Coping with Exercise Induced Spatial Memory Improvement in Morphine Dependent Rats by Inhibiting Brain Derived Neurotrophic Factor (BDNF)

2021 ◽  
Author(s):  
Aboozar Zare ◽  
Vali Nowzari ◽  
Tahereh Karimi-Jashni
Keyword(s):  
Spatial Memory ◽  
Learning And Memory ◽  
Potential Method ◽  
Voluntary Exercise ◽  
Morphine Dependence ◽  
Spatial Learning And Memory ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Neurotropic Factor ◽  
Exercise Induced

Background: Addiction as a chronic disorder that requires long treatment. One way to treating this chronic disease is exercise. Chronic exposure to opiates impairs spatial learning and memory. Given the well-known beneficial effects of voluntary exercise on cognitive functions, we investigated whether voluntary exercise would ameliorate the cognitive deficits that are induced by morphine dependence. If an effect of exercise was observed, we aimed to investigate the possible role of hippocampal brain-derived neurotropic factor (BDNF) in the exercise-induced enhancement of learning and memory in morphine-dependent rats. Methods: The rats were injected with bi-daily doses (10 mg/kg, at 12 hr. intervals) of morphine over a period of 10 days of voluntary exercise. Following these injections, a water maze task was performed twice a day for 5 consecutive days, followed by a probe trial 2 days later. A specific BDNF inhibitor (TrkB-IgG chimera) was used to block the hippocampal BDNF action during the 10 days of voluntary exercise. Results: The voluntary exercise diminished the severity of the rats’ dependency on morphine. A blockade of the BDNF action blunted the exercise-induced improvement of spatial memory, hippocampal neuron counting and BDNF protein levels in the dependent rats. Our results indicate that voluntary exercise could be increase the expression of LTP by lowering the induction threshold for LTP in the DG of morphine-dependent rats. Conclusion: Thus, voluntary exercise might be considered as a potential method to ameliorate some of the deleterious behavioral consequences of the abuse of morphine and other opiates.

scholarly journals A Long-Term Enriched Environment Ameliorates the Accelerated Age-Related Memory Impairment Induced by Gestational Administration of Lipopolysaccharide: Role of Plastic Mitochondrial Quality Control

2021 ◽  
Vol 14 ◽  
Author(s):  
Zhan-Qiang Zhuang ◽  
Zhe-Zhe Zhang ◽  
Yue-Ming Zhang ◽  
He-Hua Ge ◽  
Shi-Yu Sun ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Memory Impairment ◽  
Spatial Learning And Memory ◽  
Mitochondrial Quality Control ◽  
Protein Levels ◽  
Age Related ◽  
Old Mice ◽  
Lps Treatment

Studies have shown that gestational inflammation accelerates age-related memory impairment in mother mice. An enriched environment (EE) can improve age-related memory impairment, whereas mitochondrial dysfunction has been implicated in the pathogenesis of brain aging. However, it is unclear whether an EE can counteract the accelerated age-related memory impairment induced by gestational inflammation and whether this process is associated with the disruption of mitochondrial quality control (MQC) processes. In this study, CD-1 mice received daily intraperitoneal injections of lipopolysaccharide (LPS, 50 μg/kg) or normal saline (CON group) during gestational days 15–17 and were separated from their offspring at the end of normal lactation. The mothers that received LPS were divided into LPS group and LPS plus EE (LPS-E) treatment groups based on whether the mice were exposed to an EE until the end of the experiment. At 6 and 18 months of age, the Morris water maze test was used to evaluate spatial learning and memory abilities. Quantitative reverse transcription polymerase chain reaction and Western blot were used to measure the messenber RNA (mRNA) and protein levels of MQC-related genes in the hippocampus, respectively. The results showed that all the aged (18 months old) mice underwent a striking decline in spatial learning and memory performances and decreased mRNA/protein levels related to mitochondrial dynamics (Mfn1/Mfn2, OPA1, and Drp1), biogenesis (PGC-1α), and mitophagy (PINK1/parkin) in the hippocampi compared with the young (6 months old) mice. LPS treatment exacerbated the decline in age-related spatial learning and memory and enhanced the reduction in the mRNA and protein levels of MQC-related genes but increased the levels of PGC-1α in young mice. Exposure to an EE could alleviate the accelerated decline in age-related spatial learning and memory abilities and the accelerated changes in MQC-related mRNA or protein levels resulting from LPS treatment, especially in aged mice. In conclusion, long-term exposure to an EE can counteract the accelerated age-related spatial cognition impairment modulated by MQC in CD-1 mother mice that experience inflammation during pregnancy.

