lithium-chloride and Brain-Infarction

lithium-chloride has been researched along with Brain-Infarction* in 1 studies

Other Studies

1 other study(ies) available for lithium-chloride and Brain-Infarction

Article	Year
Lithium-induced activation of Akt and CaM kinase II contributes to its neuroprotective action in a rat microsphere embolism model. Brain research, 2006, Sep-07, Volume: 1108, Issue:1 Lithium used in bipolar mood disorder therapy protects neurons from brain ischemic cell death. Here, we documented that lithium administration under microsphere-embolism (ME)-induced brain ischemia restored decreased protein kinase B (Akt) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activities 24 h after ischemia in rat brain. Akt activation was associated with increased phosphorylation of its potential targets forkhead transcription factor (FKHR) and glycogen synthase kinase-3beta (GSK-3beta). In parallel with decreased CaMKII autophosphorylation, we also found marked dephosphorylation of tau proteins 24-72 h after ME. Increased protein phosphatase 2A (PP2A) activity was found 24 h after ME. Inhibition of increased PP2A activity by lithium treatment apparently mediated restored tau phosphorylation. Taken together, activation of Akt and CaMKII by lithium was associated with neuroprotective activity in ME-induced neuronal injury. Topics: Animals; Antimanic Agents; Brain Infarction; Brain Ischemia; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases; Disease Models, Animal; Enzyme Activation; Forkhead Transcription Factors; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Intracranial Embolism; Lithium Chloride; Male; Nerve Tissue Proteins; Neuroprotective Agents; Phosphoprotein Phosphatases; Protein Phosphatase 2; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Serine; tau Proteins; Up-Regulation	2006

Article

Year

Lithium-induced activation of Akt and CaM kinase II contributes to its neuroprotective action in a rat microsphere embolism model.

Brain research, 2006, Sep-07, Volume: 1108, Issue:1

Lithium used in bipolar mood disorder therapy protects neurons from brain ischemic cell death. Here, we documented that lithium administration under microsphere-embolism (ME)-induced brain ischemia restored decreased protein kinase B (Akt) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activities 24 h after ischemia in rat brain. Akt activation was associated with increased phosphorylation of its potential targets forkhead transcription factor (FKHR) and glycogen synthase kinase-3beta (GSK-3beta). In parallel with decreased CaMKII autophosphorylation, we also found marked dephosphorylation of tau proteins 24-72 h after ME. Increased protein phosphatase 2A (PP2A) activity was found 24 h after ME. Inhibition of increased PP2A activity by lithium treatment apparently mediated restored tau phosphorylation. Taken together, activation of Akt and CaMKII by lithium was associated with neuroprotective activity in ME-induced neuronal injury.

Topics: Animals; Antimanic Agents; Brain Infarction; Brain Ischemia; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases; Disease Models, Animal; Enzyme Activation; Forkhead Transcription Factors; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Intracranial Embolism; Lithium Chloride; Male; Nerve Tissue Proteins; Neuroprotective Agents; Phosphoprotein Phosphatases; Protein Phosphatase 2; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Serine; tau Proteins; Up-Regulation

2006