Alternative splicing of the eag potassium channel gene in Drosophila generates a novel signal transduction scaffolding protein.

The Drosophila eag gene has been shown to regulate neuronal excitability, olfaction, associative learning and larval locomotion. Not all of the roles of this gene in these processes can be explained by its function as a voltage-gated potassium channel. In this study, we show that the eag gene is spliced in a PKA- and PKC-regulated manner to produce a protein lacking channel domains.

CaMKII, an enzyme on the move: regulation of temporospatial localization.

Calcium-calmodulin-dependent protein kinase II (CaMKII) is an important regulator of neuronal and behavioral plasticity. Studies in which the subcellular distribution of CaMKII has been altered argue that targeting of this enzyme to specific subcellular compartments is crucial to many of its roles. Understanding how a very abundant enzyme can achieve specificity of action over time and space requires an understanding of the functional diversity of the enzyme and its distribution.

The eag potassium channel binds and locally activates calcium/calmodulin-dependent protein kinase II.

Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been implicated in the regulation of neuronal excitability in many systems. Recent studies suggest that local regulation of membrane potential can have important computational consequences for neuronal function. In Drosophila, CaMKII regulates the eag potassium channel, but if and how this regulation was spatially restricted was unknown.

Regulation of the Ca2+/CaM-responsive pool of CaMKII by scaffold-dependent autophosphorylation.

CaMKII is critical for structural and functional plasticity. Here we show that Camguk (Cmg), the Drosophila homolog of CASK/Lin-2, associates in an ATP-regulated manner with CaMKII to catalyze formation of a pool of calcium-insensitive CaMKII. In the presence of Ca(2+)/CaM, CaMKII complexed to Cmg can autophosphorylate at T287 and become constitutively active.

Melatonin reduces memory changes and neural oxidative damage in mice treated with D-galactose.

To investigate the role of melatonin in D-galactose-induced amnesic mice, the avoidance/escape and water maze tests were performed to evaluate their learning and memory function. Spectrophotometry was employed to determine the content of thiobarbituric acid-reactive substances (TBARS) and the activities of antioxidative enzymes in the brain. The present results demonstrate that D-galactose-induced amnesic mice had significantly decreased learning and memory function.