scholarly journals Neurotrophic factor for parasympathetic neurons: Neurite outgrowth of ciliary neurons by gizzard extract

1981 ◽  
Vol 31 ◽  
pp. 97
Author(s):  
Yokichi Hayashi ◽  
Haruhiro Higashida ◽  
Naomasa Miki
2015 ◽  
Vol 68 ◽  
pp. 222-233 ◽  
Author(s):  
Prabhuanand Selvaraj ◽  
Jane S.W. Huang ◽  
Alexander Chen ◽  
Nir Skalka ◽  
Rina Rosin-Arbesfeld ◽  
...  

2012 ◽  
Vol 18 (5) ◽  
pp. 534-543 ◽  
Author(s):  
Djoere Gaublomme ◽  
Tom Buyens ◽  
Lieve Moons

Despite intensive research efforts over the past years, regeneration of injured axons in the central nervous system remains elusive. In the quest for neurostimulatory agents that promote regeneration, well-defined models and analysis methods are required. Tissue explant cultures closely resemble the in vivo situation, making them ideal to study the effect of compounds on the neuro-glial network. This study reports the optimization of an explant culture technique using retinas of neonatal mice and the development of an analysis script that allows for rapid and automated analysis of neurite outgrowth from these explants. The key features of this script (i.e., local thresholding and form selection) allow for swift and unbiased detection of neurite outgrowth. The novel analysis method is compared with two commonly used manual methods and successfully validated by performing dose-response studies with molecules known to either inhibit (anti–β1-integrin antibody) or stimulate (brain-derived neurotrophic factor and ciliary neurotrophic factor) neurite outgrowth from retinal explants. Finally, the new analysis script is used to study whether retinal explant origin has any effect on neurite outgrowth.


1993 ◽  
Vol 123 (6) ◽  
pp. 1555-1566 ◽  
Author(s):  
T E Allsopp ◽  
M Robinson ◽  
S Wyatt ◽  
A M Davies

We have investigated the role of trkA, the tyrosine kinase NGF receptor, in mediating the survival response of embryonic neurons to NGF. Embryonic trigeminal mesencephalic (TMN) neurons, which normally survive in the presence of brain-derived neurotrophic factor (BDNF) but not NGF, become NGF-responsive when microinjected with an expression vector containing trkA cDNA. In contrast, microinjection of ciliary neurotrophic factor (CNTF)-dependent embryonic ciliary neurons with the same construct does not result in the acquisition of NGF responsiveness by these neurons despite de novo expression of trkA mRNA and protein. The failure of trkA to result in an NGF-promoted survival response in ciliary neurons is not due to absence of the low-affinity NGF receptor, p75, in these neurons. Quantitative RT/PCR and immunocytochemistry showed that TMN and ciliary neurons both express p75 mRNA and protein. These findings not only provide the first direct experimental demonstration of trkA mediating a physiological response in an appropriate cell type, namely NGF-promoted survival of embryonic neurons, but indicate that not all neurons are able to respond to a trkA-mediated signal transduction event.


2000 ◽  
Vol 43 (2) ◽  
pp. 198-205 ◽  
Author(s):  
Antti Laurikainen ◽  
Jukka O. Hiltunen ◽  
Judith Thomas-Crusells ◽  
Sampsa Vanhatalo ◽  
Urmas Arum�e ◽  
...  

2007 ◽  
Vol 283 (10) ◽  
pp. 6546-6560 ◽  
Author(s):  
Mark A. Ozog ◽  
Geetanjalee Modha ◽  
John Church ◽  
Rayne Reilly ◽  
Christian C. Naus

2008 ◽  
Vol 181 (1) ◽  
pp. 37-41 ◽  
Author(s):  
Philip Van Damme ◽  
Annelies Van Hoecke ◽  
Diether Lambrechts ◽  
Peter Vanacker ◽  
Elke Bogaert ◽  
...  

Recently, mutations in the progranulin (PGRN) gene were found to cause familial and apparently sporadic frontotemporal lobe dementia (FTLD). Moreover, missense changes in PGRN were identified in patients with motor neuron degeneration, a condition that is related to FTLD. Most mutations identified in patients with FTLD until now have been null mutations. However, it remains unknown whether PGRN protein levels are reduced in the central nervous system from such patients. The effects of PGRN on neurons also remain to be established. We report that PGRN levels are reduced in the cerebrospinal fluid from FTLD patients carrying a PGRN mutation. We observe that PGRN and GRN E (one of the proteolytic fragments of PGRN) promote neuronal survival and enhance neurite outgrowth in cultured neurons. These results demonstrate that PGRN/GRN is a neurotrophic factor with activities that may be involved in the development of the nervous system and in neurodegeneration.


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