Implication of Monoamines, Cortisol, Brain Derived Neurotrophic Factor and Opioid Receptors Genes in the Depressive-like Effect of Isotretinoin in Adult Male Rats: Comparison with Clonidine

2014 ◽  
Vol 11 (3) ◽  
pp. 1065-1080
Author(s):  
Wafaa A Hassan ◽  
Mariam G Eshak ◽  
Nashwa M Saied

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3655-3665 ◽  
Author(s):  
Erich N. Ottem ◽  
Laurel A. Beck ◽  
Cynthia L. Jordan ◽  
S. Marc Breedlove

Castration of adult male rats causes the dendrites of androgen-sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB) to retract. Brain-derived neurotrophic factor (BDNF), via activation of tyrosine receptor kinase B (trkB), has been implicated in mediating androgen effects on SNB dendrites. We used in situ hybridization to demonstrate that SNB motoneurons in gonadally intact adult male rats contain mRNA for both BDNF and trkB. Two weeks after gonadectomy, both transcripts were significantly decreased in SNB motoneurons but not in the non-androgen-responsive motoneurons of the adjacent retrodorsolateral nucleus (RDLN). In a second experiment, target perineal and foot muscles of SNB and RDLN motoneurons, respectively, were injected with the retrograde tracer Fluorogold, and then immunocytochemistry was performed to examine the distribution of BDNF and trkB proteins in SNB and RDLN motoneurons and their glutamatergic afferents. Confocal analysis revealed that gonadectomy induces a loss of BDNF protein in SNB dendrites but not in RDLN dendrites. Testosterone treatment of castrates prevented the loss of BDNF from SNB dendrites. Confocal analysis also revealed trkB protein in SNB and RDLN dendrites and in their glutamatergic afferents. Gonadectomy had no discernable effect on trkB protein in SNB or RDLN motoneurons or in their glutamatergic afferents. These results suggest that androgen maintains a BDNF-signaling pathway in SNB motoneurons that may underlie the maintenance of dendritic structure and synaptic signaling.



2019 ◽  
Vol 26 (36) ◽  
pp. 36615-36622
Author(s):  
Iman Zangiabadi ◽  
Mohammad Reza Afarinesh ◽  
Ali Shamsara ◽  
Seyed Hasan Eftekhar-Vaghefi


2004 ◽  
Vol 27 (3) ◽  
pp. 280-295 ◽  
Author(s):  
Laurent Givalois ◽  
Gaëlle Naert ◽  
Florence Rage ◽  
Guy Ixart ◽  
Sandor Arancibia ◽  
...  




Author(s):  
Farouk Kamel Elbaz ◽  
Hanan F Aly ◽  
Wagdy Kb Khalil ◽  
Hoda F Booles ◽  
Gamila H Al

ABSTRACTObjective: The present study is aimed to investigate the promising action of Dunaliella salina extract as a natural protector against Alzheimer’sdisease (AD) and reported to possess a variety of activities, including antioxidant effects due to its ability to create large amount of carotenoids.Methods: D. salina is a type of halophile green microalgae was used in the present study. 50 male rats were used in this study, where aluminumchloride was orally administered to induce AD in a dose of 100 mg/kg, daily for 6 weeks. Al-intoxicated rats treated orally daily with D. salinaethanolic extract for 6 weeks in a dose of 150 mg/kg b.wt., whereas standard anti-Alzheimer drug donepezil tartrate was administered at the doseof 10 mg/kg b.wt./day for 6 consecutive weeks. The anti-Alzheimer properties of D. salina extract were achieved through measuring the calmodulin(CaM) level, paraoxonase 1 (PON1) activity, the antiapoptotic marker (Bcl2), brain-derived neurotrophic factor (BDNF), the generation of the DNAadducts (8-hydroxy-2-deoxyguanosine [8-OHdG]/2-deoxy guanosine [2-dG]), and alteration in the expression of amyloid precursor protein, β-siteAPP-cleaving enzyme 1 (BACE1), and β-site APP-cleaving enzyme 2 (BACE2) in AD rats.Results: The current results demonstrated that supplementation of AD rats with D. salina extract-enhanced CaM level, and increased PON1 activity,upregulated Bcl2 and BDNF, decreased the levels of DNA adducts (8-OHdG/2-dG), and suppressed the alterations of the expression levels of APP,BACE1, and BACE2-m RNAs as compared with those in AD rats.Conclusion: It could be concluded that the biological activity of D. salina extract might be regulated by 9-cis b-carotene protecting the brain cells fromthe oxidative stress in AD rats.Keywords: Dunaliella salina, Calmodulin, Paraoxonase 1, Bcl2, Brain-derived neurotrophic factor, Alzheimer’s disease, DNA adduct, Amyloid precursorprotein.





Sign in / Sign up

Export Citation Format

Share Document