title: Opposing actions of protein kinase A and C mediate Hebbian synaptic plasticity.
abstract: 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.
authors.affiliation: Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, Building 49, Room 5A38, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: M X
authors.initials: MX
authors.lastname: Li
authors.forename: M
authors.initials: M
authors.lastname: Jia
authors.forename: H
authors.initials: H
authors.lastname: Jiang
authors.forename: V
authors.initials: V
authors.lastname: Dunlap
authors.forename: P G
authors.initials: PG
authors.lastname: Nelson
mesh_terms: 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
chemical_list: D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate