Bidirectional modulation of behavior with CaMKII

More recently, we have developed a system that enables us to control transgene expression in both spatial and temporal domains (Mehren and Griffith, 2004). This technical breakthrough is important for differentiating developmental from ongoing requirements for CaMKII activity. It also allows us to use manipulations of CaMKII (e.g. expression of constitutively active CaMKII) that would be lethal if expressed early in development. Expression of CaMKII in a subset of antennal lobe neurons resulted in an enhancement of courtship suppression during the training period with Ca²⁺-independent (T287D), but not Ca²⁺-dependent (T287A) CaMKII. During training, control animals have a lag before active suppression of courtship begins. Animals expressing Ca²⁺-independent CaMKII have no lag, implying that there is a threshold level of Ca²⁺-independent activity that must be present in order to suppress courtship. This was the first demonstration, in any organism, of enhanced behavioral plasticity with overexpression of constitutively active CaMKII. Interestingly, immediate memory was unaffected by expression of T287D CaMKII in mushroom bodies, even though previous studies had shown that CaMKII activity is required in this brain region for memory formation. These results suggest that the biochemical mechanisms of CaMKII-dependent memory formation are threshold-based in only a subset of neurons.

Additional behavior topics:

• Courtship conditioning
• Anatomical mapping of behavioral circuits
• Bidirectional modulation of behavior with CaMKII
• Dissection of the chemical cues underlying courtship learning
• Motor Behaviors

 

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