scholarly journals Neuropathic Pain Causes Memory Deficits and Dendrite Tree Morphology Changes in Mouse Hippocampus

2020 ◽  
Vol Volume 13 ◽  
pp. 345-354
Author(s):  
Anna Tyrtyshnaia ◽  
Igor Manzhulo
Pain ◽  
2019 ◽  
Vol 160 (4) ◽  
pp. 805-823 ◽  
Author(s):  
Helder Cardoso-Cruz ◽  
Pedro Paiva ◽  
Clara Monteiro ◽  
Vasco Galhardo

2015 ◽  
Vol 67 (5) ◽  
pp. 934-942 ◽  
Author(s):  
Pradeep Jayarajan ◽  
Ramakrishna Nirogi ◽  
Anil Shinde ◽  
Venkatesh Goura ◽  
Vuyyuru Arun Babu ◽  
...  

2020 ◽  
Vol 19 (4) ◽  
pp. 823-828
Author(s):  
Ang Cai ◽  
Liu Xiao ◽  
Yan-Ping Zhou ◽  
Zhi-Guo Zhang ◽  
Quan-Wei Yang

Purpose: To investigate the protective effect of Evodia rutaecarpa (Juss.) Benth. extract (ERBE) against Alzheimer's disease in 3xTg-AD mice. Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ERBE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in the animals treated with 400 mg/kg ERBE (20.5 ± 1.3 s) was significantly higher than untreated 3xTg-AD mice (12.4 ± 1.3 s, p < 0.01). In addition, ERBE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expressions of BDNF (1.4 ± 0.2, p < 0.05) and TrkB (1.1 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: The results suggest that ERBE administration may be a useful strategy for treating memory impairment induced by several neurodegenerative diseases. Keywords: Evodia rutaecarpa, Alzheimer, Memory impairment, NeuN-positive cells


2013 ◽  
Vol 5;16 (5;9) ◽  
pp. E563-E575
Author(s):  
Prof. Xian-Guo Liu

Background: Clinical studies have shown that about two-thirds of patients with chronic pain suffer from short-term memory (STM) deficits and an effective drug for treatment of the neurological disorder is lacking at present. Objective: We tested whether chronic oral application of magnesium L-threonate (MgT), which has been shown to improve memory in normal and aging animals by elevating Mg2+ in the brain, could prevent or restore the STM deficits induced by spared nerve injury (SNI), an animal model of chronic neuropathic pain. The mechanisms underlying the effect of MgT on STM deficits were also investigated. Study Design: The experiments were conducted in a random and double-blind fashion in adult male rats. MgT was administrated via drinking water at a dose of 609 mg/kg/d for 2 weeks, starting either one week before SNI (preventative group) or one week after SNI (therapeutic group), and water without the drug served as control. Methods: STM was accessed with a novel object recognition test (NORT), followed by recording of long-term potentiation (LTP) in the hippocampus in vivo and the measurement of the expression of tumor necrosis factor-α (TNF-α) with Western Blot or Immunohistochemistrical staining. α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor (NMDAR) currents were recorded with patch clamp in CA1 neurons in acute and cultured hippocampal slices. Result: We found that chronic oral application of MgT was able to prevent and restore the deficits of STM and of LTP at CA3-CA1 synapses in the hippocampus induced by SNI. Furthermore, both preventative and therapeutic chronic oral application of MgT blocked the up-regulation of TNF-α in the hippocampus, which has been previously shown to be critical for memory deficits. SNI reduced NMDAR current and the effect was dramatically attenuated by elevating extracellular Mg2+ concentration ([Mg2+]o). In cultured hippocampal slices, chronic application of recombinant rat TNF-α (rrTNF-α) for 3 days reduced NMDAR current in a concentration-dependent manner and the effect was again blocked by elevating [Mg2+]o. Limitations: We showed that oral application of MgT inhibited the over-expression of TNF-α and rescued the dysfunction of the NMDAR, but the causal relationship between them remains elusive. Conclusions: Our data suggested that oral application of MgT was able to prevent and restore the STM deficits in an animal model of chronic neuropathic pain by reversing the dysfunction of the NMDAR, and normalization of TNF-α expression may play a role in the effect. Oral application of MgT may be a simple and potent means for handling this form of memory deficit. Key words: Magnesium L-threonate, short-term memory, tumor necrosis factor-α, NMDA receptor, neuropathic pain


