The role of CaMKII in cerebellar learning
Year: 2006
Type: article
Abstract: The molecular mechanisms underlying learning and memory are conserved between \\nprimitive and higher organized organisms. Memory formation requires plasticity \\nbetween synaptic connections, and Ca2+ serves as an essential second messenger \\nin the regulation of this plasticity. Calcium-calmodulin dependent protein kinase II \\n(CaMKII) detects the amplitude and frequency of the Ca2+ signal, and transforms this \\ntransient signal into a graded, long-lasting Ca2+ independent signal. Activated \\nCaMKII phosphorylates itself and various other proteins, which eventually leads to \\nenhancement of synaptic efficacy. \\n\\n Because of these unique properties, it is not surprising that the CaMKII knock-\\nout mouse was the first mouse to be studied in the field of Neuroscience. Since then, \\nits role in hippocampal plasticity and hippocampal learning and memory has been \\nintensely studied. These studies were subsequently replicated for cortical areas, for \\nwhich the molecular mechanisms are very similar as the hippocampus. \\n\\nThe molecular mechanisms underlying cerebellar motor learning are markedly \\ndifferent compared to excitatory neurons of the forebrain. Influx of high amounts of \\ncalcium into cerebellar Purkinje cells results in synaptic weakening rather than \\nstrengthening. In this thesis we explored the possibility that CaMKII might be \\ninvolved in this weakening process and in cerebellar motor learning.
Author: Dmitri Andreev
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W1501414294