FGF21 improves cognition by restored synaptic plasticity, dendritic spine density, brain mitochondrial function and cell apoptosis in obese-insulin resistant male rats

2016 ◽  
Vol 85 ◽  
pp. 86-95 ◽  
Author(s):  
Piangkwan Sa-nguanmoo ◽  
Pongpan Tanajak ◽  
Sasiwan Kerdphoo ◽  
Pattarapong Satjaritanun ◽  
Xiaojie Wang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Mitochondrial Function ◽  
Dendritic Spine ◽  
Cell Apoptosis ◽  
Male Rats ◽  
Spine Density ◽  
Insulin Resistant ◽  
Dendritic Spine Density ◽  
Brain Mitochondrial Function

scholarly journals Energy restriction combined with dipeptidyl peptidase-4 inhibitor exerts neuroprotection in obese male rats

2016 ◽  
Vol 116 (10) ◽  
pp. 1700-1708 ◽  
Author(s):  
Hiranya Pintana ◽  
Pongpan Tanajak ◽  
Wasana Pratchayasakul ◽  
Piangkwan Sa-nguanmoo ◽  
Titikorn Chunchai ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Insulin Sensitivity ◽  
Mitochondrial Function ◽  
Male Rats ◽  
Insulin Resistant ◽  
Hippocampal Synaptic Plasticity ◽  
Brain Insulin ◽  
Brain Mitochondrial Function

AbstractDipeptidyl peptidase-4 (DDP-4) inhibitors and energy restriction (ER) are widely used to treat insulin resistance and type 2 diabetes mellitus. However, the effects of ER or the combination with vildagliptin on brain insulin sensitivity, brain mitochondrial function, hippocampal synaptic plasticity and cognitive function in obese insulin-resistant rats have never been investigated. We hypothesised that ER with DDP-4 inhibitor exerts better efficacy than ER alone in improving cognition in obese insulin-resistant male rats by restoring brain insulin sensitivity, brain mitochondrial function and hippocampal synaptic plasticity. A total of twenty-four male Wistar rats were divided into two groups and fed either a normal diet or a high-fat diet (HFD) for 12 weeks. At week 13, the HFD rats were divided into three subgroups (n 6/subgroup) to receive one of the following treatments: vehicle, ER (60 % of energy received during the previous 12 weeks) or ER plus vildagliptin (3 mg/kg per d, p.o.) for 4 weeks. At the end of the treatment, cognitive function, metabolic parameters, brain insulin sensitivity, hippocampal synaptic plasticity and brain mitochondrial function were determined. We found that HFD-fed rats demonstrated weight gain with peripheral insulin resistance, dyslipidaemia, oxidative stress, brain insulin resistance, impaired brain mitochondrial function and cognitive dysfunction. Although HFD-fed rats treated with ER and ER plus vildagliptin showed restored peripheral insulin sensitivity and improved lipid profiles, only ER plus vildagliptin rats had restored brain insulin sensitivity, brain mitochondrial function, hippocampal synaptic plasticity and cognitive function. These findings suggest that only a combination of ER with DPP-4 inhibitor provides neuroprotective effects in obese insulin-resistant male rats.

"Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats": Correction to Eilam-Stock et al. (2011).

2012 ◽  
Vol 126 (1) ◽  
pp. 195-195
Author(s):  
Tehila Eilam-Stock ◽  
Peter Serrano ◽  
Maya Frankfurt ◽  
Victoria Luine
Keyword(s):  
Bisphenol A ◽  
Adult Male ◽  
Dendritic Spine ◽  
Male Rats ◽  
Spine Density ◽  
Dendritic Spine Density

scholarly journals Necrostatin-1 Mitigates Cognitive Dysfunction in Prediabetic Rats With no Alteration in Insulin Sensitivity

2020 ◽  
Author(s):  
Ada Admin ◽  
Kewarin Jinawong ◽  
Nattayaporn Apaijai ◽  
Supawit Wongsuchai ◽  
Wasana Pratchayasakul ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Insulin Sensitivity ◽  
Cognitive Decline ◽  
High Fat Diet ◽  
Spine Density ◽  
High Fat ◽  
Dendritic Spine Density ◽  
Microglial Morphology ◽  
Brain Mitochondrial Function

Previous studies show that 12-week of high-fat diet (HFD) consumption caused not only prediabetes, but also cognitive decline and brain pathologies. Recently, necrostatin-1 (nec-1), a necroptosis inhibitor, showed beneficial effects in brain against stroke. However, the comparative effects of nec-1 and metformin on cognition and brain pathologies in prediabetes have not been investigated. We hypothesized that nec-1 and metformin equally attenuated cognitive decline and brain pathologies in prediabetic rats. Rats (n=32) were fed with either normal diet (ND) or high-fat diet (HFD) for 20 weeks. At week 13, ND-fed rats were given a vehicle (n=8) and HFD-fed rats were randomly assigned into 3 subgroups (n=8/subgroup) with vehicle, nec-1 or metformin for 8 weeks. Metabolic parameters, cognitive function, brain insulin receptor function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, Alzheimer’s protein, and cell death were determined.<b> </b>HFD-fed rats exhibited prediabetes, cognitive decline, and brain pathologies. Nec-1 and metformin equally improved cognitive function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, reduced hyperphosphorylated-tau and necroptosis in HFD-fed rats. Interestingly metformin, but not nec-1, improved brain insulin sensitivity in those rats.<b> </b><b> </b>In conclusion, necroptosis inhibition directly improved cognition in prediabetic rats without alteration in insulin sensitivity.

