Pheromones cause disease: pheromone/odourant transduction

This paper compares two models of the sense of smell and demonstrates that the new model has advantages over the accepted model with implications for medical research. The accepted transduction model had an odourant or pherom one contacting an aqueous sensory lymph then movement through it to a recep tor membrane beneath. If the odourant or pheromone were non-soluble, the od ourant/pheromone supposedly would be bound to a soluble protein in the lymp h to be carried across. Thus, an odourant/carrier protein complex physicall y moved through the receptor lymph/mucus to interact with a membrane bound receptor. After the membranous receptor interaction, the molecule would be deactivated and any odourant/pheromone-binding protein recycled. This new electrical chemosensory model being proposed here has the pheromon e or other odourant generating an electrical event in the extra-cellular mu cus. Before the pheromone arrives, proteins of the 'carrier class' dissolve d in the receptor mucus slowly and continuously sequester ions. A sensed ph eromonal chemical species sorbs to the mucus and immediately binds to the n ow ion-holding dissolved protein. The binding of the pheromone to the prote in causes a measurable conformational change in the pheromone/odourant-bind ing protein, desequestering ions. Releasing the bound ions changes the pote ntial differences across a nearby super-sensitive dendritic membrane result ing in dendrite excitation. Pheromones will be implicated in the aetiology of the infectious, psychiatr ic and autoimmune diseases. This is the third article in a series of twelve to systematically explore this contention (see references 1-9). (C) 2001 H arcourt Publishers Ltd.