The first sting is delivered to the prothoracic ganglion (mass of nerve tissue) which causes a 2- to 3-minute paralysis of the front legs. This sting injects significant quantities of
γ amino-butyric acid (GABA) and complementary agonists
taurine and
β alanine. The concoction temporarily blocks the motor action potentials in the prothoracic ganglion by depressing cholinergic transmission through the increased chloride conductance across nerve synapses. Individually, all of these substances induce short-term paralysis of the cockroach. When they are injected together in a ratio of , the effect is longer lasting. GABA activates
ligand-gated chloride channels by binding to GABA receptors. Taurine and beta-alanine likely extend the duration of the paralytic effect by slowing the uptake of GABA by the
synaptic cleft. Combined, this cocktail of compounds prevents the cockroach from moving and defending itself while the wasp administers the second sting/series of stings. The second sting is administered to the subesophageal ganglion (SEG) and the supraesophageal ganglion (SupOG) and is much more precise, hence the need for paralysis. It is also significantly longer. The wasp actively searches for the SEG during this sting. The second sting inhibits the cockroach's ability to walk spontaneously or of its own will, but cockroaches can right themselves and swim while under the influence, and when startled, will jump but not run. It also causes excessive grooming and alterations in the metabolism of the cockroach. The metabolic change is thought to preserve nutrients for the wasp larva. Researchers have simulated this zombie state by injecting
procaine into the SEG. They also determined using extracellular bipolar electrodes that neuronal activity was less in stung cockroaches. The venom may disturb the octopaminergic modulation in structures within the roach's ganglion. Basically, it limits the effectiveness of octopamine, the neurotransmitter that controls muscle contraction in sudden movements. ==See also==