scholarly journals A Noradrenergic Lesion Attenuates Surgery-Induced Cognitive Impairment in Rats by Suppressing Neuroinflammation

2021 ◽  
Vol 14 ◽  
Author(s):  
Jiayu Wang ◽  
Ying Zhou ◽  
Ke Li ◽  
Xiaofeng Li ◽  
Meimei Guo ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Locus Coeruleus ◽  
Neurodegenerative Disorders ◽  
Mesenteric Artery ◽  
Memory Impairment ◽  
High Performance ◽  
Open Field Test ◽  
Postoperative Cognitive Dysfunction ◽  
New Perspective ◽  
Dependent Learning

Postoperative cognitive dysfunction (POCD) is a common postoperative neurocognitive complication in elderly patients. However, the specific pathogenesis is unknown, and it has been demonstrated that neuroinflammation plays a key role in POCD. Recently, increasing evidence has proven that the locus coeruleus noradrenergic (LCNE) system participates in regulating neuroinflammation in some neurodegenerative disorders. We hypothesize that LCNE plays an important role in the neuroinflammation of POCD. In this study, 400 μg of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) was injected intracerebroventricularly into each rat 7 days before anesthesia/surgery to deplete the locus coeruleus (LC) noradrenaline (NE). We applied a simple laparotomy and brief upper mesenteric artery clamping surgery as the rat POCD model. The open field test, novel objection and novel location (NL) recognition, and Morris water maze (MWM) were performed to assess postoperative cognition. High-performance liquid chromatography (HPLC) was used to measure the level of NE in plasma and brain tissues, and immunofluorescence staining was applied to evaluate the activation of microglia and astrocytes. We also used enzyme-linked immune-sorbent assay (ELISA) to assess the levels of inflammatory cytokines and brain-derived neurotrophic factor (BDNF). Pretreatment with DSP-4 decreased the levels of systemic and central NE, increased the level of interleukin-6 (IL-6) in the plasma at 6 h after the surgery, decreased the concentration of IL-6 in the prefrontal cortex and hippocampus, and decreased the level of interleukin-1β (IL-1β) in the plasma, prefrontal cortex, and hippocampus at 1 week postoperatively. In addition, DSP-4 treatment attenuated hippocampal-dependent learning and memory impairment in rats with POCD, with a downregulation of the activation of microglia and astrocytes in the prefrontal cortex and hippocampus. In conclusion, these findings provide evidence of the effects of LCNE in modulating neuroinflammation in rats with POCD and provide a new perspective in the prevention and treatment of POCD.

scholarly journals Anxiogenic and memory impairment effect of food color exposure: upregulation of oxido-neuroinflammatory markers and acetyl-cholinestrase activity in the prefrontal cortex and hippocampus

Heliyon ◽  
2021 ◽  
Vol 7 (3) ◽  
pp. e06378
Author(s):  
Iheanyichukwu Wopara ◽  
Emmanuel U. Modo ◽  
Olusegun G. Adebayo ◽  
Samuel K. Mobisson ◽  
Jovita O. Nwigwe ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Memory Impairment ◽  
Effect Of Food

scholarly journals A novel dephosphorylation targeting chimera selectively promoting tau removal in tauopathies

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Jie Zheng ◽  
Na Tian ◽  
Fei Liu ◽  
Yidian Zhang ◽  
Jingfen Su ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Protein Phosphatase ◽  
High Efficiency ◽  
Microtubule Assembly ◽  
Hyperphosphorylated Tau ◽  
Phosphatase 2A ◽  
Dependent Learning ◽  
The Brain

AbstractIntraneuronal accumulation of hyperphosphorylated tau is a hallmark pathology shown in over twenty neurodegenerative disorders, collectively termed as tauopathies, including the most common Alzheimer’s disease (AD). Therefore, selectively removing or reducing hyperphosphorylated tau is promising for therapies of AD and other tauopathies. Here, we designed and synthesized a novel DEPhosphorylation TArgeting Chimera (DEPTAC) to specifically facilitate the binding of tau to Bα-subunit-containing protein phosphatase 2A (PP2A-Bα), the most active tau phosphatase in the brain. The DEPTAC exhibited high efficiency in dephosphorylating tau at multiple AD-associated sites and preventing tau accumulation both in vitro and in vivo. Further studies revealed that DEPTAC significantly improved microtubule assembly, neurite plasticity, and hippocampus-dependent learning and memory in transgenic mice with inducible overexpression of truncated and neurotoxic human tau N368. Our data provide a strategy for selective removal of the hyperphosphorylated tau, which sheds new light for the targeted therapy of AD and related-tauopathies.

