Ca(2+)- and CaMKII-mediated processes in early LTP
- PMID: 25452677
- PMCID: PMC4248478
- DOI: 10.5214/ans.0972.7531.210408
Ca(2+)- and CaMKII-mediated processes in early LTP
Abstract
Learning methods determine the degree of stimulation of engrams encoding information to be memorised. More enriching modes of learning allow more enduring long-term potentiation of the synapses associated with these memories. The additional activity causes a prolonged increase in [Ca2+] in the dendritic spine of the postsynaptic neuron. This allows Ca(2+)-mediated molecular pathways to bring about cytoskeletal remodeling, posttranslational modifications, and protein trafficking. These processes contribute to early long-term potentiation of the synapses, strengthening the memory they store and lead to improved performance on tests of memory recall.
Keywords: AMPARs; Calcium signalling; Calcium/calmodulin-dependent protein kinase II; Long-term potentiation; Signal transduction.
Figures
References
-
- Sheng M, Hoogenraad CC. The postsynaptic architecture of excitatory synapses: a more quantitative view. Annu Rev Biochem. 2007;76:823–847. - PubMed
-
- Lench AM, Massey PV, Pollegioni L et al. Astroglial d-serine is the endogenous co-agonist at the presynaptic NMDA receptor in rat entorhinal cortex. Neuropharmacology. 2014;83C:118–127. - PubMed
-
- Panatier A, Theodosis DT, Mothet JP et al. Glia-derived D-serine controls NMDA receptor activity and synaptic memory. Cell. 2006;125(4):775–784. - PubMed
-
- Okamoto K, Bosch M, Hayashi Y. The roles of CaMKII and F-actin in the structural plasticity of dendritic spines: a potential molecular identity of a synaptic tag? Physiology (Bethesda) 2009;24:357–366. - PubMed
Publication types
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous