The expression of α-Spec^{dsRNA.Scer\UAS} under the control of Scer\GAL4^Or47b.7.467 leads to adult olfactory receptor neurons Or47b with a significant decrease in the number of pre-synaptic sites, as assessed by an active zone marker, as compared to controls; expression under the control of Scer\GAL4^Or67d-GAL4-1 results in no obvious morphological defects in adult antennal lobe glomeruli DA1 but their associated adult olfactory receptor neurons Or67d present a significant decrease in the number of pre-synaptic sites, as compared to controls.

Expression of β-Spec^{dsRNA.Scer\UAS} (together with UAS-Dicer2 to enhance RNAi efficiency) under the control of Scer\GAL4^GMR.PU has no effect on adult eye appearance.

Ubiquitous expression of two copies of β-Spec^{dsRNA.Scer\UAS} with Scer\GAL4^αTub84B.PL produces a lethal phenotype. However, expression under the control of Scer\GAL4^elav-C155, Scer\GAL4^2-21, Scer\GAL4^P2.4.Pdf, Scer\GAL4^bab1-Agal4-5, Scer\GAL4^how-24B, Scer\GAL4^mex1.2.1, Scer\GAL4^Bx-MS1096, Scer\GAL4^hs.PB or Scer\GAL4^rn-GAL4-14 doesn't result in any visible phenotype.

Expression of β-Spec under the control of Scer\GAL4^elav.PLu results in defects in the neuromuscular junction, including larger boutons.

Expression of β-Spec^{dsRNA.Scer\UAS} in the muscle (under the control of Scer\GAL4^C57) significantly reduces the number of synaptic boutons.

Synapses lacking postsynaptic β-Spec (through the expression of β-Spec^{dsRNA.Scer\UAS} under the control of Scer\GAL4^C57) exhibit severe defects in the postsynaptic muscle membrane folds (SSR). The SSR is generally thinned above and below the synaptic bouton (orthogonal to the muscle surface) and stretched laterally. In mnay cases, muscle tissue directly abuts the presynaptic bouton membrane and active zones, a phenotype that is never observed in wild-type. In addition, the SSR membranes are generally less compact compared with wild-type.

Active zones are significantly larger at neuromuscular junctions that lack postsynaptic β-Spec (due to expression of β-Spec^{dsRNA.Scer\UAS} under the control of Scer\GAL4^C57). The spacing between active zones is also disturbed, with some active zones forming in very close proximity to each other.

Expression of β-Spec^{dsRNA.Scer\UAS} postsynaptically in the muscle (under the control of Scer\GAL4^C57) results in a dramatic increase in the average amplitude of spontaneous miniature relase events (mepsp<up>miniature excitory postsynaptic potential; quantal size). After the loss of β-Spec EPSP amplitudes are only slightly increased, despite the large increase in quantal size. However, there isn't a significant change in muscle input resistance nor average membrane resting potential. Ultrastructural analysis of neurotransmitter vesicle sizes at active zones reveals no significant difference between animals lacking postsynaptic β-Spec.

Although expression of β-Spec^{dsRNA.Scer\UAS}, under the control of Scer\GAL4^sca-537.4, causes late larval lethality, a small proportion of escapers survive to early adult stages. Expression of β-Spec^{dsRNA.Scer\UAS} in the presynapse, driven by Scer\GAL4^sca-537.4, causes an increase in the number and extent of synaptic retraction events compared to wild-type synapses. The severity of synapse retraction correlates with a decrease in frequency, but not amplitude, of spontaneous miniature release events and a decreased quantal content, but no change in quantal size. Bouton morphology is perturbed. There are large accumulations of vesicles in the axons, although changes in axonal microtubule organization are minor. Postsynaptic β-Spec^{dsRNA.Scer\UAS} expression, driven by Scer\GAL4^C57, causes defects in the integrity of the subsynaptic membrane folds but does not cause increased synapse retraction.