Calbindin D28K Overexpression Protects Striatal Neurons From Transient Focal Cerebral Ischemia

Calbindin d28k overexpression protects striatal neurons from transient focal cerebral ischemia.

BACKGROUND AND PURPOSE Increased intracellular calcium accumulation is known to potentiate ischemic injury. Whether endogenous calcium-binding proteins can attenuate this injury has not been clearly established, and existing data are conflicting. Calbindin D28K (CaBP) is one such intracellular calcium buffer. We investigated whether CaBP overexpression is neuroprotective against transient focal...

Ferulic Acid Modulates Calbindin-D28K Expression in Focal Cerebral Ischemia and Glutamate-Exposed HT22 Cells

Calbindin-D28k is a calcium-binding protein that mediates intracellular calcium concentrations and exerts a neuroprotective effect against ischemic injury. Ferulic acid provides a neuroprotective effect against focal cerebral ischemia through its anti-oxidative and anti-inflammatory mechanisms. In this study, we investigated whether ferulic acid regulates calbindin-D28k expression during focal ...

Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia

Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning (2-minute transient cerebral ischemia) on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subseque...

Inhibitory Synaptic Transmission in Striatal Neurons after Transient Cerebral Ischemia

Research Paper: Optimization of Transient Focal Cerebral Ischemia Model by Middle Cerebral Artery Occlusion

Introduction: Cerebral ischemia is one of the most common causes of death in human populations in the industrial communities. The need for animal models is inevitable to study the pathophysiology and treatment of cerebral ischemia in human. The current study aimed at evaluating the strengths and weaknesses of different techniques used to create ischemia in previous studies and optimizing the tr...