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• W2149579087 abstract "We investigated the role of the neurotrophin BDNF signalling via the TrkB receptor in rat adrenomedullary chromaffin cells (AMCs) exposed to normoxia (Nox; 21% O2) and chronic hypoxia (CHox; 2% O2) in vitro for ∼ 48 h. TrkB receptor expression was upregulated in primary AMCs and in immortalized chromaffin (MAH) cells exposed to CHox; this effect was absent in MAH cells deficient in the transcription factor, hypoxia inducible factor (HIF)-2α. Relative to normoxic controls, activation of the TrkB receptor in chronically hypoxic AMCs led to a marked increase in membrane excitability, intracellular [Ca(2+)], and catecholamine secretion. The BDNF-induced rise of intracellular [Ca(2+)] in CHox cells was sensitive to the selective T-type Ca(2+) channel blocker TTA-P2 and tetrodotoxin (TTX), suggesting key roles of low threshold T-type Ca(2+) and voltage-gated Na(+) channels in the signalling pathway. Environmental stressors, including chronic hypoxia, enhance the ability of adrenomedullary chromaffin cells (AMCs) to secrete catecholamines; however, the underlying molecular mechanisms remain unclear. Here, we investigated the role of brain-derived neurotrophic factor (BDNF) signalling in rat AMCs exposed to chronic hypoxia. In rat adrenal glands, BDNF and its tropomyosin-related kinase B (TrkB) receptor are highly expressed in the cortex and medulla, respectively. Exposure of AMCs to chronic hypoxia (2% O2; 48 h) in vitro caused a significant increase to TrkB mRNA expression. A similar increase was observed in an immortalized chromaffin cell line (MAH cells); however, it was absent in MAH cells deficient in the transcription factor HIF-2α. A specific TrkB agonist, 7,8-dihydroxyflavone (7,8-DHF), stimulated quantal catecholamine secretion from chronically hypoxic (CHox; 2% O2) AMCs to a greater extent than normoxic (Nox; 21% O2) controls. Activation of TrkB by BDNF or 7,8-DHF increased intracellular Ca(2+) ([Ca(2+)]i), an effect that was significantly larger in CHox cells. The 7,8-DHF-induced [Ca(2+)]i rise was sensitive to the tyrosine kinase inhibitor K252a and nickel (2 mm), but not the Ca(2+) store-depleting agent cyclopiazonic acid. Blockade of T-type calcium channels with TTA-P2 (1 μm) or voltage-gated Na(+) channels with TTX inhibited BDNF-induced [Ca(2+)]i increases. BDNF also induced a dose-dependent enhancement of action potential firing in CHox cells. These data demonstrate that during chronic hypoxia, enhancement of BDNF-TrkB signalling increases voltage-dependent Ca(2+) influx and catecholamine secretion in chromaffin cells, and that T-type Ca(2+) channels play a key role in the signalling pathway." @default.
• W2149579087 created "2016-06-24" @default.
• W2149579087 creator A5053204257 @default.
• W2149579087 creator A5072838097 @default.
• W2149579087 creator A5088213319 @default.
• W2149579087 date "2015-07-31" @default.
• W2149579087 modified "2023-10-02" @default.
• W2149579087 title "Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells" @default.
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• W2149579087 doi "https://doi.org/10.1113/jp270725" @default.
• W2149579087 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4553053" @default.
• W2149579087 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26095976" @default.
• W2149579087 hasPublicationYear "2015" @default.
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