scholarly journals TrkB-Mediated Neuroprotective and Antihypoxic Properties of Brain-Derived Neurotrophic Factor

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Maria V. Vedunova ◽  
Tatiana A. Mishchenko ◽  
Elena V. Mitroshina ◽  
Irina V. Mukhina
Keyword(s):  
Neurotrophic Factor ◽  
Acute Hypoxia ◽  
Brain Derived Neurotrophic Factor ◽  
Bioelectrical Activity ◽  
Multielectrode Arrays ◽  
Protective Effects ◽  
Hippocampal Cultures ◽  
Tropomyosin Related Kinase B ◽  
Posthypoxic Period

The neuroprotective and antihypoxic effects of brain-derived neurotrophic factor (BDNF) on dissociated hippocampal cultures in a hypoxia model were investigated. These experiments demonstrate that 10 minutes of normobaric hypoxia increased the number of dead cells in primary culture, whereas a preventive application of BDNF increased the number of viable cells. Spontaneous bioelectrical and calcium activity in neural networks was analyzed using multielectrode arrays and functional intravital calcium imaging. The results indicate that BDNF affects the functional parameters of neuronal networks in dissociated hippocampal cultures over the 7-day posthypoxic period. In addition, the effects of k252a, an antagonist of tropomyosin-related kinase B (TrkB), on functional bioelectrical activity during and after acute hypoxia were investigated. It was shown that the protective effects of BDNF are associated with binding to the TrkB receptor. Finally, intravital fluorescent mRNA probes were used to study the role of NF-κB1 in the protective effects of BDNF. Our experiments revealed that BDNF application stimulates NF-κB1 mRNA synthesis in primary dissociated hippocampal cells under normal conditions but not in hypoxic state.

scholarly journals Progesterone Increases the Release of Brain-Derived Neurotrophic Factor from Glia via Progesterone Receptor Membrane Component 1 (Pgrmc1)-Dependent ERK5 Signaling

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4389-4400 ◽  
Author(s):  
Chang Su ◽  
Rebecca L. Cunningham ◽  
Nataliya Rybalchenko ◽  
Meharvan Singh
Keyword(s):  
Progesterone Receptor ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Experimental Models ◽  
Protective Effects ◽  
Membrane Component ◽  
Signaling Mechanism ◽  
Receptor Membrane ◽  
Bdnf Signaling

Progesterone (P4) is cytoprotective in various experimental models, but our understanding of the mechanisms involved is still incomplete. Our laboratory has implicated brain-derived neurotrophic factor (BDNF) signaling as an important mediator of P4's protective actions. We have shown that P4 increases the expression of BDNF, an effect mediated by the classical P4 receptor (PR), and that the protective effects of P4 were abolished using inhibitors of Trk receptor signaling. In an effort to extend our understanding of the interrelationship between P4 and BDNF signaling, we determined whether P4 influenced BDNF release and examined the role of the classical PR and a putative membrane PR, progesterone receptor membrane component-1 (Pgrmc1), as mediators of this response. Given recent data from our laboratory that supported the role of ERK5 in BDNF release, we also tested whether P4-induced BDNF release was mediated by ERK5. In this study, we found that P4 and the membrane-impermeable P4 (P4-BSA) both induced BDNF release from cultured C6 glial cells and primary astrocytes. Both these cells lack the classical nuclear/intracellular PR but express high levels of membrane-associated PR, including Pgrmc1. Using RNA interference-mediated knockdown of Pgrmc1 expression, we determined that P4-induced BDNF release was dependent on the expression of Pgrmc1, although pharmacological inhibition of the PR failed to alter the effects of P4. Furthermore, the BDNF release elicited by P4 was mediated by ERK5, and not ERK1/2. Collectively, our data describe that P4 elicits an increase in BDNF release from glia via a Pgrmc1-induced ERK5 signaling mechanism and identify Pgrmc1 as a potential therapeutic target for future hormone-based drug development for the treatment of such degenerative diseases as Alzheimer's disease as well as other diseases wherein neurotrophin dysregulation is noted.

Role of Tropomyosin-related kinase B receptor and brain-derived neurotrophic factor in cancer

Cytokine ◽  
2020 ◽  
Vol 136 ◽  
pp. 155270
Author(s):  
Vilson Serafim Junior ◽  
Glaucia Maria de Mendonça Fernandes ◽  
Juliana Garcia de Oliveira-Cucolo ◽  
Erika Cristina Pavarino ◽  
Eny Maria Goloni-Bertollo
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Tropomyosin Related Kinase B

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
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