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Hippocampal synaptic plasticity characterization of defective deiodinase 2 mice

AuthorsBosch-García, Daniel ; Montero-Pedrazuela, Ana ; Guadaño-Ferraz, Ana
Issue Date2010
Citation7th FENS Forum (2010)
AbstractThyroid hormones (TH) play an important role in Central Nervous System (CNS) development. The thyroid gland produces 30% of the nuclear active form Triiodothyronine (T3) and 70% of the non-nuclear active form Thyroxine (T4). Type 2 deiodinase (D2), that is expressed in the brain, is the main enzyme responsible for T4 deiodination to T3 for local use. The reduction of TH levels in developmental hypothyroidism is associated with neurological disorders in the adult, such as learning and memory impairment. The hippocampus participates in many learning and memory processes and is a target region of TH. In fact, in hypothyroid experimental animals, this brain area shows a severe deficiency in long-term potentiation (LTP), a well accepted cellular model for learning and memory. The goal of this study is to clarify the relation between local deregulation of TH metabolism and the synaptic plasticity capability of the hippocampal CA1 region in D2 deficient mutant mice (D2KO). We have observed a reduction of T3 and T4 levels in several brain regions of the adult D2KO mice. In the hippocampus this reduction reached 40%. We have performed the electrophysiological characterization of D2KO and WT mice stimulating and recording field EPSPs in CA1 region of hippocampal slices. The stimulus/response curve revealed an increment of synaptic responses in D2KO mice while the paired-pulse facilitation ratio, which estimates glutamate release probability, was not altered. However, early and late phases of LTP induced by one or three trains of high frequency stimulation, respectively, were not modified in D2KO mice. Nor did these animals show changes in long-term depression (LTD) induced by 1 Hz synaptic stimulation for 15 min. These results suggest that a 40% reduction in TH levels in the hippocampus affect basal synaptic transmission in CA3 - CA1 synapses but does not modify long-lasting changes of synaptic efficacy evoked by several protocols of synaptic stimulation.
DescriptionResumen del póster presentado al 7th Federation of European Neurosciences Societies (FENS) Forum, celebrado en Amsterdam (Netherlands) del 3 al 7 de julio de 2010.
Appears in Collections:(IIBM) Comunicaciones congresos
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