Rapid Effects of Estradiol on Dendritic Spines and Synaptic Plasticity in the Male and Female Hippocampus

2020 ◽  
pp. 38-47
Author(s):  
Asami Kato ◽  
Gen Murakami ◽  
Yasushi Hojo ◽  
Sigeo Horie ◽  
Suguru Kawato
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Molecular Mechanisms ◽  
Hippocampal Slices ◽  
Spine Density ◽  
Male And Female ◽  
Dendritic Spine Density ◽  
Male And Female Rats ◽  
Rapid Modulation

Although the potent estrogen, 17β‎-estradiol (E2), has long been known to regulate the hippocampal dendritic spine density and synaptic plasticity, the molecular mechanisms through which it does so are less well understood. This chapter discusses the rapid modulation of hippocampal dendritic spine density and synaptic plasticity in male and female rats, with particular attention to studies in hippocampal slices from male rats. Among the mechanisms described are the roles of specific cell-signaling kinases and estrogen receptors in mediating the effects of E2 and progesterone on hippocampal neurons. In addition, dynamic changes of spine structures over time and sex differences in spine regulation are also considered. Finally, the chapter ends by discussing the importance of local hippocampal synthesis of E2 and androgens to hippocampal spine morphology and plasticity.

scholarly journals Reelin supplementation enhances cognitive ability, synaptic plasticity, and dendritic spine density

2011 ◽  
Vol 18 (9) ◽  
pp. 558-564 ◽  
Author(s):  
J. T. Rogers ◽  
I. Rusiana ◽  
J. Trotter ◽  
L. Zhao ◽  
E. Donaldson ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Ability ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density

scholarly journals Eps8 controls dendritic spine density and synaptic plasticity through its actin-capping activity

2013 ◽  
Vol 32 (12) ◽  
pp. 1730-1744 ◽  
Author(s):  
Elisabetta Menna ◽  
Stefania Zambetti ◽  
Raffaella Morini ◽  
Andrea Donzelli ◽  
Andrea Disanza ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Actin Capping

scholarly journals Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.

2012 ◽  
Vol 126 (1) ◽  
pp. 175-185 ◽  
Author(s):  
Tehila Eilam-Stock ◽  
Peter Serrano ◽  
Maya Frankfurt ◽  
Victoria Luine
Keyword(s):  
Bisphenol A ◽  
Adult Male ◽  
Dendritic Spine ◽  
Male Rats ◽  
Spine Density ◽  
Dendritic Spine Density

scholarly journals Systemic or Forebrain Neuron-Specific Deficiency of Geranylgeranyltransferase-1 Impairs Synaptic Plasticity and Reduces Dendritic Spine Density

Neuroscience ◽  
2018 ◽  
Vol 373 ◽  
pp. 207-217 ◽  
Author(s):  
David Hottman ◽  
Shaowu Cheng ◽  
Andrea Gram ◽  
Kyle LeBlanc ◽  
Li-Lian Yuan ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density

scholarly journals Necrostatin-1 Mitigates Cognitive Dysfunction in Prediabetic Rats With no Alteration in Insulin Sensitivity

2020 ◽  
Author(s):  
Ada Admin ◽  
Kewarin Jinawong ◽  
Nattayaporn Apaijai ◽  
Supawit Wongsuchai ◽  
Wasana Pratchayasakul ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Insulin Sensitivity ◽  
Cognitive Decline ◽  
High Fat Diet ◽  
Spine Density ◽  
High Fat ◽  
Dendritic Spine Density ◽  
Microglial Morphology ◽  
Brain Mitochondrial Function

Previous studies show that 12-week of high-fat diet (HFD) consumption caused not only prediabetes, but also cognitive decline and brain pathologies. Recently, necrostatin-1 (nec-1), a necroptosis inhibitor, showed beneficial effects in brain against stroke. However, the comparative effects of nec-1 and metformin on cognition and brain pathologies in prediabetes have not been investigated. We hypothesized that nec-1 and metformin equally attenuated cognitive decline and brain pathologies in prediabetic rats. Rats (n=32) were fed with either normal diet (ND) or high-fat diet (HFD) for 20 weeks. At week 13, ND-fed rats were given a vehicle (n=8) and HFD-fed rats were randomly assigned into 3 subgroups (n=8/subgroup) with vehicle, nec-1 or metformin for 8 weeks. Metabolic parameters, cognitive function, brain insulin receptor function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, Alzheimer’s protein, and cell death were determined.<b> </b>HFD-fed rats exhibited prediabetes, cognitive decline, and brain pathologies. Nec-1 and metformin equally improved cognitive function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, reduced hyperphosphorylated-tau and necroptosis in HFD-fed rats. Interestingly metformin, but not nec-1, improved brain insulin sensitivity in those rats.<b> </b><b> </b>In conclusion, necroptosis inhibition directly improved cognition in prediabetic rats without alteration in insulin sensitivity.

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