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Figure 3 | Neural Development

Figure 3

From: Molecular components underlying nongenomic thyroid hormone signaling in embryonic zebrafish neurons

Figure 3

Rohon-Beard cells in Na v 1.6a morphants did not show a rapid T4 response. (A-C) The representative traces show Rohon-Beard cell (RB) INa before (black) and 5 minutes after (red) acute T4 application. Embryos had been injected with either the 1.6 missense control morpholino (Ctl MO) (A), or MOs targeting sodium channels Nav1.1l (1.1 MO) or Nav1.6a (1.6 MO) (C). (D) Injection of 1.6 MO or 1.1 MO reduced RB INa peak amplitude compared to control. The reductions in INa peak amplitudes were consistent with previously reported values for successful knockdown of either Nav1.6a or nav1.1la [18]. Injection of 5-missense control MO did not significantly alter INa peak amplitude. The data presented in (D) were recorded in the presence of 30 mM extracellular Na+. (E) Embryos injected with 5-missense MO or 1.1 MO showed significant increases in RB INa peak amplitude after 5 minutes of T4 application. In contrast, RBs in 1.6 morphant embryos did not show an increase in INa amplitude after T4 application. (F) Injection of 1.6 MO (n = 3) reduced peak INa amplitude in 125 mM extracellular recording solution compared to controls (n = 5; P < 0.05). In control embryos, thyroid hormone antagonism (tetrac) or αVβ3 blockade (LM609) injection reduced INa amplitudes [11]. However, in 1.6 morphant embryos, neither LM609 (n = 5) nor tetrac (n = 9) altered INa amplitudes compared to 1.6 morphants unexposed to LM609 or tetrac (n = 3). Asterisks represent a p-value of < 0.05 and error bars represent standard errors.

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