nonC¹ mutants exhibit robust phototransduction while synaptic transients are not detectable. Neither on-transients, nor off-transients of any significant amplitude can be elicited from nonC¹ mutants over a range of light intensities. The peak phototransduction responses of photoreceptors are slightly depressed in nonC¹ mutants.

With basal stimulation (0.5Hz), nonC¹ mutant synapses show an approximate 50% decrease in EJC amplitude with a significant loss of transmission fidelity. nonC¹ mutants exhibit a mean amplitude of 39nA. There is no detectable change in mEJC amplitude.

nonC¹/nonC^rst2 transheterozygous synapses exhibit a decreased EJC amplitude compared with nonC¹ heterozygotes.

nonC¹ mutants exhibit under-elaborated neuromuscular junctions with reduced terminal areas, fewer synaptic branches and boutons, and a synapse that is generally conifed closer to the muscle nerve entry site. Overall, mutant synaptic area is significantly reduced. Wild-type controls have a mean area of 2414υm[2] compared with 1502υm[2] in nonC¹ mutants. The transheterozygous mutant nonC¹/nonC^rst2 exhibits an area of 1524.8υm[2] compared with the transheterozygous control nonC¹/+ of 2315.2Δm[2]. There is also a reduction in the number of synaptic terminal branches. nonC¹ mutants exhibit on average 5.8 branches, with nonC¹/nonC^rst2 transheterozygotes having 6.2 branches, approximately half that in wild-type.

There is a noticeable but statistically insignificant reduction in bouton number in nonC¹ and nonC¹/nonC^rst2 mutants.

Bouton size is significantly larger in nonC¹ mutants compared with controls. Consistently, the mutant contains significantly more synaptic vesicles, although mean vesicle density is still significantly reduced, owing to the enlarged bouton area. In addition, vesicle pool distributions are slightly altered. The number of docked vesicles is significantly elevated in nonC¹ mutants compared to controls. The number of vesicles clustered around the active zone is also significantly increased in mutants compared to controls. By contrast, there is highly significant reduction in the number of internal synaptic vesicles in mutants compared with controls.

nonC¹ heterozygous neuromuscular junctions maintain a nearly constant level of transmission at 0.5mM external "["Ca[2+]"]", with no significant tendency to facilitate or fatigue. By contrast, nonC¹ homozygous and heterozygous nonC¹/nonC^MC45 mutant neuromuscular junctions start out impaired by ~50% and then experience further significant fatigue during high frequency training. Initially, normalized EJC amplitudes demonstrate a small amount of facilitation but this facilitation is not maintained. However, from ~20 seconds, nonC¹ mutants show an overall steady decline in transmission amplitudes for the remainder of the stimulus train. Upon return to basal (0.2Hz) stimulation, nonC¹ mutant EJC amplitudes gradually recover towards their initial basal level.