CaM Kinase II and Visual Input Modulate Memory Formation in the Neuronal Circuit Controlling Courtship Conditioning

Abstract

In Drosophila, calcium/calmodulin-dependent protein kinase II (CaM kinase) has been shown to be important in the expression of both learning and memory for the associative behavior courtship conditioning. In this study we examine the role of visual input in producing this behavior and the effects of modifying visual input on CaM kinase-dependent memory formation. Inhibition of CaM kinase blocked apparent learning regardless of visual input. Visual input selectively affected the memory phase of courtship conditioning: normal visual input masked the memory effects of inhibition of CaM kinase resulting in generation of memory without apparent learning, whereas disruption of visual input revealed the CaM kinase-dependence of memory. Visual input was found to be important only during the training period, which implies that vision and CaM kinase are interacting in the formation rather than the retrieval of memory. Our results suggest a model for courtship conditioning in which multiple sensory inputs are integrated at a CaM-kinase-dependent neuronal switch to modulate courtship behavior.

Genetics and genomics of Drosophila mating behavior

“…These include mutations in genes required for normal morphology [white (13,14), yellow (14), and curved (15)], as well as genes involved in learning and memory [Calcium calmodulin kinase II (16), dunce (17,18), rutabaga (19,20), turnip (19,21), and amnesiac (20,22,23)], circadian rhythm [period (18,(24)(25)(26)] and dopamine and serotonin synthesis [Dopa decarboxylase (27), pale (28,29), tan (30,31), and ebony (32)(33)(34)], sex determination [doublesex (35)(36)(37), transformer (38)(39)(40)(41)(42)(43), fruitless (44)(45)(46)(47), and sex lethal (48)], pheromone production [desaturase 2 (49)], and accessory gland-specific peptides (6-8, 50-52). a subset of loci identified by mutational analysis, or will the analysis of natural variants reveal novel loci?…”

Calcium-Independent Calcium/Calmodulin-Dependent Protein Kinase II in the AdultDrosophilaCNS Enhances the Training of Pheromonal Cues

“…Tetracycline concentrations of as little as 0.1 g/ml food have been shown to inactivate tTA (tetracycline-controlled transactivator protein) when combined with tetO-lacZ (Bello et al, 1998). With our system, however, we detected a low level of GFP (green fluorescent protein) in third-instar larvae carrying one copy each of pan-neuronal MJ85b-GAL4 (Joiner and Griffith, 1997), UAS-tTA, and tetO-GFP grown on food containing tc at 5 g/ml food (data not shown). Full suppression of tetO-GFP expression was seen with tetracycline at 10 g/ml food, and therefore this was the concentration used for all experiments described in this paper.…”

“…Each CI was subjected to arcsine, arcsine squared, or arcsine square root transformation to effect approximation of normal distributions (Villella and Hall, 1996;Joiner and Griffith, 1997;Villella et al, 1997). Transformed learning or memory scores were subjected to a one-way ANOVA with genotype as the main effect, using JMP (version 5.0 for Macintosh; SAS Institute, Cary, NC), and planned comparisons of means were performed with Student's t test (adjusted for experimentwise error) (Sokal and Rohlf, 1995).…”

“…Table 1 displays the results of crossing GAL4 lines MJ85b, 29BD, or C155 to UAStTA; tetO-T287D flies, with or without tetracycline in the larval medium. MJ85b expresses GAL4 throughout the CNS and PNS (Joiner and Griffith, 1997). The C155-GAL4 transgene is inserted near elav and expresses in all neurons, beginning during embryogenesis .…”

The Metabotropic Glutamate Receptor Activates the Lipid Kinase PI3K in Drosophila Motor Neurons Through the Calcium/Calmodulin-Dependent Protein Kinase II and the Nonreceptor Tyrosine Protein Kinase DFak

“…It was previously found that motor neuron expression of CaMKII T287D increased synapse number and decreased excitability in motor neurons (Park et al 2002); both of these phenotypes are also exhibited in larvae expressing the constitutively active PI3K-CAAX (Martin-Pena et al 2006;Howlett et al 2008). Similarly, CaMKII inhibition accomplished by transgenic expression of the CaMKII inhibitory peptide "ala" (Joiner and Griffith, 1997) increases motor neuron excitability and decreases synapse number (Park et al 2002); both of these phenotypes are also exhibited in transgenic larvae in which PI3K activity is blocked. Taken together, these results support the notion that levels of PI3K activity are specified, at least in part, by activity of CaMKII.…”