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Targeting the interaction of GABA receptors with CaMKII with an interfering peptide restores receptor expression after cerebral ischemia and inhibits progressive neuronal death in mouse brain cells and slices

Brain Pathol. 2022-06; 
Karthik Balakrishnan, Mohammad Hleihil, Musadiq A Bhat, Robert P Ganley, Markus Vaas, Jan Klohs, Hanns Ulrich Zeilhofer, Dietmar Benke
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Proteins, Expression, Isolation and Analysis … directed against the N-terminus of GABAB1b (affinity-purified, 1:100 for IF; custom made by GenScript) [26], rabbit GABAB2 directed against the N-terminus of GABAB2 (affinity-purified, … Get A Quote

摘要

Cerebral ischemia is the leading cause for long-term disability and mortality in adults due to massive neuronal death. Currently, there is no pharmacological treatment available to limit progressive neuronal death after stroke. A major mechanism causing ischemia-induced neuronal death is the excessive release of glutamate and the associated overexcitation of neurons (excitotoxicity). Normally, GABA receptors control neuronal excitability in the brain via prolonged inhibition. However, excitotoxic conditions rapidly downregulate GABA receptors via a CaMKII-mediated mechanism and thereby diminish adequate inhibition that could counteract neuronal overexcitation and neuronal death. To prevent the deleterious downr... More

關鍵詞

CaMKII, GABAB receptor, cerebral ischemia, interfering peptide, neuroprotection
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