Mutant larvae show significantly increased green-light avoidance compared to controls, but blue-light avoidance is normal in the mutant larvae.

The amplitude of glutamate-gated currents is reduced in mutant embryos compared to wild-type (312 +/- 55 pA compared to 1691 +/- 71 pA), when glutamate is pressure-ejected onto the postsynaptic neuromuscular junction. Single-channel current amplitude of postsynaptic glutamate receptors is not different from wild type in the mutant embryonic neuromuscular junction. The amplitude of spontaneous excitatory junctional currents is significantly reduced in the mutant embryonic neuromuscular junction compared to wild type (70 +/- 17 pA compared to 141 +/- 14 pA).

Those few homozygous animals that do survive to hatch, diplay grossly abnormal movement and behaviour and always die as early as first instar larvae. Electrophysiological analysis of neuromuscular function of mature mutant embryos display a severe disruption in neurotransmission. Evoked excitatory junctional currents (EJCs) are reduced to about 15% of normal amplitude. Also, glutamate activated currents are dramatically reduced, indicating that the defect in synaptic transmission is entirely due to a reduction in postsynaptic receptor current. When the step size on the falling phase of spontaneous synaptic currents are measured, the single channel glutamate receptor current amplitude does not differ between wild-type and Gad1 flies. This indicates a reduced number of postsynaptic glutamate receptors. Consistent with this, the amplitude of spontaneous synaptic activity is reduced in mutants. Experiments with focally applied glutamate show that the defect is not due to glutamate receptor mislocalisation. No difference in endogenous motor neuron activity is observed between wild-type and Gad1^L352F mutant embryos.