scholarly journals EXPERIMENTAL RESEARCH ON FORECASTING INDEX OF BIOLOGICAL IMAGE AEROBIC EXERCISE ANALYSIS OF ARTIFICIAL NEURAL NETWORK

2021 ◽  
Vol 27 (4) ◽  
pp. 405-409
Author(s):  
Min Lin
Keyword(s):  
Neural Network ◽  
Aerobic Exercise ◽  
Low Frequency ◽  
Exercise Group ◽  
Sleep State ◽  
Gamma Energy ◽  
Hippocampal Ca1 ◽  
Gamma Rhythm ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area

ABSTRACT Objective: The paper uses artificial neural network images to explore the effects of aerobic exercise on the gamma rhythm of theta period in the awake hippocampal CA1 area of APP/PS1/tau mice and the low-frequency gamma rhythm of the sleep state hippocampal CA1 area SWR period. Methods: Clean grade 6-month-old APP/PS1/tau mice were randomly divided into quiet group (AS) and exercise group (AE), C57BL/6J control group mice were randomly divided into quiet group (CS) and exercise group (CE). The AE group and the CE group performed 12-week treadmill exercise, 5d/week, 60min/d, the first 10min exercise load was 12m/min, the last 50min was 15m/min treadmill slope was 0°. Eight-arm maze detection of behavioral changes in mice; multi-channel in vivo recording technology to record the electrical signals of the awake state and sleep state in the hippocampal CA1 area, MATLAB extracts the awake state theta period and sleep state SWR period, multi-window spectrum estimation method Perform time-frequency analysis and power spectral density analysis. Results: 12 weeks of aerobic exercise can significantly improve the working memory and reference memory of the AS group, increase the gamma energy in theta period of the awake hippocampus CA1 area and the low-frequency gamma energy in the sleep state CA1 area SWR period. Conclusions: Aerobic exercise can improve the neural network state of the AD model and increase the gamma energy in theta period of the hippocampus CA1 area, and the low-frequency gamma energy in the SWR period is one of the neural network mechanisms for its overall behavioral improvement. Level of evidence II; Therapeutic studies - investigation of treatment results.

scholarly journals Oxytocin protects neurons from hypoxic-ischemic brain injury by enhancing inhibitory neurotransmission in neonatal rats

2021 ◽  
Vol 20 (9) ◽  
pp. 1909-1914
Author(s):  
Linhua Xiang ◽  
Rong Wu ◽  
Kangling Liu ◽  
Jing Wang
Keyword(s):  
Protective Effect ◽  
Hippocampal Slices ◽  
Time Lapse ◽  
Oxytocin Receptor ◽  
Neonatal Rats ◽  
Model Group ◽  
Ischemic Brain ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area

Purpose: To study the protective effect of oxytocin on hypoxic-ischemic brain neuron injury in neonatal rats, and the mechanism of action involved.Methods: Hippocampal slices from neonatal SD rats were cultured in oxygen/glucose-deprived (OGD) solution, leading to establishment of hypoxic-ischemic model of hippocampal slices in vitro. The slices were assigned to 3 groups: control (ACSF solution), model (OGD solution), and oxytocin (OGD solution + 1 μM oxytocin). The effect of oxytocin on vertebral neurons in hippocampal CA1 region of HIBD rats was determined using TOPRO-3 staining, while the effects of oxytocin on hypoxic depolarization (AD) and inhibitory postsynaptic currents (iPSCs) were measured by cell patch clamp technique.Results: The fluorescence intensity of vertebral lamina in hippocampal CA1 area of model group was significantly higher than that of control group, while the corresponding value for oxytocin group was significantly lower than that of model group (p < 0.05). The time lapse before occurrence of AD in hippocampal CA1 area was significantly longer in oxytocin group than in model group, while the time lapse before neuronal AD in oxytocin receptor antagonist group was lower than that in oxytocin group. The frequency and amplitude of iPSCs in oxytocin group were markedly higher than the corresponding control values.Conclusion: Oxytocin exerts protective effect against hypoxic-ischemic brain neuronal damage in neonatal rats by regulating the activation of oxytocin receptor and GABA receptor, and inhibiting nerve transmission. These findings may be of benefit in the development of a suitable therapy for HIBD.

