threshold voltage. The early synapse also causes current to leak through the active synapse, resulting in weak EPSPs that are ultimately unable to generate the tail flip. A number of processes are inhibited once the initial flexion has begun. Further LGI spiking, influx of sensory information from the tail, MoG spiking and FF contraction are all inhibited so that a flexion and extension cycle can be completed before another flexion begins. Long IPSPs are generated to prevent these events. The extensor muscles are inhibited to prevent competition between the extensor and flexors. Rapid IPSPs presented at the muscle receptor organ (MRO) prevent the stretch receptor from initiating extension while they are also presented at the fast extensor motor neurons and the fast extensor muscles. The circuits responsible for slow flexion and extension are also inhibited. 2 – Reextension When the LGI-mediated inhibition subsides, the reextension process begins. This process is mediated by the MRO and tail fan hair receptors, which were inhibited during the flexion portion of the escape behavior. The MRO is responsible for the initiation of extension and the inhibition of flexion through a reflex like mechanism. The muscle fibers of the MRO are located on the dorsal side of the abdomen, each spanning the joint of two segments. They are innervated by proprioreceptors that detect the stretch in extensor muscles when the flexors are contracted. They then fire phasically or tonically. It then excites the motor neurons in the fast extensor muscles while directly exciting an inhibitory neuron that prevents contractions in the FF muscles. The hair cells detect the resulting movement caused by the tail flip when activated, they would fire and excite the fast extensor motor neurons. 3 – Swimming Non-giant-mediated responses are initiated after the tail flip, creating cycles of flexion followed by extension. This non-giant system is activated parallel to the LGI circuit when the hair cells receive input. However, this behavior has a longer delay that allows the onset of swimming to occur after the completion of the tail flip. The non-giant swimming occurs independently of the LGI response since direct stimulation of the LGI with the electrodes results in a tail flip but not the subsequent non-giant swimming. This swimming response seems to be a fixed action pattern mediated by a central pattern generator since it does not require sensory feedback for physical and temporal maintenance. Modulation and plasticity of the