Pyramidal cortical cell morphology studied by multivariate analysis: effects of neonatal thyroidectomy, ageing and thyroxine-substitution therapy

Ipiña, Santiago L.; Ruiz-Marcos, Antonio; Rey, Francisco Escobar del; Escobar, Gabriella Morreale de

doi:10.1016/0165-3806(87)90243-4

Cited by 19 publications

(7 citation statements)

References 8 publications

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“…In 60-day-old animals, the recovery was not complete, though treatment with T4 starting at 12 or 15 days of age had an ameliorating effect on the pyramids. However, in another work of the pyramidal cortical cell morphology studied by multivariate analysis, treatment with T4 started at 12 days of age did not prevent the changes due to T performed at 10 days of age ( 43 ). In the present work, the authors observed a clear-cut ameliorating effect of T4 administration on adult-onset hypothyroidism-induced morphological changes in the PFC.…”

Section: Discussionmentioning

confidence: 92%

Concurrent administration of thyroxine and donepezil induces plastic changes in the prefrontal cortex of adult hypothyroid rats

Wang

Zha

et al. 2017

Molecular Medicine Reports

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The aim of the present study was to observe the effects of the concurrent administration of thyroxine (T4) and an acetylcholinesterase (AChE) inhibitor, donepezil (DON), on the hypothyroidism-induced ultrastructural changes of the prefrontal cortex (PFC) in adult rats. The acetylcholine (ACh) content and AChE activity was assessed, as well as the expressions of synaptotagmin-1 (syt-1) and SNAP-25 were analyzed in the rats. Adding 0.05% propylthiouracil to rats' drinking water induced a hypothyroid rat model. The animals were treated with T4 and DON administered separately or in combination from the fifth week. Transmission electron microscope analysis revealed that hypothyroidism induced marked ultrastructural changes, including the neurons, the synapses and the myelin sheath in the PFC. T4 or DON treatment improved the morphologic features of the PFC, and the performance of the T4 combined DON group was the closest to the control group. Moreover, hypothyroidism significantly decreased the content of ACh (29.8%) and activity of AChE (27.8%), which were restored to control values by T4 administration. In addition, DON treatment restored ACh content to normal. At the protein level, hypothyroidism increased the levels of syt-1 and SNAP-25 in the PFC, both of which were not restored to control values following T4 administration, while concurrent administration of T4 and DON was able to induce this effect. These results suggested that adult-onset hypothyroidism induce morphological, biochemical and molecular alterations in the PFC, combined administration of T4 and DON induce plastic changes in the PFC, different from that of the standard T4 therapy, and that the DON treatment may facilitate the recovery of synaptic protein impairments induced by hypothyroidism.

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Section: Discussionmentioning

confidence: 92%

Concurrent administration of thyroxine and donepezil induces plastic changes in the prefrontal cortex of adult hypothyroid rats

Wang

Zha

et al. 2017

Molecular Medicine Reports

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“…Thyroid hormone has been demonstrated to affect morphological characteristics of several other neuronal populations, including cerebellar Purkinje cells (Legrand, 1977;Morreale de Escobar et al, 1983), dopaminergic hypothalamic neurons (Puymirat et al, 1983) and pyramidal cells of the neocortex (Ipina et al, 1987) and hippocampus (Rami et al, 1986). Nonetheless, the lack of apparent effect of thyroid hormone on the development of cholinergic PMT neurons suggests that thyroid hormone can influence specific neuronal configurations, including selected cells within categories ofneurons having the same transmitter phenotype.…”

Section: Thyroid Hormone Effects On the Morphology Of Cholinergic Neumentioning

confidence: 99%

“…It is now generally accepted that thyroid hormone plays a critical role in the development of several species (Kaltenbach, 1953;Kollros and McMurray, 1956;Eayrs, 1964;Sokoloff, 1977). A deficit or an excess of thyroid hormone during critical periods of development leads to profound and permanent biochemical (Kalaria et al, 198 1;Kalaria and Prince, 1985a, b) and morphological (Rami et al, 1986;Ipina et al, 1987) abnormalities in the mammalian nervous system. Biochemical evidence suggests that developing forebrain choline@ neurons are sensitive to thyroid hormone.…”