Lipopolysaccharide inhibits induction of long-term potentiation and depression in the rat hippocampal CA1 area

2001 ◽  
Vol 422 (1-3) ◽  
pp. 69-76 ◽  
Author(s):  
Ji-Hoon Jo ◽  
Eun-Jin Park ◽  
Jae-Kwang Lee ◽  
Min-Whan Jung ◽  
Chang-Joong Lee
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area

scholarly journals Protective Effects of a New C-Jun N-terminal Kinase Inhibitor in the Model of Global Cerebral Ischemia in Rats

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1722 ◽  
Author(s):  
Mark B. Plotnikov ◽  
Galina A. Chernysheva ◽  
Oleg I. Aliev ◽  
Vera I. Smol’iakova ◽  
Tatiana I. Fomina ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Ischemia ◽  
Endothelial Dysfunction ◽  
Neurological Deficit ◽  
Neuroprotective Effect ◽  
Global Cerebral Ischemia ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area ◽  
The Brain

c-Jun N-terminal kinase (JNK) is activated by various brain insults and is implicated in neuronal injury triggered by reperfusion-induced oxidative stress. Some JNK inhibitors demonstrated neuroprotective potential in various models, including cerebral ischemia/reperfusion injury. The objective of the present work was to study the neuroprotective activity of a new specific JNK inhibitor, IQ-1S (11H-indeno[1,2-b]quinoxalin-11-one oxime sodium salt), in the model of global cerebral ischemia (GCI) in rats compared with citicoline (cytidine-5′-diphosphocholine), a drug approved for the treatment of acute ischemic stroke and to search for pleiotropic mechanisms of neuroprotective effects of IQ-1S. The experiments were performed in a rat model of ischemic stroke with three-vessel occlusion (model of 3VO) affecting the brachiocephalic artery, the left subclavian artery, and the left common carotid artery. After 7-min episode of GCI in rats, 25% of animals died, whereas survived animals had severe neurological deficit at days 1, 3, and 5 after GCI. At day 5 after GCI, we observing massive loss of pyramidal neurons in the hippocampal CA1 area, increase in lipid peroxidation products in the brain tissue, and decrease in local cerebral blood flow (LCBF) in the parietal cortex. Moreover, blood hyperviscosity syndrome and endothelial dysfunction were found after GCI. Administration of IQ-1S (intragastrically at a dose 50 mg/kg daily for 5 days) was associated with neuroprotective effect comparable with the effect of citicoline (intraperitoneal at a dose of 500 mg/kg, daily for 5 days).The neuroprotective effect was accompanied by a decrease in the number of animals with severe neurological deficit, an increase in the number of animals with moderate degree of neurological deficit compared with control GCI group, and an increase in the number of unaltered neurons in the hippocampal CA1 area along with a significant decrease in the number of neurons with irreversible morphological damage. In rats with IQ-1S administration, the LCBF was significantly higher (by 60%) compared with that in the GCI control. Treatment with IQ-1S also decreases blood viscosity and endothelial dysfunction. A concentration-dependent decrease (IC50 = 0.8 ± 0.3 μM) of tone in isolated carotid arterial rings constricted with phenylephrine was observed after IQ-1S application in vitro. We also found that IQ-1S decreased the intensity of the lipid peroxidation in the brain tissue in rats with GCI. 2.2-Diphenyl-1-picrylhydrazyl scavenging for IQ-1S in acetonitrile and acetone exceeded the corresponding values for ionol, a known antioxidant. Overall, these results suggest that the neuroprotective properties of IQ-1S may be mediated by improvement of cerebral microcirculation due to the enhanced vasorelaxation, beneficial effects on blood viscosity, attenuation of the endothelial dysfunction, and antioxidant/antiradical IQ-1S activity.

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