Ethanol exposure enhances cell death in the developing cerebral cortex: Role of brain-derived neurotrophic factor and its signaling pathways

2002 ◽  
Vol 68 (2) ◽  
pp. 213-225 ◽  
Author(s):  
E. Climent ◽  
M. Pascual ◽  
J. Renau-Piqueras ◽  
C. Guerri
Keyword(s):  
Cell Death ◽  
Cerebral Cortex ◽  
Signaling Pathways ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Ethanol Exposure

scholarly journals Brain-derived neurotrophic factor enhances cholinergic contraction of longitudinal muscle of rabbit intestine via activation of phospholipase C

2014 ◽  
Vol 306 (4) ◽  
pp. G328-G337 ◽  
Author(s):  
M. Al-Qudah ◽  
C. D. Anderson ◽  
S. Mahavadi ◽  
Z. L. Bradley ◽  
H. I. Akbarali ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Signaling Pathways ◽  
Phospholipase C ◽  
Neurotrophic Factor ◽  
Longitudinal Muscle ◽  
Muscle Cells ◽  
Brain Derived Neurotrophic Factor ◽  
Trkb Receptors ◽  
Rabbit Intestine

Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family of proteins best known for its role in neuronal survival, differentiation, migration, and synaptic plasticity in central and peripheral neurons. BDNF is also widely expressed in nonneuronal tissues including the gastrointestinal tract. The role of BDNF in intestinal smooth muscle contractility is not well defined. The aim of this study was to identify the role of BDNF in carbachol (CCh)- and substance P (SP)-induced contraction of intestinal longitudinal smooth muscle. BDNF, selective tropomyosin-related kinase B (TrkB) receptor agonists, and pharmacological inhibitors of signaling pathways were examined for their effects on contraction of rabbit intestinal longitudinal muscle strips induced by CCh and SP. BDNF activation of intracellular signaling pathways was examined by Western blot in homogenates of muscle strips and isolated muscle cells. One-hour preincubation with BDNF enhanced intestinal muscle contraction induced by CCh but not by SP. The selective synthetic TrkB agonists LM 22A4 and 7,8-dihydroxyflavone produced similar effects to BDNF. The Trk antagonist K-252a, a TrkB antibody but not p75NTR antibody, blocked the effect of BDNF. The enhancement of CCh-induced contraction by BDNF was blocked by the phospholipase C (PLC) antagonist U73122, but not by ERK1/2 or Akt antagonists. Direct measurement in muscle strips and isolated muscle cells showed that BDNF caused phosphorylation of TrkB receptors and PLC-γ, but not ERK1/2 or Akt. We conclude that exogenous BDNF augments the CCh-induced contraction of longitudinal muscle from rabbit intestine by activating TrkB receptors and subsequent PLC activation.

Neurological And Non Neurological Role of Brain-Derived Neurotrophic Factor (BDNF) in Developing Jaw

2020 ◽  
Vol 11 (2) ◽  
pp. 1577
Author(s):  
Noor Natik Raheem ◽  
Mohammed Faris ◽  
Athraa Y. Al-Hijazi ◽  
Ali I Alqurshi
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor

Role of brain-derived neurotrophic factor in the control of D3 receptor expression

1999 ◽  
Vol 9 ◽  
pp. 184-185 ◽  
Author(s):  
O. Guillin ◽  
L. Damier ◽  
N. Griffon ◽  
J. Diaz ◽  
P. Carroll ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Receptor Expression ◽  
D3 Receptor

Good proteins gone bad: brain-derived neurotrophic factor and its receptors in endometriotic implants and the role of estrogen

2014 ◽  
Vol 102 (3) ◽  
pp. e10-e11
Author(s):  
J.M. Wessels ◽  
N.A. Leyland ◽  
S.K. Agarwal ◽  
W.G. Foster
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor
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