scholarly journals Histology and Brain Derived Neurotrophic Factor immunoreaction of the neurons in the corpora quadrigemina of the African grasscutter (Thryonomys swinderianus – Temminck, 1827)

2019 ◽  
Vol 52 (2) ◽  
pp. 49-58
Author(s):  
Chikera Samuel Ibe ◽  
Suleiman Olawoye Salami ◽  
Ekele Ikpegbu ◽  
Mohammed Adam

Abstract The African grasscutter is the second largest rodent in Africa, thus, a key component of the minilivestock industry. The study described the histological features and probed the distribution of Brain Derived Neurotrophic Factor (BDNF) in the corpora quadrigemina of the African grasscutter at foetal and postnatal developmental periods. Brain samples from foetuses explanted on foetal days 60 (F60) and 90 (F90) and extracted from 3 and 6-days-old pups (P3 and P6, respectively), 72-days-old juveniles (P72) and 450-days-old adults (P450) were used. They were prepared for histology and immunohistochemistry. Three laminae were distinct in the rostral colliculi at the foetal and postnatal periods; an outermost stratum zonale, middle stratum griseum superficiale and an inner stratum griseum profundum. Stratum griseum intermediale and stratum medullarium were not distinct. On F60 and F90, the stratum zonale was made of immature neurons, devoid of neurites; the central nucleus of the caudal colliculus was also made of immature migrating neurons. On P3, the neurons were already mature. The stratum zonale was made of medium-sized neuronal cells and thick processes. The thickness of this layer decreased with age. On P3, the caudal colliculus was made of all the components typical of a developed caudal colliculus. There was no BDNF immunoreactive cell in the stratum zonale at any postnatal period; a moderate BDNF-immunoreactivity in the stratum griseum superficiale on P3, a mild immunoreactivity on P6, none reactivity on P72 and mild on P450. The dorsal and lateral cortices of the caudal colliculus were none reactive to BDNF at any postnatal period. The results suggest a better auditory than visual capacity in the rodent.

Development ◽  
2000 ◽  
Vol 127 (21) ◽  
pp. 4531-4540 ◽  
Author(s):  
M.J. Donovan ◽  
M.I. Lin ◽  
P. Wiegn ◽  
T. Ringstedt ◽  
R. Kraemer ◽  
...  

Brain derived neurotrophic factor, BDNF, is a neurotrophin best characterized for its survival and differentiative effects on neurons expressing the trk B receptor tyrosine kinase. Although many of these neurons are lost in the BDNF(−)(/)(−)mouse, the early postnatal lethality of these animals suggests a wider function for this growth factor. Here, we demonstrate that deficient expression of BDNF impairs the survival of endothelial cells in intramyocardial arteries and capillaries in the early postnatal period, although the embryonic vasculature can remodel into arteries, capillaries and veins. BDNF deficiency results in a reduction in endothelial cell-cell contacts and in endothelial cell apoptosis, leading to intraventricular wall hemorrhage, depressed cardiac contractility and early postnatal death. Vascular hemorrhage is restricted to cardiac vessels, reflecting the localized expression of BDNF and trk B by capillaries and arterioles in this vascular bed. Conversely, ectopic BDNF overexpression in midgestational mouse hearts results in an increase in capillary density. Moreover, BDNF activation of endogenous trk B receptors supports the survival of cardiac microvascular endothelial cells cultured from neonatal mice. These results establish an essential role for BDNF in maintaining vessel stability in the heart through direct angiogenic actions on endothelial cells.


Nano Letters ◽  
2018 ◽  
Vol 18 (10) ◽  
pp. 6237-6247 ◽  
Author(s):  
Alexandra N. Edelbrock ◽  
Zaida Àlvarez ◽  
Dina Simkin ◽  
Timmy Fyrner ◽  
Stacey M. Chin ◽  
...  

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2461-2470 ◽  
Author(s):  
S. Biffo ◽  
N. Offenhauser ◽  
B.D. Carter ◽  
Y.A. Barde

The tyrosine kinase receptor trkB is thought to mediate the biological actions of brain-derived neurotrophic factor. This receptor is expressed by a large variety of neurons during development. Truncated trkB molecules lacking the tyrosine kinase domain have also been described, but their functions remain elusive. In order to gain insight into their role, we studied the pattern of expression and properties of these truncated receptors in the chick embryo. mRNA coding for truncated trkB was detected already early during neurogenesis and in situ hybridisation experiments indicated that the expression was in non-neuronal cells, as previously observed in the brain of adult rodents. Ependymal and leptomeningeal cells expressing high levels of truncated trkB were found to completely surround the developing brain and the spinal cord throughout development. In the otic vesicle, mesenchymal cells expressing truncated trkB surround cells producing brain-derived neurotrophic factor, as well as neurons expressing trkB with its tyrosine kinase domain. Non-neuronal cells were found not to express trkB mRNA coding for the tyrosine kinase domain. Studies with radioiodinated brain-derived neurotrophic factor performed on frozen sections of the chick embryo revealed that non-neuronal cells expressing truncated trkB bind brain-derived neurotrophic factor with high affinity and selectivity. In addition, experiments with dissociated leptomeningeal cells revealed that binding is rapidly followed by selective internalisation of the ligand. These results suggest that truncated trkB molecules form an efficient and selective barrier preventing the diffusion of brain-derived neurotrophic factor and eliminating it by internalisation.(ABSTRACT TRUNCATED AT 250 WORDS)


2016 ◽  
Vol 469 (1) ◽  
pp. 273-276 ◽  
Author(s):  
T. A. Gudasheva ◽  
K. N. Koliasnikova ◽  
T. A. Antipova ◽  
S. B. Seredenin

Molecules ◽  
2020 ◽  
Vol 25 (5) ◽  
pp. 1117 ◽  
Author(s):  
Yoshiko Furukawa ◽  
Yu-suke Washimi ◽  
Ryu-ichi Hara ◽  
Mizuki Yamaoka ◽  
Satoshi Okuyama ◽  
...  

(1) Background: Our published data have indicated that (1) auraptene (AUR), a citrus ingredient, has neuroprotective effects on the mouse brain, owing to its ability to suppress inflammation, such as causing a reduction in hyperactivation of microglia and astrocytes; (2) AUR has the ability to trigger phosphorylation (activation) of extracellular signal-related kinase (ERK) and cAMP response element-binding protein (CREB) in neuronal cells; (3) AUR has the ability to induce glial cell line-derived neurotrophic factor (GDNF) synthesis/secretion in rat C6 glioma cells. The well-established fact that the ERK-CREB pathway plays an important role in the production of neurotrophic factors, including GDNF and brain-derived neurotrophic factor (BDNF), prompted us to investigate whether AUR would also have the ability to induce BDNF expression in neuronal cells. (2) Methods: Mouse neuroblastoma neuro2a cells were cultured and the effects of AUR on BDNF mRNA expression and protein content were evaluated by RT-PCR and ELISA, respectively. (3) Results: The levels of BDNF mRNA and secreted BDNF were significantly increased by AUR in a dose- and time-dependent manner in neuro2a cells. (4) Conclusion: The induction of BDNF in neuronal cells might be, in part, one of the mechanisms accounting for the neuroprotective effects of AUR.


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