Abstract:
:Altered gene expression mediated by calcium/calmodulin-dependent protein kinase II (CaMKII) and other intracellular signaling molecules plays an important role in activity-dependent neuroplasticity. We discovered that sustained depolarization induced by KCl, a commonly used paradigm for studying activity-dependent gene expression, surprisingly caused a decrease in CaMKII activity in rat mesencephalic dopamine neurons. This decrease in CaMKII activity, after 2 days of depolarization, occurred in the presence of a continued elevation in intracellular calcium concentration. An increase in calyculin-sensitive phosphatase activity was at least partly responsible for the decrease in CaMKII activity. Phosphatase assays revealed that activity but not the abundance of protein phosphatase-2A was increased by sustained depolarization. Decreased CaMKII activity was accompanied by a selective decrease in dopamine transporter (DAT) mRNA, while tyrosine hydroxylase and actin mRNA abundance was unaltered. On the other hand, brain-derived neurotrophic factor (BDNF) mRNA abundance was increased by sustained depolarization, further demonstrating the specificity of changes. Depolarization also caused a significant decrease in DAT protein abundance and DAT-mediated uptake. Taken together, these data illustrate a novel signaling paradigm in which the activity of protein phosphatase-2A is associated with CaMKII activity and gene expression.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Padmanabhan S,Prasad BMdoi
10.1016/j.neuroscience.2009.06.041subject
Has Abstractpub_date
2009-09-29 00:00:00pages
277-85issue
1eissn
0306-4522issn
1873-7544pii
S0306-4522(09)01066-5journal_volume
163pub_type
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