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Opposing actions of protein kinase A and C mediate Hebbian synaptic plasticity

Abstract

A compartmental nerve–muscle tissue culture system expresses Hebbian1,2 activity-dependent synapse modulation. Protein kinase C (PKC) mediates a heterosynaptic loss of efficacy, and we now show that protein kinase A (PKA) is involved in homosynaptic stabilization. Both work through postsynaptic changes in the acetylcholine receptor (AChR) as measured electrophysiologically and by imaging techniques.

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Correspondence to Phillip G. Nelson.

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Figure 1: Neuronal electrical stimulation prevents the downregulation of synapse efficacy by PKC activation; this effect involves PKA.
Figure 2: PKA activation prevents stimulation-related synapse downregulation.