In utero and lactational lanthanum exposure induces olfactory dysfunction associated with downregulation of βIII-tubulin and olfactory marker protein in young rats.

Shuai Hao, Fei Yu, Aihui Yan, Yang Zhang, Jiali Han, Xuejun Jiang

Index: Biol. Trace Elem. Res. 148(3) , 383-91, (2012)

Full Text: HTML

Abstract

We evaluated the role of βIII-tubulin in the morphology of olfactory receptor neuron (ORN) and olfactory dysfunction in offspring caused by prenatal and postnatal lanthanum exposure. Pregnant rats were exposed to 0.25% lanthanum chloride in drinking water from gestational day (GD) 7 until postnatal day 21. From postnatal day 23 until postnatal day 28, pups were examined with buried food pellet and olfactory maze test. The ultrastructural features of ORNs in the olfactory epithelium (OE) were observed by transmission electron microscope. The expression of βIII-tubulin and olfactory marker protein (OMP) in the tissue sections and homogenates of OE were, respectively, measured by immunodetection and western blot. Behavioral analysis of olfaction showed that lanthanum chloride exposure induced olfactory dysfunction. Offsprings exposed to lanthanum chloride showed enlarged ORN knobs and a decreased number of cilia. In addition, the levels of OMP and βIII-tubulin expression in lanthanum chloride exposure offsprings significantly decreased. Developmental lanthanum exposure could impair olfaction, and this deficit may be attributed to the downregulation of βIII-tubulin and OMP in the OE.