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Abstract: Olfactory neurons in the nasal mucosa have the capacity to regenerate continuously along the lifespan by neurogenesis processes starting with progenitor cells close to the basal lamina. The cellular turnover into olfactory neuroepithelium may be modified by environmental stimuli insofar as nasal mucosa is directly in contact with airborne chemicals. However, few studies have been focused on selective changes, especially those concerning mature olfactory neurons and basal cells during specific inhalation exposure. Among chemicals, solvents are known to induce changes in smell abilities and concomitant histological and cellular modifications related to the type of molecule, concentration and time of exposure. This study was designed to characterize smell sensitivity (using behavioral tests) and immunohistochemical effects on olfactory neuroepithelium induced by pyridine exposure in mice. Olfactory marker protein (OMP) and proliferating cell nuclear antigen (PCNA) were used to characterize respectively mature olfactory neurons and basal cells. Results showed that inhalation exposure to pyridine had no impact on smell sensitivity whatever the concentration used and the time of exposure. These findings were in agreement with immunohistochemical measurements showing the same cellular kinetic whatever the condition of exposition to pyridine. Indeed, OMP-positive cells increased and PCNA-positive cells decreased as early as the beginning of exposure and cell amounts remained stable at this level until the end of exposure. These findings suggest that pyridine could have the property to rapidly activate a cellular turnover from basal cell progenitors. Rather than toxic effects, the present findings suggest that the metabolites of pyridine might have cell cycle activation properties. [Copyright &y& Elsevier]

Although recent studies have documented compensatory generation of neurons in adult brains in response to various insults, a noninjurious short episode of hypoxia in rat neonates has been shown to trigger neurogenesis within the ensuing weeks, without apparent brain lesions. Very little is known of the long-term consequences. We therefore investigated the effects of such a conditioning-like hypoxia (100% N(2), 5 min) on the brain and the cognitive outcomes of rats at 40 to 100 days of age. Control and posthypoxic rats developed similar learning capacities over postnatal days 14 to 18, but hypoxia was associated with enhanced scores in a test used to evaluate memory retrieval between 40 and 100 days. A striking sexual dimorphism was observed, with an earlier functional gain observed in female (40 days) compared with male (100 days) rats; gains were associated with matching structural changes in areas involved in cognition, including the hippocampus and frontal cortex. Therefore, it is proposed that brief neonatal hypoxia may exert long-term beneficial effects through neurogenesis stimulation. © Elsevier Inc. All rights reserved. [ABSTRACT FROM AUTHOR]