Influence of Thyroidectomy and Subsequent Replacement Therapy Upon Conditioned Avoidance Learning in the Rat

Abstract

1.A shuttle-box technique (unconditioned stimulus\p=m-\electricshock; conditioned stimulus\p=m-\buzzer) has been used to study conditioned avoidance learning in rats thyroidectomized on the day of birth and during adult life. The effects of medication with thyroid hormone have also been examined.2. Both classes of thyroidectomized rat made significantly more errors than did normal litter-mates, an effect which was more marked following neonatal thyroidectomy than in animals thyroidectomized when adult. As a result of thyroidectomy the latencies of the response to both conditioned and unconditioned stimuli increased but rate of performance and the number of inter-trial crossings was reduced.3. Replacement therapy restored all these measures in the direction of normal. In most instances the differences in performance between normal and thyroidectomized rats of both classes was eliminated by medication, the behaviour of medicated thyroidectomized rats differing significantly from that of unmedicated animals and but little from the controls. 4. The relationship of these findings to the developmental and metabolic functions of the thyroid and to earlier behavioural studies on the significance of the age of thyroidectomy and medication are discussed.

An Appropriate Model for Congenital Hypothyroidism in the Rat Induced by Neonatal Treatment with Propylthiouracil and Surgical Thyroidectomy: Studies on Learning Ability and Biochemical Parameters

“…This result is consistent with reports by Eayrs and Le vine [7] and Tsukada et al [11], suggesting that in rats thyroid hormone is essential for a critical period of less than 3 weeks after birth. Therefore, we tried to induce a hypothyroid state in younger rats without using ra dioiodine.…”

“…However, the activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase and the brain myelin remained low throughout life unless thyroxine was administered. Though a critical correlation between biochemical pa rameters and learning ability is still uncertain, these results suggest that the formation of myelin in the neonatal period is at least dependent on thyroid hormone and would play an important role in mental development.Thyroid hormone is known to be important for growth and maturation of the central nervous system [1], However, it has an effect on development of brain tissue only for a certain critical period after birth [2][3][4][5][6], and the exact length of this critical period is still uncertain; in rats, Eayrs and Levine [7] concluded from behavioral studies that this pe riod is the first 24 days after birth, but other authors [8][9][10] have proposed shorter periods from biochemical and pathological studies.Tsukada et al [11] reported that in rats which had been radiothyroidectomized within 3 weeks after birth retarded learning ability was restored by treatment with growth hor mone but not by replacement therapy with thyroid hor mone. The same therapeutic effect of growth hormone has also been reported in neonatally radiothyroidectomized rats on the maze learning of Lashley [12].…”

The inhibitory effect of ACTH 1–10 on extinction of a conditioned avoidance response: Its independence of thyroid function

“…Similar ACTH-analogues have been shown to stimulate thyroid gland activity [3,7,9,27]. The thyroid seems implicated in acquisition and retention of avoidance behavior as well as in spontaneous behavior [2,12,13,14,15,16,18,21,23,24]. It might be possible therefore that ACTHanalogues exert their influence on avoidance behavior by mediation of the thyroid gland.…”

Induction of the UDP-Glucuronosyltransferase 1A1 during the Perinatal Period Can Cause Neurodevelopmental Toxicity

“…In rodents, perinatal hypothyroidism induced by propylthiouracil (PTU), methimazole, and thyroidectomy leads to impaired performance on a variety of motor and behavioral learning tasks (Eayrs and Levine, 1963;Davenport and Dorcey, 1972;Hasebe et al, 2008). It has been reported that, in the cerebellum, perinatal hypothyroidism induced various anatomic alterations, including delayed migration of granule cells, reduction of growth and branching of dendritic arborization of Purkinje cells, reduction of synaptogenesis between Purkinje cells and granule cell axons, delayed myelination, and changes in the synaptic connection among cerebellar neurons and afferent neuronal fibers in the cerebellum in rodents (Nicholson and Altman, 1972a,b,c;Legrand, 1979Legrand, , 1980.…”