SGK1 knockdown in the medial prefrontal cortex reduces resistance to stress-induced memory impairment

2021 ◽  
Vol 45 ◽  
pp. 29-34
Author(s):  
Jung-Cheol Park ◽  
Yong-Jae Jeon ◽  
Yoon-Sun Jang ◽  
Jeiwon Cho ◽  
Dong-Hee Choi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Memory Impairment ◽  
Resistance To Stress

scholarly journals Kynurenine pathway in post-mortem prefrontal cortex and cerebellum in schizophrenia: relationship with monoamines and symptomatology

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Amira Ben Afia ◽  
Èlia Vila ◽  
Karina S. MacDowell ◽  
Aida Ormazabal ◽  
Juan C. Leza ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
High Performance ◽  
Interaction Analysis ◽  
Kynurenine Pathway ◽  
Psychotic Symptoms ◽  
Post Mortem ◽  
Control Subjects ◽  
Network Interaction ◽  
Hydroxyindoleacetic Acid ◽  
Cortical Circuit

Abstract Background The cortico-cerebellar-thalamic-cortical circuit has been implicated in the emergence of psychotic symptoms in schizophrenia (SZ). The kynurenine pathway (KP) has been linked to alterations in glutamatergic and monoaminergic neurotransmission and to SZ symptomatology through the production of the metabolites quinolinic acid (QA) and kynurenic acid (KYNA). Methods This work describes alterations in KP in the post-mortem prefrontal cortex (PFC) and cerebellum (CB) of 15 chronic SZ patients and 14 control subjects in PFC and 13 control subjects in CB using immunoblot for protein levels and ELISA for interleukins and QA and KYNA determinations. Monoamine metabolites were analysed by high-performance liquid chromatography and SZ symptomatology was assessed by Positive and Negative Syndrome Scale (PANSS). The association of KP with inflammatory mediators, monoamine metabolism and SZ symptomatology was explored. Results In the PFC, the presence of the anti-inflammatory cytokine IL-10 together with IDO2 and KATII enzymes decreased in SZ, while TDO and KMO enzyme expression increased. A network interaction analysis showed that in the PFC IL-10 was coupled to the QA branch of the kynurenine pathway (TDO-KMO-QA), whereas IL-10 associated with KMO in CB. KYNA in the CB inversely correlated with negative and general PANSS psychopathology. Although there were no changes in monoamine metabolite content in the PFC in SZ, a network interaction analysis showed associations between dopamine and methoxyhydroxyphenylglycol degradation metabolite. Direct correlations were found between general PANSS psychopathology and the serotonin degradation metabolite, 5-hydroxyindoleacetic acid. Interestingly, KYNA in the CB inversely correlated with 5-hydroxyindoleacetic acid in the PFC. Conclusions Thus, this work found alterations in KP in two brain areas belonging to the cortico-cerebellar-thalamic-cortical circuit associated with SZ symptomatology, with a possible impact across areas in 5-HT degradation.

The Antioxidant Resveratrol from Polygonum Cuspidatum Reverses Memory Impairment and Brain Oxidative Stress in SAMP8 Mice

2011 ◽  
Vol 422 ◽  
pp. 470-473
Author(s):  
Gui Shan Liu ◽  
Ze Sheng Zhang ◽  
Bo Yang ◽  
Wei He
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Open Field ◽  
Field Test ◽  
Memory Impairment ◽  
Open Field Test ◽  
Pharmacological Action ◽  
Age Related ◽  
Brain Oxidative Stress ◽  
Samp8 Mice