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confidence: 99%

Developing cholinergic basal forebrain neurons are sensitive to thyroid hormone

1989

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The influence of thyroid hormone on the development of cholinergic neurons in nucleus basalis was assessed in hyperthyroid, hypothyroid, and euthyroid rats by use of CAT immunohistochemistry and single-section Golgi-impregnation histology. Animals were made either hyperthyroid by daily injections of 1.0 micrograms/gm body weight triiodothyronine starting at postnatal day (P) 3 or hypothyroid by providing 0.4% propylthiouracil in the diet of dams from P2. Compared to developing control rats, increased exposure to thyroid hormone resulted in accelerated expression of CAT in nucleus basalis neurons. Overshoot in cell body size, a normal developmental phenomenon of cholinergic neurons in the basal nuclear complex, occurred earlier in hyperthyroid brains and was of a greater magnitude than in controls. Furthermore, increased numbers of primary dendrites and dendritic branchpoints accompanied by dendritic and perisomal filopodia-like structures were observed for nucleus basalis neurons in hyperthyroid rats. These dendritic changes persisted throughout the second postnatal month. After the fifth postnatal week, cell body sizes of these hyperthyroid CAT-positive neurons began to decrease and by P50 were significantly less than controls or similarly treated animals at earlier ages. By P64, the number of cholinergic neurons in nucleus basalis was appreciably less than in age-matched controls. Hypothyroidism resulted in a delay of normal CAT expression that persisted throughout the third postnatal week. After this time, CAT staining increased until normal immunoreactivity was attained in cell bodies, fibers, and terminal regions by P35. A deficit in thyroid hormone during development prevented overshoot in perikaryal size and resulted in diminished cross-sectional areas throughout the cholinergic nucleus basalis at all ages examined. Hypothyroidism also prevented the normal overproduction of dendrites in those cells and produced stunted dendritic trees at all ages examined. These morphological abnormalities persisted throughout the second postnatal month. The effects of thyroid hormone on cholinergic projection neurons in the rat brain appeared relatively selective for cells in the basal nuclear complex because neither hypothyroid nor hyperthyroid treatment produced changes in the cell body areas of the phenotypically similar CAT-positive neurons of the pontomesencephalotegmental complex.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…A Golgi study by Armstrong and coworkers (42) provides a direct comparison between the dendritic anomalies of Rett and Down syndrome, pointing out that basal dendrites of the frontal cortex in individuals affected by Rett syndrome are strongly impaired both in supra- and infragranular layers, while apical dendrites are affected only in supragranular layers. In experimental models of early-onset hypothyroidism, finally, both apical and basal dendrites of PNs appear to be strongly reduced (43). …”

Section: Dendrites and Connectivitymentioning

confidence: 99%

Alterations of Neocortical Pyramidal Neurons: Turning Points in the Genesis of Mental Retardation

Granato

Giorgio

2014

Front. Pediatr.

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Pyramidal neurons (PNs) represent the majority of neocortical cells and their involvement in cognitive functions is decisive. Therefore, they are the most obvious target of developmental disorders characterized by mental retardation. Genetic and non-genetic forms of intellectual disability share a few basic pathogenetic signatures that result in the anomalous function of PNs. Here, we review the key mechanisms impairing these neurons and their participation in the cortical network, with special focus on experimental models of fetal exposure to alcohol. Due to the heterogeneity of PNs, some alterations affect selectively a given cell population, which may also differ depending on the considered pathology. These specific features open new possibilities for the interpretation of cognitive defects observed in mental retardation syndromes, as well as for novel therapeutic interventions.

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Pyramidal cortical cell morphology studied by multivariate analysis: effects of neonatal thyroidectomy, ageing and thyroxine-substitution therapy

Cited by 19 publications

References 8 publications

Concurrent administration of thyroxine and donepezil induces plastic changes in the prefrontal cortex of adult hypothyroid rats

Concurrent administration of thyroxine and donepezil induces plastic changes in the prefrontal cortex of adult hypothyroid rats

Developing cholinergic basal forebrain neurons are sensitive to thyroid hormone

Alterations of Neocortical Pyramidal Neurons: Turning Points in the Genesis of Mental Retardation

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