Abstract：
:Thyroid hormone deficiency during early developmental stages causes a multitude of functional and morphological deficits in the brain. In the present study we investigate the effects of a mutated thyroid hormone receptor TR alpha 1 and the resulting receptor-mediated hypothyroidism on the development of GABAergic neurotransmission and seizure susceptibility of neuronal networks. We show that mutant mice have a strong resistance to seizures induced by antagonizing the GABA(A) receptor complex. Likewise the hippocampal network of mutant mice shows a decreased likelihood to transform physiological into pathological rhythmic network activity such as seizure-like interictal waves. As we demonstrate the cellular basis for this behavior is formed by the excitatory nature of GABAergic neurotransmission in the mutant mice, possibly caused by altered Cl(-) homeostasis, and/or the altered patterning of calretinin-positive cells in the hippocampal hilus. This study is, to our knowledge, the first to show an effect of maternal and early postnatal hypothyroidism via TR alpha 1 on the development of GABAergic neurotransmission and susceptibility to epileptic seizures.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Hadjab-Lallemend S,Wallis K,van Hogerlinden M,Dudazy S,Nordström K,Vennström B,Fisahn Adoi
10.1016/j.neuropharm.2010.02.005subject
Has Abstractpub_date
2010-06-01 00:00:00pages
1130-9issue
7eissn
0028-3908issn
1873-7064pii
S0028-3908(10)00038-9journal_volume
58pub_type
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journal_title：Neuropharmacology
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