Analysis of plasma membrane Ca2+-ATPase gene expression during epileptogenesis employing single hippocampal CA1 neurons

2011 ◽  
Vol 236 (4) ◽  
pp. 409-417 ◽  
Author(s):  
Jorge Bravo-Martínez ◽  
Blanca Delgado-Coello ◽  
David E García ◽  
Jaime Mas-Oliva
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Atpase Gene

scholarly journals Calcium Movement in Ischemia-Tolerant Hippocampal CA1 Neurons after Transient Forebrain Ischemia in Gerbils

1996 ◽  
Vol 16 (5) ◽  
pp. 915-922 ◽  
Author(s):  
Shinsuke Ohta ◽  
Shigeru Furuta ◽  
Ichiro Matsubara ◽  
Keiji Kohno ◽  
Yoshiaki Kumon ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Neuronal Death ◽  
Pyramidal Neurons ◽  
Forebrain Ischemia ◽  
Electron Microscopic ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Before And After ◽  
Intracellular Ca

Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ischemia, acquired tolerance to a subsequent lethal 5-min period of ischemia, which usually causes delayed-type neuronal death. Intracelluar Ca2+ movements before and after the 5 min of forebrain ischemia were evaluated in gerbil hippocampal CA1 pyramidal neurons, had acquired tolerance in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distribution and the Ca2+ adenosine triphosphatase (Ca2+-ATPase) activity using electron microscopic cytochemistry. In comparison with nonischemia-tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons sequestered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapidly decreased. Plasma membrane Ca2+-ATPase activities were already significantly elevated before the 5 min of ischemia, and remained at a higher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca2+-ATPase activities in ischemia-tolerant CA1 neurons after the 5-min period of ischemia showed a strong resemblance to those in CA3 neurons, which originally possess resistance to such periods of ischemia. These findings suggest that enhanced or maintained activities of mitochondrial Ca2+ sequestration and plasma membrane Ca2+-ATPase reduced Ca2+ toxicity following 5-min ischemia in terms of time, resulting in escape from delayed neuronal death.

Ischemic preconditioning protects the hippocampal CA1 neurons by inhibiting synaptic activity in rat

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S300-S300
Author(s):  
Thomas J Sick ◽  
Ami P Raval ◽  
Isabel Saul ◽  
Kunjan R Dave ◽  
Raul Busto ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Synaptic Activity ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

Plasma Membrane Calcium ATPase Gene Expression in Bovine Lens Epithelium

2000 ◽  
Vol 32 (2-3) ◽  
pp. 100-105 ◽  
Author(s):  
Lijun Bian ◽  
Junwen Zeng ◽  
Douglas Borchman ◽  
Christopher A. Paterson
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Calcium Atpase ◽  
Lens Epithelium ◽  
Plasma Membrane Calcium Atpase ◽  
Bovine Lens ◽  
Atpase Gene

Diazepam delays the death of hippocampal CA1 neurons following global ischemia

2008 ◽  
Vol 214 (2) ◽  
pp. 309-314 ◽  
Author(s):  
Dale Corbett ◽  
Jennifer Larsen ◽  
Kristopher D. Langdon
Keyword(s):  
Global Ischemia ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1
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