The role of the central histaminergic receptors in the exercise-induced improvements of the spatial learning and memory in rats

2014 ◽  
Vol 1587 ◽  
pp. 112-118 ◽  
Author(s):  
Majid Taati ◽  
Mehrnoush Moghaddasi ◽  
Masoumeh Esmaeili ◽  
Soheila Pourkhodadad ◽  
Hassan Nayebzadeh
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Spatial Learning And Memory ◽  
Exercise Induced

The effect of preventive exercise on the neuroprotection in 6-hydroxydopamine-lesioned rat brain

2019 ◽  
Vol 44 (12) ◽  
pp. 1267-1275 ◽  
Author(s):  
Zeinab Rezaee ◽  
Sayed Mohammad Marandi ◽  
Hojjatallah Alaei ◽  
Fahimeh Esfarjani
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Treadmill Running ◽  
Spatial Learning And Memory ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Protein Levels ◽  
6 Hydroxydopamine

Parkinson’s disease is characterized by neurodegeneration and learning deficiency. Physical exercise can alleviate these symptoms by increasing the expression of some effective and relevant factors. The preventive effect of 16-week treadmill running in a rat model of Parkinson’s disease, before 6-hydroxydopamine (6-OHDA) induction, was assessed. Experimental groups consisted of sedentary (SED), SED+6-OHDA, exercised (EX), and EX+6-OHDA rats. Forty-eight hours after the last session of exercise, 6-OHDA was injected into the medial forebrain bundle (MFB). One week after the injection, behavioral tests, including spatial learning and memory, were assessed through Morris water maze (MWM) and apomorphine-induced rotation. Three weeks after the injection, mRNA expression and protein levels of the transcriptional co-activator peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α), fibronectin type III domain-containing protein 5 (FNDC5), brain-derived neurotrophic factor (BDNF), and tyrosine hydroxylase (TH) were measured in the striatum and the hippocampus of rats by applying real-time PCR and Western blotting. The findings indicate that exposure to 6-OHDA leads to impairments in behavioral and molecular functions. Exercise training prevents and reduces the symptoms caused by dopamine toxins. The results suggest that treadmill running can exert neuroprotective and have preventive effects to reduce Parkinson’s disease symptoms. Novelty Parkinson’s disease impairs spatial learning and memory. Parkinson’s disease reduced levels of PGC-1α, FNDC5, and BDNF and increased neurodegeneration in the striatum and the hippocampus. Treadmill running before disease attenuated 6-OHDA-induced memory deficit and elevated neuroprotection. Exercise has multiple effects on memory and biochemical factors.

The glucocorticoid system is required for the voluntary exercise-induced enhancement of learning and memory in rats

2011 ◽  
Vol 219 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Razieh Hajisoltani ◽  
Ali Rashidy-Pour ◽  
Abbas A. Vafaei ◽  
Behshid Ghaderdoost ◽  
Ahmad Reza Bandegi ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Voluntary Exercise ◽  
Exercise Induced

scholarly journals Naloxone Ameliorates Spatial Memory Deficits and Hyperthermia Induced by a Neurotoxic Methamphetamine Regimen in Male Rats

2019 ◽  
Vol 8 ◽  
pp. 1182 ◽  
Author(s):  
Solmaz Khalifeh ◽  
Mehdi Khodamoradi ◽  
Vahid Hajali ◽  
Hamed Ghazvini ◽  
Lelia Eliasy ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Spatial Memory ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Memory Impairment ◽  
Memory Performance ◽  
Poor Performance ◽  
Male Rats ◽  
Spatial Learning And Memory ◽  
Opiate Antagonist

Background: Methamphetamine (METH) as a synthetic psychostimulant is being increasingly recognized as a worldwide problem, which may induce memory impairment. On the other hand, it is well established that naloxone, an opiate antagonist, has some beneficial effects on learning and memory. The present research aimed at evaluating naloxone effects on spatial learning and memory impairment triggered by a neurotoxic regimen of METH in male rats. Materials and Methods: The animals received the subcutaneous (sc) regimen of METH (4×6 mg/kg at 2-h intervals), intraperitoneal (ip) naloxone (4×1 mg/kg at 2-h intervals), or normal saline at four events. The Nal-METH group of rats received four naloxone injections (1 mg/kg, ip) 30 min before each METH injection (6 mg/kg, sc) at 2-h intervals. Seven days later, they were evaluated for spatial learning and memory in the Morris Water Maze (MWM) task. Result: METH regimen induced hyperthermia, as well as a poor performance, in the acquisition and retention phases of the task, indicating spatial learning and memory impairment compared to the controls. Naloxone administration (1 mg/kg, ip) before each METH injection led to significant attenuations of both hyperthermia and METH adverse effects on the rat performance in the MWM task. Conclusion: The results revealed that pretreatment with the opiate antagonist naloxone could prevent METH adverse effects on body temperature and memory performance. It seems that the opioidergic system and hyperthermia may, at least partially, be involved in METH effects on spatial memory. [GMJ. 2019;8:e1182]

scholarly journals Thyroidectomy- And Ptu-Induced Hypothyroidism: Effect of L-Thyroxine on Suppression of Spatial and Non-Spatial Memory Related Signaling Molecules

