|ZFIN ID: ZDB-PUB-030211-14|
Translocation of CaM kinase II to synaptic sites in vivo
Gleason, M.R., Higashijima, S.I., Dallman, J., Liu, K., Mandel, G., and Fetcho, J.R.
|Source:||Nature Neuroscience 6(3): 217-218 (Journal)|
|Registered Authors:||Fetcho, Joseph R., Higashijima, Shin-ichi, Liu, Katharine S.|
|PubMed:||12563265 Full text @ Nat. Neurosci.|
Gleason, M.R., Higashijima, S.I., Dallman, J., Liu, K., Mandel, G., and Fetcho, J.R. (2003) Translocation of CaM kinase II to synaptic sites in vivo. Nature Neuroscience. 6(3):217-218.
ABSTRACTThe idea that calcium/calmodulin-dependent protein kinase II (CaMKII) is strategically localized to excitatory synapses to exert its important role in long-term potentiation and other forms of neuronal plasticity is supported by the binding of CaMKII to isolated postsynaptic densities (PSD) in biochemical assays and by the finding in cultured neurons that PSD clusters of green fluorescent protein (GFP)-tagged CaMKII form in response to glutamate application or direct electrical stimulation. The observation that CaMKII also forms large clusters in response to ischemic insults, however, questions the physiological relevance of such translocations. Here we show that in intact zebrafish, repeated sensory stimulation resulted in reproducible and reversible translocation of GFP-CaMKII to the PSD in an identified interneuron in a sensorimotor circuit.
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