Resveratrol (RVT) is a phytoalexin polyphenolic compound found in various plants, including grapes, berries and peanuts. Recently, studies have documented various health benefits of resveratrol including cardiovascular and cancer-chemopreventive properties. The aim of the present study was to demonstrate the effects of resveratrol on the learning and memory impairment. The senescence-accelerated mice (SAM) were introgastric gavage administrated resveratrol (25,100mg/(kg•bw)) for 60 days. The learning and memory behavior was assessed using open-field test while the parameters of oxidative stress assessed were malondialdehyde (MDA) and superoxide dismutases (SOD).The results showed that resveratrol significantly improved the learning and memory ability in open-field test. Further investigation showed that resveratrol restored SOD levels, but decreased MDA level in the mouce brain. These results indicated that the pharmacological action of RVT may offer a novel therapeutic strategy for the treatment of age-related conditions.

scholarly journals The Role of Alteration of Glutamic Acid and Gaba in Learning and Memory Impairment of Rats Induced by Aluminum

2005 ◽  
Vol 3 (2) ◽  
pp. 97-101
Author(s):  
Q. Niu ◽  
P. Niu ◽  
Q. Zhang ◽  
L. Wang ◽  
S. He ◽  
...  
Keyword(s):  
Amino Acids ◽  
Cerebral Cortex ◽  
Glutamic Acid ◽  
Learning And Memory ◽  
Memory Impairment ◽  
High Performance ◽  
Gamma Aminobutyric Acid ◽  
Aluminum Exposure ◽  
Step Down

Aluminum exposure has been reported to be related to learning and memory impairment. This study examines the role of aluminum in alterating amino acids of the cerebral cortex of rats. The Step-down type tests were performed to investigate the alteration of learning and memory of rats induced by aluminum. The amino acids in the cerebral cortex were detected by high performance liquid chromatography (HLPC). Results show that the amounts of aluminum in the cerebral cortex increased by 5.0mgAl3+/(Kg·BW) group and 10.0mg Al3+/(Kg·BW) group. In the Step-down type test, the EN1 increased significantly in the Al3+ 10.0mg/(Kg·BW) group. The latency shortened obviously and the EN2 increased significantly in the 10.0mg Al3+/(Kg·BW) group. The content of Glu (Glutamic acid) increased but the content of GABA (gamma-aminobutyric acid) decreased significantly in the 10.0mg Al3+/(Kg·BW) group. This present study shows evidence that the disorder of amino acid neurotransmitters system plays an important role in the impairment of learning and memory of rats induced by aluminum.

scholarly journals Monoaminergic Involvement in Decreased Locomotor Activity of Mice Treated with α and β-amyrin from Protium heptaphyllum

2018 ◽  
Vol 13 (8) ◽  
pp. 1934578X1801300
Author(s):  
Gislei F. Aragão ◽  
Manoel O. de Moraes Filho ◽  
Paulo N. Bandeira ◽  
Antônio P. Frota Junior ◽  
Yasmin Ingrid S. Oliveira de ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Locomotor Activity ◽  
Open Field ◽  
Field Test ◽  
High Performance ◽  
Open Field Test ◽  
Inhibitory Effect ◽  
Pharmacological Agents ◽  
Tissue Homogenates ◽  
The Central Nervous System

A triterpenic mixture of α and β-amyrin (AMY) extracted from Protium heptaphyllum has demonstrated several pharmacological effects, including activity in the central nervous system. The aim of this study was to evaluate the effect of AMY administration on locomotor activity of mice by the open field test using some monoaminergic agonists and antagonists and the cerebral cortex levels of monoamines and their major metabolites by high-performance liquid chromatography. Mice were treated acutely with AMY at doses of 1, 2.5 and 5 mg/kg given intraperitoneally and with the pharmacological agents and placed in open field test, then the animals were sacrificed and the cerebral cortex extracted, and monoamines were assayed in tissue homogenates. AMY at 1, 2.5 and 5 mg/kg decreased locomotor activity of animals by 25, 31 and 39%, respectively in the open field test. Ondasentron, doxazosin, oxymetazoline and clonidine did not reverse the inhibitory effect of 5 mg/kg AMY. Venlafaxine and yohimbine reversed the inhibitory effect of 5 mg AMY. In the cortex, the 5-HT and 5-HIAA were significantly reduced by the administration of AMY. NE and HVA were also reduced with 2.5 and 5 mg/kg AMY, while Dopamine and DOPAC were not increased with AMY. In conclusion, AMY decreased locomotor activity of animals accompanied by a decrease in 5-HT and NE levels in the cerebral cortex, this locomotor effect is reversed by drug that blocker the α-2-adrenoreceptor.

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