In Drosophila, mutations in specific ion channel genes can increase or
decrease the level of neural/synaptic activity. We have used these ge
netic tools, in combination with classical pharmacological agents, to
modulate neural activity during embryogenesis and examined effects on
the differentiation of an identified neuromuscular junction. We find t
hat electrical activity is required for the neural induction of transm
itter receptor expression during synaptogenesis. Likewise, neural elec
trical activity is required to localize transmitter receptors to the s
ynaptic site. In muscles with activity blocked synapses, a low level o
f receptors is expressed homogeneously in the muscle membrane as in mu
scles developing without innervation. Thus, presynaptic electrical act
ivity is required to mediate the neural induction of the transmitter r
eceptor field in the postsynaptic membrane.