Effects of volatile anaesthetics on a high conductance calcium dependent potassium channel in cultured hippocampal neurons

1998 ◽  
Vol 100-101 ◽  
pp. 271-276 ◽  
Author(s):  
James McLarnon ◽  
Dale Sawyer
Keyword(s):  
Potassium Channel ◽  
Hippocampal Neurons ◽  
Volatile Anaesthetics ◽  
Calcium Dependent ◽  
High Conductance ◽  
Cultured Hippocampal Neurons

scholarly journals Amyloid-β oligomers induce tau-independent disruption of BDNF axonal transport via calcineurin activation in cultured hippocampal neurons

2013 ◽  
Vol 24 (16) ◽  
pp. 2494-2505 ◽  
Author(s):  
Elisa M. Ramser ◽  
Kathlyn J. Gan ◽  
Helena Decker ◽  
Emily Y. Fan ◽  
Matthew M. Suzuki ◽  
...  
Keyword(s):  
Axonal Transport ◽  
Hippocampal Neurons ◽  
Glycogen Synthase ◽  
Amyloid Β ◽  
Protein Phosphatase 1 ◽  
Organelle Transport ◽  
Calcium Dependent ◽  
Pathological Event ◽  
Cultured Hippocampal Neurons

Disruption of fast axonal transport (FAT) is an early pathological event in Alzheimer's disease (AD). Soluble amyloid-β oligomers (AβOs), increasingly recognized as proximal neurotoxins in AD, impair organelle transport in cultured neurons and transgenic mouse models. AβOs also stimulate hyperphosphorylation of the axonal microtubule-associated protein, tau. However, the role of tau in FAT disruption is controversial. Here we show that AβOs reduce vesicular transport of brain-derived neurotrophic factor (BDNF) in hippocampal neurons from both wild-type and tau-knockout mice, indicating that tau is not required for transport disruption. FAT inhibition is not accompanied by microtubule destabilization or neuronal death. Significantly, inhibition of calcineurin (CaN), a calcium-dependent phosphatase implicated in AD pathogenesis, rescues BDNF transport. Moreover, inhibition of protein phosphatase 1 and glycogen synthase kinase 3β, downstream targets of CaN, prevents BDNF transport defects induced by AβOs. We further show that AβOs induce CaN activation through nonexcitotoxic calcium signaling. Results implicate CaN in FAT regulation and demonstrate that tau is not required for AβO-induced BDNF transport disruption.

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