Abstract
A model is proposed to suggest that the mechanism of action of DEET on the mosquito Aedes aegypti is through interaction of the repellent molecules with the lipid portion of cell membranes. DEET in the vapor state would have access to the membranes of neurons in the chemosensilla and to the membranes of a great many body cells via pores in the cuticle and the tracheal system, respectively. In host location, a behavior chiefly mediated by olfactory cues, interaction of DEET molecules with lipids perturbs the organization of the dendritic membranes in such a way that the normal responses to attractants are altered. Sufficient quantity of DEET would alter significantly the sensory pattern, largely composed of responses from all the olfactory neurons, that impinges on the central nervous system (CNS). Consequently, the CNS would not elicit the muscular contractions needed to make the appropriate turning responses that would keep the mosquito within the stream of host-related attractants. DEET, having entered the body through the spiracles, may indirectly interfere with nonolfactory-mediated behaviors by interaction with membranes of a large number of body cells, initially affecting respiration. Other physiological processes would be affected that could eventually cause the observed behavioral changes. This indirect action on the nervous system would not be important in DEET's interference with host location, because the proposed alteration of the sensory pattern mechanism would occur more quickly.