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Volume 17, Number 12, Issue of June 15, 1997 pp. 4600-4611
Copyright ©1997 Society for NeurosciencePostsynaptic Calcineurin Activity Downregulates Synaptic Transmission by Weakening Intracellular Ca2+ Signaling Mechanisms in Hippocampal CA1 Neurons
Received Nov. 20, 1996; revised March 20, 1997; accepted April 2, 1997.
Jin-Hui Wang and Paul T. Kelly Department of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, Texas 77225
Protein phosphorylation and dephosphorylation are believed to functionally couple neuronal activity and synaptic plasticity. Our previous results indicated that postsynaptic Ca2+/calmodulin (CaM) signaling pathways play an important role in setting synaptic strength, and calcineurin (CaN) activity limits synaptic responses during basal synaptic transmission and long-term potentiation expression. The inhibition of postsynaptic CaN activity by FK-506 or an autoinhibitory peptide induced synaptic potentiation in hippocampal slices, which occludes tetanus-induced LTP. FK-506-induced synaptic potentiation was expressed in adult but not young rats. To elucidate mechanisms underlying CaN-inhibited synaptic potentiation, we co-injected certain agents affecting Ca2+ signaling pathways with CaN inhibitors into CA1 neurons. Synaptic potentiation induced by FK-506 was significantly attenuated by co-injecting BAPTA, heparin/dantrolene (inhibitors of intracellular Ca2+ release), a CaM-binding peptide, or CaM-KII/PKC pseudosubstrate peptides. These results indicate that postsynaptic CaN activity can downregulate evoked synaptic transmission by weakening intracellular Ca2+ signals and downstream protein kinase activities.
Key words: synaptic potentiation; calcineurin inhibitor; calcium/calmodulin; IP3/ryanodine receptors; positive feedback; postsynaptic manipulation
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