Zamponi ◽  
Ray W. Turner

AbstractT-type calcium channels are important regulators of neuronal excitability. The mammalian brain expresses three T-type channel isoforms (Cav3.1, Cav3.2 and Cav3.3) with distinct biophysical properties that are critically regulated by temperature. Here, we test the effects of how temperature affects spike output in a reduced firing neuron model expressing specific Cav3 channel isoforms. The modeling data revealed only a minimal effect on baseline spontaneous firing near rest, but a dramatic increase in rebound burst discharge frequency for Cav3.1 compared to Cav3.2 or Cav3.3 due to differences in window current or activation/recovery time constants. The reduced response by Cav3.2 could optimize its activity where it is expressed in peripheral tissues more subject to temperature variations than Cav3.1 or Cav3.3 channels expressed prominently in the brain. These tests thus reveal that aspects of neuronal firing behavior are critically dependent on both temperature and T-type calcium channel subtype.


1998 ◽  
Vol 82 (2) ◽  
pp. 215-231 ◽  
Author(s):  
Jin Y. Ro ◽  
Daniel Debowy ◽  
Stanley Lu ◽  
Soumya Ghosh ◽  
Esther P. Gardner

1984 ◽  
Vol 298 (1) ◽  
pp. 75-90 ◽  
Author(s):  
T.J. Marczynski ◽  
L.L. Burns ◽  
G.T. Livezey ◽  
R.L.P. Vimal ◽  
E. Chen

2006 ◽  
Vol 18 (10) ◽  
pp. 1654-1662 ◽  
Author(s):  
Indre V. Viskontas ◽  
Barbara J. Knowlton ◽  
Peter N. Steinmetz ◽  
Itzhak Fried

Different structures within the medial-temporal lobe likely make distinct contributions to declarative memory. In particular, several current psychological and computational models of memory predict that the hippocampus and parahippocampal regions play different roles in the formation and retrieval of declarative memories [e.g., Norman, K. A., & O'Reilly, R. C. Modeling hippocampal and neocortical contributions to recognition memory: A complementary-learning systems approach. Psychological Review, 110, 611–646, 2003]. Here, we examined the neuronal firing patterns in these two regions during recognition memory. Recording directly from neurons in humans, we find that cells in both regions respond to novel stimuli with an increase in firing (excitation). However, already on the second presentation of a stimulus, neurons in these regions show very different firing patterns. In the parahippocampal region there is dramatic decrease in the number of cells responding to the stimuli, whereas in the hippocampus there is recruitment of a large subset of neurons showing inhibitory (decrease from baseline firing) responses. These results suggest that inhibition is a mechanism used by cells in the human hippocampus to support sparse coding in mnemonic processing. The findings also provide further evidence for the division of labor in the medial-temporal lobe with respect to declarative memory processes.


2004 ◽  
Vol 279 (11) ◽  
pp. 9681-9684 ◽  
Author(s):  
Houman Khosravani ◽  
Christophe Altier ◽  
Brett Simms ◽  
Kevin S. Hamming ◽  
Terrance P. Snutch ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
William Plumbly ◽  
Nick Brandon ◽  
Tarek Z. Deeb ◽  
Jeremy Hall ◽  
Adrian J. Harwood

Abstract The combination of in vitro multi-electrode arrays (MEAs) and the neuronal differentiation of stem cells offers the capability to study human neuronal networks from patient or engineered human cell lines. Here, we use MEA-based assays to probe synaptic function and network interactions of hiPSC-derived neurons. Neuronal network behaviour first emerges at approximately 30 days of culture and is driven by glutamate neurotransmission. Over a further 30 days, inhibitory GABAergic signalling shapes network behaviour into a synchronous regular pattern of burst firing activity and low activity periods. Gene mutations in L-type voltage gated calcium channel subunit genes are strongly implicated as genetic risk factors for the development of schizophrenia and bipolar disorder. We find that, although basal neuronal firing rate is unaffected, there is a dose-dependent effect of L-type voltage gated calcium channel inhibitors on synchronous firing patterns of our hiPSC-derived neural networks. This demonstrates that MEA assays have sufficient sensitivity to detect changes in patterns of neuronal interaction that may arise from hypo-function of psychiatric risk genes. Our study highlights the utility of in vitro MEA based platforms for the study of hiPSC neural network activity and their potential use in novel compound screening.


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