Neonatal olfactory sensory deprivation decreases BDNF in the olfactory bulb of the rat.

We hypothesized that brain-derived neurotrophic factor (BDNF) may be down-regulated in the olfactory bulb ipsilateral to experimental naris occlusion. Unilateral naris occlusion was performed on rats at postnatal day three (P3). On P10, P30, and P60 olfactory bulbs were weighed and assayed for tyrosine hydroxylase (TH), BDNF, and TrkB by Western blotting to determine the response of BDNF and its cognate receptor, TrkB, both during the acute phase of sensory loss (P10) and longer term. TH levels, which are highly dependent on intact input from the olfactory epithelium, were assayed as a means of determining the success of occlusion in each animal. At P10, BDNF protein expression was variable but most often increased ipsilateral to deprivation. In contrast, by P30 and P60 TH levels were found to be significantly decreased in the ipsilateral bulbs as were the levels of BDNF. TrkB protein levels changed little relative to the control side. Immunohistochemical localization of BDNF within the control-side olfactory bulb revealed small cells located mainly in the mitral cell layer and internal plexiform layer. Very few of the BDNF immunoreactive cells were visible in the bulb ipsilateral to the occlusion by P30. Given the roles of BDNF in survival of cells and plasticity during development, the decrease in BDNF expression subsequent to olfactory sensory deprivation may contribute to cellular and synaptic deficits observed by others following olfactory sensory deprivation.