Opposing actions of protein kinase A and C mediate Hebbian synaptic plasticity.
A compartmental nerve-muscle tissue culture system expresses Hebbian 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.
Li
M X
MX
Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, Building 49, Room 5A38, National Institutes of Health, Bethesda, Maryland 20892, USA.
Jia
M
M
Jiang
H
H
Dunlap
V
V
Nelson
P G
PG
D017868:Cyclic AMP-Dependent Protein Kinases / Q000502:physiology*; D004558:Electric Stimulation; D004789:Enzyme Activation; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000502:physiology*; D011493:Protein Kinase C / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate