Mutant nmjs appear morphologically wild type though the nerve terminals are slightly smaller than normal. In electrophysiological recordings at the embryonic nmj nerve stimulation produces muscle contraction demonstrating that presynaptic depolarization evokes transmitter release and that muscle excitation-secretion response is intact. However evoked EJC peak amplitudes are significantly reduced and the release of neurotransmitter at mutant synapses is markedly asynchronous due to delayed presynaptic vesicle fusion. Mutants have an impaired ability to synchronously trigger calcium-mediated vesicle fusion. The overall level of neurotransmitter release is reduced. Variability in EJC peak amplitudes is increased approximately twofold, compared to wild type. Transmission fidelity is lost. Calcium sensitivity is unaltered. MEJC frequency is not significantly altered, though amplitude is increased, perhaps because of increased quantity of neurotransmitter in some vesicles. Mutant synapses exhibit severe fatigue after prolonged stimulation. Embryonic synapses show decreased synaptic vesicle density and accumulate membrane-recycling intermediates, though this defect is not apparent in mature larval nmjs.

stnA¹⁵ larvae show approximately threefold enhancement in the frequency of spontaneous miniature events at the neuromuscular junction compare to wild-type. Postsynaptic responses in the muscle evoked by motor nerve stimulation are substantially altered compared to wild-type; the excitatory junctional potentials (EJPs) are substantially smaller than normal and the excitatory junctional current amplitude is only 15% of wild-type. EJP amplitudes are twice as variable in individual stnA¹⁵ larvae compared to individual wild-type larvae. Neuromuscular junctions show an enhanced rate of transmission failure compared to wild-type under low Ca²⁺ conditions. Mean quantal content is smaller than at wild-type neuromuscular junctions. The fractional area occupied by vesicles is not significantly different from wild-type in stnA¹⁵ boutons at the neuromuscular junction, although there is a trend towards wider synaptic vesicle distribution than in wild-type. There is a small but significant increase in synaptic vesicle density. The synaptic vesicles are indistinguishable from wild-type. The number of boutons per arbor is slightly, but significantly, increased compared to wild-type.

At 22^oC flies become paralyzed after an mechanical shock. At 29^oC flies die after a mechanical shock. ERG phenotype shows loss of both off and on transients. Flies heterozygous for stnA¹⁵ and any of the lethal stnA alleles show either a small or no off transient in ERGs. Flies heterozygous for stnA¹⁵ and a ts allele show ERG off transients significantly lower than for the control class, and lower than for the heterozygotes between ts and lethal alleles of stnA.

Electroretinograms (ERG) lack the on- and off-transients.

Homozygotes are paralysed when subjected to a mechanical shock and die when tested at 29^oC. Hemizygotes with Df(1)JC4, Df(1)EA113 and Df(1)GA22 have greatly reduced viability and usually become mired in the food medium. stnA¹⁵/stnA¹ flies are ill, have no jump response and show uncoordinated behaviour after exposure to stress such as mechanical shock. stnA¹⁵/stnA^VE814 flies do not survive. stnA¹⁵/stnA⁶ flies are very sedentary, are bang sensitive, uncoordinated and show marked debilitation at 35^oC.

temperature-sensitive lethal allele

stnA¹⁵, stnB¹⁵ has abnormal neurophysiology phenotype

Scer\GAL4^elav-C155, stnA¹⁵, stnB¹⁵, stnB^AB.UAS has viable phenotype

Scer\GAL4^elav-C155, stnA¹⁵, stnA^UAS.cEa, stnB¹⁵ has lethal phenotype

Scer\GAL4^elav-C155, stnA¹⁵, stnA^AB.UAS, stnB¹⁵, stnB^AB.UAS has viable phenotype

Syt1^D27/Syt1^AD4, Syt1^elav.PD, stnA¹⁵, stnB¹⁵ has viable phenotype