Abstract:
:Glycogen synthase kinase-3 (GSK3) has been implicated in major neurological disorders, but its role in normal neuronal function is largely unknown. Here we show that GSK3beta mediates an interaction between two major forms of synaptic plasticity in the brain, N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) and NMDA receptor-dependent long-term depression (LTD). In rat hippocampal slices, GSK3beta inhibitors block the induction of LTD. Furthermore, the activity of GSK3beta is enhanced during LTD via activation of PP1. Conversely, following the induction of LTP, there is inhibition of GSK3beta activity. This regulation of GSK3beta during LTP involves activation of NMDA receptors and the PI3K-Akt pathway and disrupts the ability of synapses to undergo LTD for up to 1 hr. We conclude that the regulation of GSK3beta activity provides a powerful mechanism to preserve information encoded during LTP from erasure by subsequent LTD, perhaps thereby permitting the initial consolidation of learnt information.
journal_name
Neuronjournal_title
Neuronauthors
Peineau S,Taghibiglou C,Bradley C,Wong TP,Liu L,Lu J,Lo E,Wu D,Saule E,Bouschet T,Matthews P,Isaac JT,Bortolotto ZA,Wang YT,Collingridge GLdoi
10.1016/j.neuron.2007.01.029subject
Has Abstractpub_date
2007-03-01 00:00:00pages
703-17issue
5eissn
0896-6273issn
1097-4199pii
S0896-6273(07)00070-0journal_volume
53pub_type
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