DEVELOPMENTAL PLASTICITY OF THE RAT OLFACTORY RECEPTOR SHEET AS SHOWNBY COMPLETE RECOVERY OF SURFACE-AREA AND CELL NUMBER FROM EXTENSIVE EARLY HYPOTHYROID GROWTH-RETARDATION
Ma. Paternostro et E. Meisami, DEVELOPMENTAL PLASTICITY OF THE RAT OLFACTORY RECEPTOR SHEET AS SHOWNBY COMPLETE RECOVERY OF SURFACE-AREA AND CELL NUMBER FROM EXTENSIVE EARLY HYPOTHYROID GROWTH-RETARDATION, Developmental brain research, 76(2), 1993, pp. 151-161
To assess the effects of early thyroid deficiency, and recovery from t
his 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 were allowed to recove
r 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 num
ber of olfactory receptor neurons, basal cells and supporting cells, u
sing 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 unchan
ged. In the post-weaning hypothyroid rats, the expansion of surface ar
ea 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 complete
ly; 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-weanin
g rats. This pronounced ability to recover from early growth retardati
on contrasts with that seen in central neural structures, and indicate
s the great potential of OE for use as a model neural system for the s
tudy of recovery from early damage and growth retardation.