Hypothyroidsm alters the development of radial glial cells in the term fetal and postnatal neocortex of the rat

Martinez-Galán, Juan R.; Rey, Francisco Escobar del; Escobar, Gabriella Morreale de; Santacana, Marı́a; Ruiz-Marcos, Antonio

doi:10.1016/j.devbrainres.2004.08.002

Cited by 44 publications

(30 citation statements)

References 40 publications

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“…Maternal hypothyroidism in the rat causes a temporal delay in the postnatal development of radial glia leading to a reduced number of neurons in layers IV and V but an increased number in layer VI (Lavado-Autric et al, 2003;Auso et al, 2004;Martinez-Galan et al, 2004). It is likely that the receptor-mediated hypothyroidism of the TR␣1ϩ/m mice also causes aberrancies in neocortical layering, a hypothesis supported by the decreased thickness of layers II-III observed by the CB immunostaining at P14.…”

Section: Development Of Interneuronsmentioning

confidence: 52%

Locomotor Deficiencies and Aberrant Development of Subtype-Specific GABAergic Interneurons Caused by an Unliganded Thyroid Hormone Receptor α1

Wallis¹,

Sjögren²,

Hogerlinden³

et al. 2008

J. Neurosci.

105

102

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Thyroid hormone (TH) deficiency during development causes severe and permanent neuronal damage, but the primary insult at the tissue level has remained unsolved. We have defined locomotor deficiencies in mice caused by a mutant thyroid hormone receptor ␣1 (TR␣1) with potent aporeceptor activity attributable to reduced affinity to TH. This allowed identification of distinct functions that required either maternal supply of TH during early embryonic development or sufficient innate levels of hormone during late fetal development. In both instances, continued exposure to high levels of TH after birth and throughout life was needed. The hormonal dependencies correlated with severely delayed appearance of parvalbumin-immunoreactive GABAergic interneurons and increased numbers of calretinin-immunoreactive cells in the neocortex. This resulted in reduced numbers of fast spiking interneurons and defects in cortical network activity. The identification of locomotor deficiencies caused by insufficient supply of TH during fetal/perinatal development and their correlation with subtype-specific interneurons suggest a previously unknown basis for the neuronal consequences of endemic cretinism and untreated congenital hypothyroidism, and specifies TR␣1 as the receptor isoform mediating these effects.

show abstract

Section: Development Of Interneuronsmentioning

confidence: 52%

Locomotor Deficiencies and Aberrant Development of Subtype-Specific GABAergic Interneurons Caused by an Unliganded Thyroid Hormone Receptor α1

Wallis¹,

Sjögren²,

Hogerlinden³

et al. 2008

J. Neurosci.

105

102

View full text Add to dashboard Cite

show abstract

“…Therefore, efforts should be on going made to establish the optimal therapy that leads to the possibility that children with CH reach their complete intellectual potential. Experimental studies at the cellular level found that hypothyroidism impaired neuronal progenitor proliferation and migration, which may contribute to persistent cognitive deficits and learning impairments [12][13][14]. Furthermore, cell proliferation, neuronal differentiation, and cognitive function are environmentally related and could be stimulated and improved by environmental stimulation [15].…”

mentioning

confidence: 99%

Risk factors for neurodevelopmental deficits in congenital hypothyroidism after early substitution treatment

et al. 2011

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“…Taken together, the findings from this and our 2013 psychometric study support the role of TH in brain development; various animal models have demonstrated that TH deficiency during critical periods of brain development results in irreversible morphological disturbances (Farwell & Leonard, 2005), impaired cortical layering (Calikoglu, Gutierrez Ospina, & D'Ercole, 1996), altered callosal connections (Berbel et al, 1993), reduced arborization (Anderson, Schoonover, & Jones, 2003), fewer synapses (Iiguez, Rodriguez-Pea, Ibarrola, Morreale de Escobar, & Bernal, 1992), and reduced and structurally abnormal myelinated axons (Freundl & Van Wynsberghe, 1978;GuadaoFerraz, Escobar del Rey, Morreale de Escobar, Innocenti, & Berbel, 1994). Importantly, the visual system is a known target for TH regulation during development (Berbel et al, 2010;Martinez-Galan, Escobar del Rey, Morreale de Escobar, Santacana, & RuizMarcos, 2004). As recently demonstrated by Clairman et al (2015), children who are deficient in TH during pregnancy, despite receiving early and continuous treatment after birth, experience aberrant neural development involving both cortical thinning and cortical thickening, including in regions belonging to both visual streams.…”

Section: Discussion Of Study 2 Resultsmentioning

confidence: 97%

Dorsal and ventral visual streams: Typical and atypical development

Simić

Rovet

2016

Child Neuropsychology

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The literature on visuospatial processing describes two distinct pathways within the brain: a dorsal route extending from the visual cortex into the parietal lobes that is critical for spatial processing and a ventral route extending from the visual cortex into the temporal lobes that is critical for form perception. These visual streams appear to differ in their developmental trajectories and their vulnerabilities to diverse neurodevelopmental conditions. The present work aims to investigate development and vulnerability in two aspects of dorsal and ventral visual-stream function, namely attention to location and attention to identity. In Study 1, we compare typically-developing (TD) youth aged 9 to 16 years with young adults aged 18 to 22 years on computerized location and identity tasks. In Study 2, we compare children and adolescents who have congenital hypothyroidism (CH), a pediatric endocrine disorder, with age-matched TD controls on the same tasks. The results from Study 1 show that the youths were less accurate than the adults at judging identity, whereas both groups were equally accurate at judging location. The results from Study 2 show that the youths with CH were slower but not less accurate than the TD youths in making both identity and location judgments. The results are interpreted as signifying later development of ventral (identity) stream functions compared to dorsal (location) but equal vulnerability of both functions in CH.

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Hypothyroidsm alters the development of radial glial cells in the term fetal and postnatal neocortex of the rat

Cited by 44 publications

References 40 publications

Locomotor Deficiencies and Aberrant Development of Subtype-Specific GABAergic Interneurons Caused by an Unliganded Thyroid Hormone Receptor α1

Locomotor Deficiencies and Aberrant Development of Subtype-Specific GABAergic Interneurons Caused by an Unliganded Thyroid Hormone Receptor α1

Risk factors for neurodevelopmental deficits in congenital hypothyroidism after early substitution treatment

Dorsal and ventral visual streams: Typical and atypical development

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