CONCOMITANT ALTERATIONS OF PHYSIOLOGICAL AND DEVELOPMENTAL PLASTICITYIN DROSOPHILA CAM KINASE II-INHIBITED SYNAPSES

Ca2+/calmodulin-dependent protein kinase II (CaM kinase) has been impl icated in neural plasticity that underlies learning and memory process es. Transformed strains of Drosophila, ala1 and ala2, expressing a spe cific inhibitor of CaM kinase are known to be impaired in an associati ve conditioning behavioral paradigm. We found that these transformants had altered short-term plasticity in synaptic transmission along with abnormal nerve terminal sprouting and directionality of outgrowth. Th ese results represent an interesting parallel with the activity-depend ent regulation of synaptic physiology and morphology by the cAMP casca de in Aplysia and Drosophila. In contrast to the learning mutants dunc e and rutabaga, which are defective in the cAMP cascade, inhibition of CaM kinase in ala transformants caused increased sprouting at larval neuromuscular junctions near the nerve entry point, rather than alteri ng the higher order branch segments. In addition, synaptic facilitatio n and potentiation were altered in a manner different from that observ ed in the cAMP mutants. Furthermore, synaptic currents in ala transfor mants were characterized by greater variability, suggesting an importa nt role of CaM kinase in the stability of transmission.