Neurotoxicological effects and the mode of action of pyrethroid insecticides

Neuroexcitatory symptoms of acute poisoning of vertebrates
by pyrethroids are related to the ability of these insecticides to
modify electrical activity in various parts of the nervous system.
Repetitive nerve activity, particularly in the sensory nervous
system, membrane depolarization, and enhanced neurotransmitter
release, eventually followed by block of excitation, result
from a prolongation of the sodium current during membrane
excitation. This effect is caused by a stereoselective and
structure-related interaction with voltage-dependent sodium
channels, the primary target site of the pyrethroids.
Near-lethal doses of pyrethroids cause sparse axonal damage
that is reversed in surviving animals. After prolonged exposure
to lower doses of pyrethroids axonal damage is not observed.
Occupational exposure to pyrethroids frequently leads to
paresthesia and respiratory irritation, which are probably due
to repetitive firing of sensory nerve endings. Massive exposure
may lead to severe human poisoning symptoms, which are
generally treated well by symptomatic and supportive measures.