nonC^MC45 mutants exhibit robust phototransduction while synaptic transients are not detectable. They display no detectable photoreceptor synaptic on-transients, and display off-transients of reduced amplitude. The peak phototransduction responses of photoreceptors are comparable with wild-type in nonC^MC45 mutants.

With basal stimulation (0.5Hz), nonC^MC45 mutant synapses show an approximate 50% decrease in EJC amplitude with a significant loss of transmission fidelity. nonC^MC45 mutants exhibit a mean amplitude of 39nA. There is no detectable change in mEJC amplitude.

nonC^MC45 mutants exhibit under-elaborated neuromuscular junctions with reduced terminal areas, fewer synaptic branches and boutons, and a synapse that is generally confined 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 1607υm[2] in nonC^MC45 mutants. There is also a reduction in the number of synaptic terminal branches. nonC^MC45 mutants exhibit on average 5.8 branches.

There is a noticeable but statistically insignificant reduction in bouton number in nonC^MC45 mutants.

Bouton size is significantly larger in nonC^MC45 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 nonC^MC45 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.

nonC^MC45 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, nonC^MC45 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, nonC^MC45 mutants show an overall steady decline in transmission amplitudes for the remainder of the stimulus train. Upon return to basal (0.2Hz) stimulation, nonC^MC45 mutant EJC amplitudes gradually recover towards their initial basal level. High frequency training decreases the mean area of bouton size in nonC^MC45 mutants (compared to increasing it in control synapses). Although control boutons show no significant change in the number of enlarged membrane cisternae, stimulated mutant boutons show a highly significant elevation of trafficking organelles. The total synaptic vesicle number is reduced in nonC^MC45 mutants following high frequency stimulation, although there is no significant difference in vesicle density. Stimulated nonC^MC45 mutants show a highly significant loss of clustered vesicles, resulting in a significantly smaller pool than the stimulated control. Similarly, nonC^MC45 mutants lose docked vesicles when stimulated.