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Transport of AMPA receptors during long-term potentiation is impaired in rats with hepatic encephalopathy.

Authors: Monfort, P  Piedrafita, B  Felipo, V 
Citation: Monfort P, etal., Neurochem Int. 2009 Dec;55(7):514-20. Epub 2009 May 18.
Pubmed: (View Article at PubMed) PMID:19450629
DOI: Full-text: DOI:10.1016/j.neuint.2009.05.006

Cognitive function is impaired in patients with hepatic encephalopathy. Learning ability is also impaired in rats with hepatic encephalopathy due to portacaval shunts. Long-term potentiation (LTP) in hippocampus, considered the basis of some forms of learning and memory, is impaired in rats with portacaval shunt. We analyzed the mechanisms by which LTP is impaired in these rats. In control rats, application of the tetanus to induce LTP increases phosphorylation of Thr286 of calcium-calmodulin dependent protein kinase II. This activates the kinase which phosphorylates the GluR1 subunit of AMPA receptors in Ser831 and induces its translocation to the post-synaptic densities. All these steps are completely prevented in rats with hepatic encephalopathy in which the tetanus does not induce phosphorylation of CaMKII or GluR1 nor translocation of this subunit to the post-synaptic membrane. This would explain the impairment in LTP in these rats.

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CRRD Object Information
CRRD ID: 4108489
Created: 2010-07-26
Species: All species
Last Modified: 2010-07-26
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.