Mutant animals show reduced 1 hour memory and normal age-related memory impairment.
Single-trial short program training in an olfactory learning assay shows that scbVol-1 flies perform poorly immediately after conditioning. The mutants are sensitive to two-trial, spaced conditioning over two-trial, massed conditioning, behaving in this respect qualitatively like control flies. The phenotype after short program training is completely recessive.
At physiological levels of external Ca2+ mutant nmjs show normal transmission. At reduced external Ca2+ levels EJC amplitudes are increased over those of controls (least pronounced for scbVol-2, but highly significant for scbVol-1, scbVol-3 and scbVol-4. scbVol-1, scbVol-3 and scbVol-4 show reduced slope of the logarithmic relationship between EJC amplitude and external Ca2+ concentration, indicating reduced Ca2+ dependence of transmission. Mutants show significant defects in two forms of short-term facilitation, paired pulse and frequency dependent short term facilitation. Mutants show impaired augmentation of transmission amplitude upon prolonged stimulation at intermediate frequencies.
Mutations produce a memory deficit as shown in the odour avoidance test. Neither sensorimotor nor gross anatomical defects can account for the memory deficit.
Mutation disrupts the expression of scb long form.