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Received for publication April 14, 2004.
Revised June 28, 2004.
Accepted for publication June 30, 2004.
The dopamine D4 receptor in prefrontal cortex (PFC) plays a key role in normal mental functions and neuropsychiatric disorders. However, the cellular mechanisms and physiological actions of D4 receptors remain elusive. In this study, we found that activation of D4 receptors in PFC exerts a complex regulation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) - a multifunctional enzyme critically involved in synaptic plasticity that is fundamental for cognitive and emotional processes. In PFC slices with high neuronal activity, application of the D4 receptor agonist PD168077 produced a potent reduction of the CaMKII activity, whereas in PFC slices with low neuronal activity, PD168077 caused a marked increase of the CaMKII activity. The D4 up-regulation of CaMKII activity was through the stimulation of phospholipase C (PLC) pathway and elevation of intracellular Ca2+ via IP3 receptors. These results reveal a bi-directional regulation of CaMKII activity by PFC D4 receptors in response to changes in neuronal activity, and a non-classical signaling pathway underlying the D4 up-regulation of CaMKII activity. This modulation provides a unique and flexible mechanism for D4 receptors to regulate CaMKII activity, which could lead to dynamic regulation of many targets of CaMKII by D4 receptors.
Key words:
Dopamine, Protein Kinases (other)
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