scholarly journals Rapid brain-derived neurotrophic factor-dependent sequestration of amygdala and hippocampal GABAA receptors via different tyrosine receptor kinase B-mediated phosphorylation pathways

Neuroscience ◽  
2011 ◽  
Vol 176 ◽  
pp. 72-85 ◽  
Author(s):  
L. Mou ◽  
S.A. Heldt ◽  
K.J. Ressler
Keyword(s):  
Gabaa Receptors ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Receptor Kinase ◽  
Tyrosine Receptor Kinase

scholarly journals Brain-Derived Neurotrophic Factor and Supraoptic Vasopressin Neurons in Hyponatremia

2019 ◽  
Vol 110 (7-8) ◽  
pp. 630-641
Author(s):  
Kirthikaa Balapattabi ◽  
Joel T. Little ◽  
Martha Bachelor ◽  
J. Thomas Cunningham
Keyword(s):  
Liver Failure ◽  
Neurotrophic Factor ◽  
Plasma Osmolality ◽  
Liver Weight ◽  
Brain Derived Neurotrophic Factor ◽  
Male Rats ◽  
Receptor Kinase ◽  
Control Shrna ◽  
Vasopressin Neurons ◽  
Tyrosine Receptor Kinase

Hyponatremia due to elevated arginine vasopressin (AVP) secretion increases mortality in liver failure patients. The mechanisms causing dysregulation of AVP secretion are unknown. Our hypothesis is that inappropriate AVP release associated with liver failure is due to increased brain-derived neurotrophic factor (BDNF) in the supraoptic nucleus (SON). BDNF diminishes GABAA inhibition in SON AVP neurons by increasing intracellular chloride through tyrosine receptor kinase B (TrkB) activation and downregulation of K+/Cl– cotransporter 2 (KCC2). This loss of inhibition could increase AVP secretion. This hypothesis was tested using shRNA against BDNF (shBDNF) in the SON in bile duct ligated (BDL) male rats. All BDL rats had significantly increased liver weight (p < 0.05; 6–9) compared to shams. BDL rats with control ­shRNA injections (BDL scrambled [SCR]) developed hyponatremia with increased plasma AVP and copeptin (CPP; all p < 0.05; 6–9) compared to sham groups. This is the first study to show that phosphorylation of TrkB is significantly increased along with significant decrease in phosphorylation of KCC2 in BDL SCR rats compared to the sham rats (p < 0.05;6–8). Knockdown of BDNF in the SON of BDL rats (BDL shBDNF) significantly increased plasma osmolality and hematocrit compared to BDL SCR rats (p < 0.05; 6–9). The BDL shBDNF rats had significant (p < 0.05; 6–9) decreases in plasma AVP and CPP concentration compared to BDL SCR rats. The BDNF knockdown also significantly blocked the increase in TrkB phosphorylation and decrease in KCC2 phosphorylation (p < 0.05; 6–8). The results indicate that BDNF produced in the SON contributes to increased AVP secretion and hyponatremia during liver failure.

miR-124 antagonizes the antidepressant-like effects of standardized gypenosides in mice

2018 ◽  
Vol 32 (4) ◽  
pp. 458-468 ◽  
Author(s):  
Li-Tao Yi ◽  
Rong-Hao Mu ◽  
Shu-Qi Dong ◽  
Shuang-Shuang Wang ◽  
Cheng-Fu Li ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Neurotrophic Factor ◽  
Glucocorticoid Receptors ◽  
Brain Derived Neurotrophic Factor ◽  
Sucrose Preference ◽  
Mild Stress ◽  
Dependent Manner ◽  
Receptor Kinase ◽  
Immobility Time ◽  
Tyrosine Receptor Kinase