2021 ◽  
Author(s):  
Karim Alkadhi ◽  
KH Alzoubi
Keyword(s):  
Spatial Memory ◽  
Learning And Memory ◽  
Molecular Level ◽  
Thyroid Stimulating Hormone ◽  
Adult Rats ◽  
Thyroxine Therapy ◽  
Protein Levels ◽  
Hippocampal Area ◽  
Dependent Learning ◽  
Memory Rats

Abstract The calcium/calmodulin protein kinase II (CaMKII) signaling cascade is crucial for hippocampus-dependent learning and memory. In adult rats, Hypothyroidism impairs hippocampus-dependent learning and memory, which can be prevented by simple replacement therapy with L-thyroxine (thyroxine, T4) treatment. In this study, we compared animal models of hypothyroidism induced by thyroidectomy and treatment with propylthiouracil (PTU). Our findings show that thyroidectomy and PTU models are equally effective as indicated by the identical plasma levels of thyroid stimulating hormone (TSH) and T4. The two model produced identical degree of inhibition of synaptic plasticity as indicated by depression of LTP. We then investigated the effect of thyroidectomy hypothyroidism and thyroxine treatment on the underlying molecular mechanism of spatial and non-spatial types of memory. To generate spatial memory, we used training in the radial arm water maze (RAWM) where rats had to locate a hidden platform. For non-spatial memory, rats were trained to swim to a clearly visible platform in an open swim field. Western blot analysis of hippocampal area CA1 revealed that training, on both mazes, of control and thyroxine-treated hypothyroid rats produced significant increases in the P-CaMKII, PKCγ, calcineurin and calmodulin protein levels, but the training failed to induce such increases in untreated thyroidectomized rats. As expected, we show that thyroxine therapy prevented the deleterious effects of hypothyroidism at the molecular level.

Voluntary exercise-induced neurogenesis in the postischemic dentate gyrus is associated with spatial memory recovery from stroke

2007 ◽  
Vol 85 (8) ◽  
pp. 1637-1646 ◽  
Author(s):  
Chun Xia Luo ◽  
Jun Jiang ◽  
Qi Gang Zhou ◽  
Xin Jian Zhu ◽  
Wei Wang ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Dentate Gyrus ◽  
Voluntary Exercise ◽  
Memory Recovery ◽  
Exercise Induced

scholarly journals Leptin in hippocampus mediates benefits of mild exercise by an antioxidant on neurogenesis and memory

2019 ◽  
Vol 116 (22) ◽  
pp. 10988-10993 ◽  
Author(s):  
Jang Soo Yook ◽  
Randeep Rakwal ◽  
Junko Shibato ◽  
Kanako Takahashi ◽  
Hikaru Koizumi ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Direct Action ◽  
Memory Function ◽  
Neuroblastoma Cell ◽  
Hippocampal Neurogenesis ◽  
Human Neuroblastoma Cell ◽  
Bioinformatics Analyses ◽  
Human Neuroblastoma ◽  
Beneficial Effects ◽  
Protein Levels

Regular exercise and dietary supplements with antioxidants each have the potential to improve cognitive function and attenuate cognitive decline, and, in some cases, they enhance each other. Our current results reveal that low-intensity exercise (mild exercise, ME) and the natural antioxidant carotenoid astaxanthin (AX) each have equivalent beneficial effects on hippocampal neurogenesis and memory function. We found that the enhancement by ME combined with AX in potentiating hippocampus-based plasticity and cognition is mediated by leptin (LEP) made and acting in the hippocampus. In assessing the combined effects upon wild-type (WT) mice undergoing ME with or without an AX diet for four weeks, we found that, when administrated alone, ME and AX separately enhanced neurogenesis and spatial memory, and when combined they were at least additive in their effects. DNA microarray and bioinformatics analyses revealed not only the up-regulation of an antioxidant gene, ABHD3, but also that the up-regulation of LEP gene expression in the hippocampus of WT mice with ME alone is further enhanced by AX. Together, they also increased hippocampal LEP (h-LEP) protein levels and enhanced spatial memory mediated through AKT/STAT3 signaling. AX treatment also has direct action on human neuroblastoma cell lines to increase cell viability associated with increased LEP expression. In LEP-deficient mice (ob/ob), chronic infusion of LEP into the lateral ventricles restored the synergy. Collectively, our findings suggest that not only h-LEP but also exogenous LEP mediates effects of ME on neural functions underlying memory, which is further enhanced by the antioxidant AX.

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