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Degui Gong ◽  
Xiangmei Yu ◽  
Menghong Jiang ◽  
Changzheng Li ◽  
Zhifu Wang

Abnormal changes in hippocampal function and neuroplasticity are involved in neuropathic pain, which induces hyperalgesia and learning and memory deficits. Previous studies from our group have shown that electroacupuncture at Huantiao (GB30) and Yanglingquan (GB34) has an obvious analgesic effect on neuropathic pain. However, the central regulatory mechanism occurring in the hippocampus remains to be investigated. In this study, behavioral and proteomic analyses were performed to identify differentially expressed hippocampal proteins involved in electroacupuncture-induced analgesia. Our results showed both upregulated (TMEM126A, RDH13, and Luc7L) and downregulated proteins (Mettl7A, GGA1 RTKN, RSBN1, and CDKN1B). Further protein verification revealed for the first time that hippocampal TMEM126A plays an important anti-inflammatory role in the treatment of neuralgia by electroacupuncture.


2019 ◽  
Vol 19 (1) ◽  
pp. 83-89
Author(s):  
Mostofa Jamal ◽  
Ayako Ito ◽  
Naoko Tanaka ◽  
Kiyoshi Ameno ◽  
Takanori Miki ◽  
...  

Background: Ethanol (EtOH) and acetaldehyde (AcH) have long been associated with many adverse effects in the central nervous system. c-fos has been used as an indirect index of neural activity. Method: Here, we investigated the effects of systemic administration of EtOH and AcH on the expression of c-fos protein in the hippocampus of Aldh2-knockout (Aldh2-KO) mice. The animals received an intraperitoneal injection of saline (control), EtOH (1.0, 2.0 and 4.0 g/kg) or AcH (50, 100 and 200 mg/kg), and the expression of c-fos protein was measured by Western blotting. Result: We found that EtOH at doses of 2.0 and 4.0 g/kg decreased c-fos in wild-type (WT) mice, whereas EtOH at all three doses tested (1.0-4.0 g/kg) decreased c-fos in Aldh 2-KO mice. Likewise, AcH at doses of 100 and 200 mg/kg had a significant effect in lowering c-fos protein in both WT and Aldh2-KO mice. Conclusion: Our observations suggest that moderate to high EtOH and AcH can decrease the expression of c-fos protein in the mouse hippocampus. This effect may support, at least in part, the link between c-fos and spatial memory deficits following EtOH and AcH exposure as we have observed in our previous study. Bangladesh Journal of Medical Science Vol.19(1) 2020 p.83-89


2018 ◽  
Vol 23 (6) ◽  
pp. 14-15
Author(s):  
Lee H. Ensalada

Abstract Symptom validity testing (SVT), also known as forced-choice testing, is a means of assessing the validity of sensory and memory deficits, including tactile anesthesias, paresthesias, blindness, color blindness, tunnel vision, blurry vision, and deafness. The common feature among these symptoms is a claimed inability to perceive or remember a sensory signal. SVT comprises two elements: a specific ability is assessed by presenting a large number of items in a multiple-choice format, and then the examinee's performance is compared to the statistical likelihood of success based on chance alone. These tests usually present two alternatives; thus the probability of simply guessing the correct response (equivalent to having no ability at all) is 50%. Thus, scores significantly below chance performance indicate that the sensory cues must have been perceived, but the examinee chose not to report the correct answer—alternative explanations are not apparent. SVT also has the capacity to demonstrate that the examinee performed below the probabilities of chance. Scoring below a norm can be explained by fatigue, evaluation anxiety, inattention, or limited intelligence. Scoring below the probabilities of chance alone most likely indicates deliberate deceptions and is evidence of malingering because it provides strong evidence that the examinee received the sensory cues and denied the perception. Even so, malingering must be evaluated from the total clinical context.


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