Effects of beta-amyloid on behavioral and amino acids spectrum in rats’ brain and their modulation by embryonic proteins

Yenkoyan, Konstantin; Safaryan, Karen; Navasardyan, G.A.; Mkrtchyan, Lusine; Aghajanov, M. I.

doi:10.1016/j.neuint.2008.12.010

Cited by 16 publications

(10 citation statements)

References 28 publications

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“…In the current study, administration of glutamate produced a significant alteration in spatial memory, as measured by the Y-maze test. This coincides with previous studies whereby Glu-excitotoxicity induced by several agents caused alteration in the SAB%, compared to control groups, in the Y-maze test ( 47 – 49 ). Previously, it was shown that bilateral intracerebroventricular administration of Aβ-35 caused impairment in the SAB% and contributed to the neurotoxicity of Aβ through increasing glutamatergic neurotransmission ( 49 ).…”

Section: Discussionsupporting

confidence: 92%

“…This coincides with previous studies whereby Glu-excitotoxicity induced by several agents caused alteration in the SAB%, compared to control groups, in the Y-maze test ( 47 – 49 ). Previously, it was shown that bilateral intracerebroventricular administration of Aβ-35 caused impairment in the SAB% and contributed to the neurotoxicity of Aβ through increasing glutamatergic neurotransmission ( 49 ). Moreover, it was observed that olfactory bulbectomy in rodents led to deficits in behavioral and cognitive deficits through glutamate-mediated excitotoxicity manifested by impairment in the SAB% ( 50 ).…”

Section: Discussionsupporting

confidence: 92%

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Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways

et al. 2018

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Overexposure of the glutamatergic N-methyl-d-aspartate (NMDA) receptor to the excitatory neurotransmitter l-glutamic acid leads to neuronal cell death by excitotoxicity as a result of increased intracellular Ca2+, mitochondrial dysfunction, and apoptosis. Moreover, it was previously reported that prolonged activation of the NMDA receptor increased beta-amyloid (Aβ) levels in the brain. Thymoquinone (TQ), the active constituent of Nigella sativa seeds, has been shown to have potent antioxidant and antiapoptotic effects. The aim of the present study was to explore the neuromodulatory effects of different doses of TQ (2.5 and 10 mg/kg) against apoptotic cell death and Aβ formation resulting from glutamate administration in rats using vitamin E as a positive control. Behavioral changes were assessed using Y-maze and Morris water maze tests for evaluating spatial memory and cognitive functions. Caspase-3, Lactate dehydrogenase, Aβ-42, and cytochrome c gene expression were determined. TQ-treated groups showed significant decreases in the levels of all tested biochemical and behavioral parameters compared with the glutamate-treated group. These findings demonstrated that TQ has a promising neuroprotective activity against glutamate-induced neurotoxicity and this effect is mediated through its anti-amyloidogenic, antioxidant, and antiapoptotic activities.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways

et al. 2018

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“…Both Exendin-4 and Aβ1-42 were purchased from Sigma (St. Louis, MO, USA) and dissolved in normal saline, and Aβ1-42 was "aged" before surgery by incubation at 37°C for 4 days (Wang et al, 2014;Yenkoyan et al, 2009). Aβ1-42 (5 nmol per rat), Exendin-4 (0.02, 0.2, 2 nmol per rat) and vehicle solutions were injected i.c.v.…”

Section: Chemicals and Drug Applicationmentioning

confidence: 99%

Exendin-4, a glucagon-like peptide 1 receptor agonist, protects against amyloid-β peptide-induced impairment of spatial learning and memory in rats

Jia

Ye-Tian

Yuanli

et al. 2016

Physiology & Behavior

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Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) share specific molecular mechanisms, and agents with proven efficacy in one may be useful against the other. The glucagon-like peptide-1 (GLP-1) receptor agonist exendin-4 has similar properties to GLP-1 and is currently in clinical use for T2DM treatment. Thus, this study was designed to characterize the effects of exendin-4 on the impairment of learning and memory induced by amyloid protein (Aβ) and its probable molecular underlying mechanisms. The results showed that (1) intracerebroventricular (i.c.v.) injection of Aβ1-42 resulted in a significant decline of spatial learning and memory of rats in water maze tests; (2) pretreatment with exendin-4 effectively and dose-dependently protected against the Aβ1-42-induced impairment of spatial learning and memory; (3) exendin-4 treatment significantly decreased the expression of Bax and cleaved caspase-3 and increased the expression of Bcl2 in Aβ1-42-induced Alzheimer's rats. The vision and swimming speed of the rats among all groups in the visible platform tests did not show any difference. These findings indicate that systemic pretreatment with exendin-4 can effectively prevent the behavioral impairment induced by neurotoxic Aβ1-42, and the underlying protective mechanism of exendin-4 may be involved in the Bcl2, Bax and caspase-3 pathways. Thus, the application of exendin-4 or the activation of its signaling pathways may be a promising strategy to ameliorate the degenerative processes observed in AD.

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“…Aβ31–35 was purchased from Sigma (St. Louis, MO) and Rattin was provided by Prof. Tomohiro Chiba from KEIO University in Japan. All drugs dissolved in normal saline, and Aβ31–35 was “aged” before surgery by incubation at 37°C for 4 days (Maurice et al, ; Yenkoyan et al, ; Li et al, ). Three days after adaptation, rats were anesthetized with Chloral hydrate (0.3 g kg −1 i.p.)…”

Section: Methodsmentioning

confidence: 99%

The neuroprotection of Rattin against amyloid β peptide in spatial memory and synaptic plasticity of rats

et al. 2013

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Rattin, a specific derivative of humanin in rats, shares the ability with HN to protect neurons against amyloid β (Aβ) peptide-induced cellular toxicity. However, it is still unclear whether Rattin can protect against Aβ-induced deficits in cognition and synaptic plasticity in rats. In the present study, we observed the effects of Rattin and Aβ31-35 on the spatial reference memory and in vivo hippocampal Long-term potentiation of rats by using Morris water maze test and hippocampal field potential recording. Furthermore, the probable molecular mechanism underlying the neuroprotective roles of Rattin was investigated. We showed that intra-hippocampal injection of Rattin effectively prevented the Aβ31-35-induced spatial memory deficits and hippocampal LTP suppression in rats; the Aβ31-35-induced activation of Caspase-3 and inhibition of STAT3 in the hippocampus were also prevented by Rattin treatment. These findings indicate that Rattin treatment can protect spatial memory and synaptic plasticity of rats against Aβ31-35-induced impairments, and the underlying protective mechanism of Rattin may be involved in STAT3 and Caspases-3 pathways. Therefore, application of Rattin or activation of its signaling pathways in the brain might be beneficial to the prevention of Aβ-related cognitive deficits.

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Effects of beta-amyloid on behavioral and amino acids spectrum in rats’ brain and their modulation by embryonic proteins

Cited by 16 publications

References 28 publications

Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways

Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways

Exendin-4, a glucagon-like peptide 1 receptor agonist, protects against amyloid-β peptide-induced impairment of spatial learning and memory in rats

The neuroprotection of Rattin against amyloid β peptide in spatial memory and synaptic plasticity of rats

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