Bioallethrin

Bioallethrin, like other pyrethroids, binds to voltage gated sodium channels in their closed state and modifies the gating kinetics. Channel opening appears to increase affinity of the channel for pyrethroids like bioallethrin. Once bound pyrethroids slow both the opening and closing of the sodium channel resulting in a need for stronger excitatory potentials to produce an action potential and a delay in repolarization. The these changes make the neuron more susceptible to large action potentials and repeated firing by both increasing the initial threshold and reducing the input needed for after-potentials. When repeated firing does occur, the nerve terminal will release more neurotransmitter which can produce muscle paralysis through tetanus. This paralysis stops the breathing of lice and scabies parasites resulting in death.

Some pyrethroids act on calcium channels to increase intracelllular calcium. Bioallethrin produces a very small increase in intracellular calcium in mouse neocortical neurons by acting on N-type calcium channels but the effect returns to baseline within 2 min. In contrast bioallethrin has been found to block L T, and P/Q-types of voltage gated calcium channels in human embryonic kidney cell cultures. Bioallethrin has been found to inhibit both sodium-calcium dependent and magnesium-calcium ATP hydrolysis in insects although it, along with other type I pyrethroids, has a greater effect on sodium-calcium dependent hydrolysis. Bioallethrin may stimulate phosphoinositol breakdown in synaptoneuromes as other type I pyrethroids have been observed to do so. Other type I pyrethoids have also been found to bind to kainate receptors.