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      Postnatal development of masseteric motoneurons in congenital hypothyroid rats.

      Brain Research

      Animals, Animals, Newborn, Cell Enlargement, Cell Shape, Cell Size, Congenital Hypothyroidism, complications, Dendrites, pathology, Disease Models, Animal, Feeding Behavior, physiology, Horseradish Peroxidase, Male, Mandibular Nerve, growth & development, physiopathology, Masseter Muscle, innervation, Mastication, Motor Neurons, Neuromuscular Junction, metabolism, Pons, Propylthiouracil, adverse effects, Rats, Rats, Sprague-Dawley, Stomatognathic System, Thyroid Gland, drug effects, Thyroid Hormones, Trigeminal Nerve Diseases, etiology

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          It has been known that an intact thyroid hormone is obligatory for the attainment of the normal masticatory function at the time of weaning. Following induced maternal thyroid hypo-function, the development of masseter motoneurons was determined at postnatal days 1, 7, 15 and 23 (weaning time), using retrograde transport of horseradish peroxidase (HRP) in the normal and hypothyroid pups. Based on the HRP labeling profile (strong and weak), the soma area of the masseteric labeled motoneurons was measured in each group. No significant morphological differences were observed at the end of the first week of life. On day 15, hypothyroid masseteric labeled motoneurons consisted of 76% small and 24% medium-sized neurons compared to 58% and 42% in normal pups, respectively. At the time of weaning (i.e., day 23) the number of large masseter motoneurons reached to 1/3 of normal value with few, short and disoriented dendrites in the hypothyroid pup. There was no statistically significant difference in the uptake of HRP from the neuromuscular junction. These results suggest that neonatal thyroid hormone deficiency considerably postponed the development of feeding behavior from sucking to chewing and biting.

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