Our previous study demonstrated that gypenosides produced antidepressant-like effects in mice exposed to chronic mild stress in a brain-derived neurotrophic factor-dependent manner. However, whether other mechanisms are involved in the antidepressant-like effects of gypenosides is not clear. miR-124 is one of the most abundant microRNAs in the hippocampus, and its dysregulation is related to the pathophysiology of depression. The glucocorticoid receptor is dysfunctional in depression, and it is a direct target of miR-124. Therefore, the present study used corticosterone-induced mice as a model to evaluate the role of miR-124 on the antidepressant-like effects of gypenosides. miR-124 agomir was intracerebrally injected prior to administration of gypenosides and corticosterone injection. Sucrose preference and forced swimming tests were performed 21 days later. Proteins related to glucocorticoid receptors and brain-derived neurotrophic factor-tyrosine receptor kinase B signaling in the hippocampus were evaluated. Our results demonstrated that gypenosides reversed the chronic corticosterone injection-induced decreased sucrose preference and increased immobility time. In contrast, this effect was antagonized by miR-124 injection. In addition, gypenosides increased glucocorticoid receptor and tyrosine receptor kinase B expression in the hippocampus, which activated brain-derived neurotrophic factor signaling. miR-124 also blocked these effects. In conclusion, this study demonstrated that a reduction in miR-124 was required for the antidepressant-like effects of gypenosides induced by chronic corticosterone injection in mice.

Extract of the Aerial Part of Polygala tenuifolia Attenuates d-Galactose/NaNO2-induced Learning and Memory Impairment in Mice

Planta Medica ◽  
2020 ◽  
Vol 86 (18) ◽  
pp. 1389-1399
Author(s):  
Dian Zhang ◽  
Xiao Wang ◽  
Rong Li ◽  
Lin Wang ◽  
Zihao Zhou ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Neurotrophic Factor ◽  
Memory Impairment ◽  
Aerial Part ◽  
Brain Derived Neurotrophic Factor ◽  
Latency Time ◽  
Receptor Kinase ◽  
Model Group ◽  
Age Related ◽  
Polygala Tenuifolia

AbstractAlzheimerʼs disease, one of the most common types of age-related dementia, is characterized by memory deterioration and behavior disorder. The aboveground part of Polygala tenuifolia is a traditional Chinese medicine used for the treatment of amnesia. This study was conducted to investigate the ameliorating effect of the aerial part of P. tenuifolia on d-galactose/NaNO2-induced learning and memory impairment in mice. d-galactose (120 mg/kg) and NaNO2 (90 mg/kg) were injected intraperitoneally for 60 days to induce learning and memory impairment in mice. The aerial part of P. tenuifolia (25, 50, and 100 mg/kg) and piracetam (200 mg/kg) were simultaneously administered orally on days 15 – 60. Results of this study showed that aerial part of P. tenuifolia significantly decreased the latency time and increased the number of platform crossings in the Morris water maze compared with the Model group. Moreover, the aerial part of P. tenuifolia significantly increased the latency time and decreased the error frequency in the step-down and step-through tests compared with the Model group. Meanwhile, the aerial part of P. tenuifolia was able to regulate the cholinergic system by increasing the levels of ACh and ChAT and decreasing the level of AChe. The aerial part of P. tenuifolia also significantly attenuated the levels of interleukin-1 beta and malonaldehyde and enhanced the interleukin-10 and glutathione levels and superoxide dismutase activity. Furthermore, treatment with aerial part of P. tenuifolia increased the protein and mRNA expression of brain-derived neurotrophic factor and tropomyosin receptor kinase B in the hippocampus. These results suggest that the aerial part of P. tenuifolia can ameliorate learning and memory impairments by modulating cholinergic activity, inhibiting neuroinflammation and oxidative stress, and regulating the brain-derived neurotrophic factor and tropomyosin receptor kinase B signaling pathway.

scholarly journals Androgen-Dependent Regulation of Brain-Derived Neurotrophic Factor and Tyrosine Kinase B in the Sexually Dimorphic Spinal Nucleus of the Bulbocavernosus

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3655-3665 ◽  
Author(s):  
Erich N. Ottem ◽  
Laurel A. Beck ◽  
Cynthia L. Jordan ◽  
S. Marc Breedlove
Keyword(s):  
Adult Male ◽  
Neurotrophic Factor ◽  
Dendritic Structure ◽  
Brain Derived Neurotrophic Factor ◽  
Male Rats ◽  
Sexually Dimorphic ◽  
Spinal Nucleus ◽  
Androgen Effects ◽  
Tyrosine Receptor Kinase

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.

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