There is an article in Neuron magazine published in 2007 that conclude that We conclude that the regulation of GSK3b 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.

During LTD, activation of PP1 leads to dephosphorylation of GSK3b at ser9 to further activate GSK3b and enable LTD to occur. PP1 also inhibits Akt. During LTP, activation of NMDA receptors leads to stimulation of the PI3K-Akt pathway, which phosphorylates GSK3b at ser9 to inhibit its activity and prevent the induction of LTD. Thus, GSK3b, under the control of Akt and PP1, is a critical determinant of the direction of NMDA receptor-dependent plasticity.

Stéphane Peineau et col. A Role for GSK3b in Synaptic Plasticity

Neuron 53, 703–717, March 1, 2007