Developmental plasticity of the rat olfactory receptor sheet as shown by complete recovery of surface area and cell number from extensive early hypothyroid growth retardation.

To assess the effects of early thyroid deficiency, and recovery from this condition on growth and development of olfactory epithelium (OE), male Sprague-Dawley rat pups were rendered hypothyroid by addition of propylthiouracil (PTU) to their drinking water from birth. At weaning some rats continued to receive PTU while others ere allowed to recover by withdrawal of PTU. Body weights and plasma thyroxine levels were determined in all groups. At the ages of 25, 50 and 90 days, the OE of these hypothyroid and 'recovery' rats were compared with age-matched controls for surface area, epithelial thickness, density and total number of olfactory receptor neurons, basal cells and supporting cells, using morphometric and cell counting methods. Normal rats showed marked and highly significant increases in the OE surface area and olfactory neuron number (2.6- and 2.3-folds) during the post-weaning period. In the hypothyroid rats, body growth and thyroxine levels were severely suppressed. The OE in the 25-day-old hypothyroid rats showed more than 40% reduction in surface area and cell number, compared to controls, but mean epithelial thickness and surface density of cells were unchanged. In the post-weaning hypothyroid rats, the expansion of surface area was severely retarded, and increase in cell number ceased entirely. In rats allowed to recover by PTU withdrawal, by 90 days of age, body weight and size had markedly increased but had not caught up completely; however, thyroxine levels were restored to normal and the surface area and cell number in the OE had increased in a compensatory manner, completely restoring the deficiencies in OE growth, including surface area, numbers of receptor neurons, basal cells and supporting cells. The results indicate marked growth plasticity of OE in the post-weaning rats. This pronounced ability to recover from early growth retardation contrasts with that seen in central neural structures, and indicates the great potential of OE for use as a model neural system for the study of recovery from early damage and growth retardation.