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Thyroid hormones regulate the frequency of miniature end‐plate currents in pre‐ and prometamorphic stages of the tadpole tail
Author(s) -
Rojas Legier V.,
Bonilla Laurie,
Baez Sheila,
LasaldeDominicci José A.
Publication year - 2002
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10522
Subject(s) - inhibitory postsynaptic potential , endocrinology , medicine , neuromuscular junction , biology , neurotransmitter , axolotl , tadpole (physics) , hormone , chemistry , microbiology and biotechnology , neuroscience , central nervous system , physics , regeneration (biology) , particle physics
Thyroid hormones (THs), primarily 3,3′,5‐triiode‐ L ‐thyronine (T 3 ), have been clearly established as natural inducers of apoptosis during metamorphosis of anuran embryos. We decided to use this phenomenon to test the hypothesis that, prior to genomic activation, T 3 has acute actions in the neuromuscular junction (NMJ) of the tail of amphibian embryos. We detected a dramatic increase in the production of miniature end‐plate currents (MEPCs) 2–5 min after continuous application of T 3 (250 nM) using focal recordings under voltage clamp. Furthermore, this increase in the spontaneous release of neurotransmitter, evaluated by the MEPC frequency, was maintained for several hours. Reverse‐T 3 , the “inhibitory” form of THs, prevented this increase in MEPC frequency, suggesting that this is probably a highly specific action of T 3 . In addition, the elevation in MEPC frequency induced by T 3 was unchanged in the presence or absence of extracellular calcium. The T 3 ‐mediated increase in MEPC frequency was blocked by niflumic acid, a nonsteroidal antinflammatory fenamate used to prevent the apoptotic volume decrease observed in many systems. The present study demonstrated that T 3 induces a remarkable nongenomic action in the NMJ of the tadpole tail at pre‐ and promatamorphic stages. © 2002 Wiley‐Liss, Inc.