A growing number of genetically encoded tools are becoming available that allow 
non-invasive manipulation of the neural activity of specific neurons in 
Drosophila melanogaster. Chief among these are optogenetic tools, which enable 
the activation or silencing of specific neurons in the intact and freely moving 
animal using bright light. Channelrhodopsin (ChR2) is a light-activated cation 
channel that, when activated by blue light, causes depolarization of neurons 
that express it. ChR2 has been effective for identifying neurons critical for 
specific behaviors, such as CO(2) avoidance, proboscis extension and giant-fiber 
mediated startle response. However, as the intense light sources used to 
stimulate ChR2 also stimulate photoreceptors, these optogenetic techniques have 
not previously been used in the visual system. Here, we combine an optogenetic 
approach with a mutation that impairs phototransduction to demonstrate that 
activation of a cluster of loom-sensitive neurons in the fly's optic lobe, 
Foma-1 neurons, can drive an escape behavior used to avoid collision. We used a 
null allele of a critical component of the phototransduction cascade, 
phospholipase C-β, encoded by the norpA gene, to render the flies blind and also 
use the Gal4-UAS transcriptional activator system to drive expression of ChR2 in 
the Foma-1 neurons. Individual flies are placed on a small platform surrounded 
by blue LEDs. When the LEDs are illuminated, the flies quickly take-off into 
flight, in a manner similar to visually driven loom-escape behavior. We believe 
that this technique can be easily adapted to examine other behaviors in freely 
moving flies.