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Olfactory physiology involves four main steps: nasal airflow perireceptor events, transduction, and central olfaction. Complex and diverse physiological processes are involved at each step and may be undermined by numerous pathological processes. Nasal airflow physiology involves fluid mechanics and specifc physicochemical properties of odorants; its main pathology is nasal polyposis. Perireceptor events involve transport molecules and enzymes which eliminate xenobiotics; its main pathology is chronic rhinitis. Transduction is the role of primary olfactory neurons, which detect and discriminate various chemical molecules across a wide range of concentrations. To fulfill this task, these cells use a large family of G protein-coupled receptors (odorant receptors). The main pathology is acute viral rhinitis affecting the olfactory organ. Finally, after olfactory signals are generated, the information is processed and coded in the olfactory bulb before being disseminated to several areas of the brain; its pathology is dominated by neurodegenerative disorders.

The pheromones are molecules, mainly aliphatic acids, with or without perceptible odor, recognized by specific receptors, the stimulation of which induces neuroendocrine reactions and affects the individual behavior. Olfactory receptors are underexpressed in human, 70 % of genes have become nonfunctional pseudogenes. But the remaining function was tested and is able to induce emotional reactions corresponding to a non-verbal signal of social interactions. In the present study, we review the actual knowledge on the olfactory receptors. They belong to the G-protein-coupled-receptors. Their signal is transduced to the hypothalamic-pituitary-gonadal axis. Some HLA-based olfactory cues are shown with reference to recent experiments. The pathophysiological hypotheses are considered with respect to studies in anorexia nervosa and Alzheimer' disease.

Recent work on the insect olfactory system has shown that its mushroom bodies (one of its major components) are involved in the fine discrimination of odours and that the temporal organisation of spike discharges plays a fundamental role. We propose here a model of a network that is able to decode the temporal patterns which characterise an odour. This model has three fundamental properties that seem to exist in all mushroom bodies of insects studied so far: a) long lasting inhibitions with rebounds, able to facilitate delayed spike generation; b) synaptic plasticity, which allows the network to learn to recognise temporal patterns; c) above all a large interconnection, which allows this network to recognise intervals of various duration. This model thus appears suited to identify combinations of temporal patterns in the dendrites of Kenyon cells (the principal cells in the calyces of the mushroom bodies). Moreover, the mushroom bodies integrate multimodal inputs, suggesting that the detection of temporal patterns may be extended to the detection of a complex environment, combining in particular olfactive and visual inputs.

Chemosensory dysfunction is relatively common. This article describes a series of 306 patients who presented with anosmia. We divided olfactory disorders into those associated with interruption of the transport of stimulus and those associated with damage to either peripheral or central nervous system structures. Nasal and paranasal sinus disease (transport interruption) was found to be causative in 67% of patients presenting with anosmia. These patients are generally 45 years old, the loss of olfaction is progressive and associated with additional nasal symptoms. Upper respiratory infection was found to be causative in 18% of patients. They are generally older, with a mean age of 58 years and are predominantly female (78%). The loss of smell is sudden and anosmia is often accompanied by troublesome parosmias (50%). CT-scan is necessary for the evaluation of a smell dysfunction.

Olfactory transduction is mediated by neuroepithelial cells localized on turbinal crests in naris. Odorant molecules are uptaked by the mucosa which flows on epithelial surface and some of the molecules enter in contact with olfactory cells tentacles. Odorant molecules interact with molecular receptors bound to cell membrane and induced successive reactions leading to ion channels opening and then to receptor potential appearance. The receptor cells degenerate when molecular receptors are saturated and, further regenerate, according a genetic program and olfactory learning action potentials which appear at the basal pole of the receptor cell are propagated along the small olfactory nerves to the olfactory bulb glomerulus. Several hundred axons enter in one glomerulus among others and make synaptic contacts with one dendritic tree of a mitral cell. The selection of the numerous signals which converge in the glomerulus, the codage in intensity, duration and contrast are made at this level. One odorant molecule activates some glomeruli (rarely one); a complex odor activates a great number of glomeruli according a complex spatial distribution. Following odor stimulation, the electrical signals are analysed in the olfactory bulb which delivers to the olfactory cortex various informations about the odor components that are to be selected and compared to anterior olfactory learning. Animal experimentation and clinical data show that memory storage is made using short, medium and long term memorization. This memory is integrated in the limbic system at the interface of neural structures which regulate the main behaviors and physiological functions. This explains the modulatory role of smell in some behaviors but complicate our understanding of access to olfactory memory.