Search results for "Tropomyosin receptor kinase A"
showing 5 items of 5 documents
Sex hormones modulate pathogenic processes in experimental traumatic brain injury.
2018
Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…
Sciences within European Young Researcher Community272The neuro-cardiac interaction defines an extracellular microdomain required for neurotrophic si…
2016
# 272 The neuro-cardiac interaction defines an extracellular microdomain required for neurotrophic signaling {#article-title-2} Purpose: Sympathetic neurons (SNs) innervate the myocardium with a defined topology that allows physiological modulation of cardiac activity. Limiting amounts of neurotrophins released by cardiac cells control SN viability and myocardial distribution, whose impairment has been described in a number of heart diseases (e.g. myocardial infarction, heart failure). Therefore, the fine control of cardiac innervation is crucial to ensure the physiological sympathetic function. It has been demonstrated that SNs directly interact with cardiomyocytes (CMs). Although it has b…
Truncated TrkB receptor-induced outgrowth of dendritic filopodia involves the p75 neurotrophin receptor.
2004
The Trk family of receptor tyrosine kinases and the p75 receptor (p75NTR) mediate the effects of neurotrophins on neuronal survival, differentiation and synaptic plasticity. The neurotrophin BDNF and its cognate receptor tyrosine kinase, TrkB.FL, are highly expressed in neurons of the central nervous system. At later stages in postnatal development the truncated TrkB splice variants (TrkB.T1, TrkB.T2) become abundant. However, the signalling and function of these truncated receptors remained largely elusive.We show that overexpression of TrkB.T1 in hippocampal neurons induces the formation of dendritic filopodia, which are known precursors of synaptic spines. The induction of filopodia by T…
Expression of neurotrophins, GDNF, and their receptors in rat thyroid tissue
1999
Levels of mRNA for neurotrophins (brain-derived neurotrophic factor, BDNF; neurotrophin 3, NT-3; neurotrophin 4, NT-4) and their receptors (trkA, trkB, trkC) and for glial cell line-derived neurotrophic factor (GDNF) and its receptors (ret, GDNFR-alpha) were measured in rat thyroid tissue by ribonuclease protection assays. In thyroid tissue the NT-3 mRNA level was threefold lower and the NT-4 mRNA level sixfold higher than those detected in adult rat hippocampus, while BDNF mRNA was undetectable. Very low levels of mRNA for truncated trkB and trkC receptors and no catalytic trkA, trkB or trkC were found. In conclusion NT-3 and NT-4, but not the corresponding functional receptors, are expres…
Tiam1 as a Signaling Mediator of Nerve Growth Factor-Dependent Neurite Outgrowth
2010
Nerve Growth Factor (NGF)-induced neuronal differentiation requires the activation of members of the Rho family of small GTPases. However, the molecular mechanisms through which NGF regulates cytoskeletal changes and neurite outgrowth are not totally understood. In this work, we identify the Rac1-specific guanine exchange factor (GEF) Tiam1 as a novel mediator of NGF/TrkA-dependent neurite elongation. In particular, we report that knockdown of Tiam1 causes a significant reduction in Rac1 activity and neurite outgrowth induced by NGF. Physical interaction between Tiam1 and active Ras (Ras- GTP), but not tyrosine phosphorylation of Tiam1, plays a central role in Rac1 activation by NGF. In add…