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Ryanodine-mediated conversion of STP to LTP is lacking in synaptopodin-deficient mice.

Brain Struct Funct. 2016 May;221(4):2393-7. Epub 2015 Mar 14
Gayane Grigoryan 1 , Menahem Segal 2
Gayane Grigoryan 1 , Menahem Segal 2

[No authors listed]

Author information
  • 1 Department of Neurobiology, The Weizmann Institute, 76100, Rehovot, Israel.
  • 2 Department of Neurobiology, The Weizmann Institute, 76100, Rehovot, Israel. Menahem.segal@weizmann.ac.il.

摘要


In previous studies we and others have found that activation of ryanodine receptors (RyRs) facilitate expression of long-term potentiation (LTP) of reactivity to afferent stimulation in hippocampal slices, with a more pronounced action in the ventral hippocampus. We have also been able to link the involvement of synaptopodin (SP), an actin-binding protein, with neuronal plasticity via its interaction with RyRs. To test this link more directly, we have now compared the ability of ryanodine to convert short-term to LTP in hippocampal slices taken from normal and SP-knockout (SPKO) mice. Indeed, SPKO hippocampus expresses lower concentrations of RyRs and in slices of these mice ryanodine is unable to facilitate conversion of short-term to LTP. These observations link functionally SP with calcium stores.

KEYWORDS: Calcium stores, Hippocampus, LTP, Ryanodine receptors, Synaptopodin