scholarly journals Cannabidiol promotes neurogenesis in the dentate gyrus during an abstinence period in rats following chronic exposure to methamphetamine

2021 ◽  
Author(s):  
Yasaman Razavi ◽  
Fariborz Keyhanfar ◽  
Abbas Haghparast ◽  
Ronak Shabani ◽  
Mehdi Mehdizadeh
Keyword(s):  
Dentate Gyrus ◽  
Chronic Exposure ◽  
Neuronal Degeneration ◽  
Hippocampal Neurogenesis ◽  
Control Group ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Promising Therapeutic Approach ◽  
Abstinence Period

Abstract Chronic methamphetamine (meth) abuse can lead to certain deficits in the hippocampal function by affecting the hippocampal neurogenesis and plasticity. To determine whether cannabidiol (CBD) can promote proliferation and maturation of neuronal progenitor cells, this study investigated the CBD effect on neurogenesis in the hippocampal dentate gyrus (DG) following chronic exposure to meth in rats. The rats received 2 mg/kg of meth twice a day for ten days. Next, immunofluorescence was performed to evaluate the effect of intracerebroventricular (ICV) administration of CBD (50 µg/5 µL) over an abstinence period (ten days) on the expression levels of neurogenesis markers, such as Ki67, NeuN, and doublecortin (DCX). Moreover, neuronal degeneration in the hippocampus was assessed using Nissl staining. According to our findings, repeated ICV administration of CBD improved cell proliferation and neurogenesis and increased the number of Ki-67 and DCX-positive cells in the abstinence period. Meanwhile, meth treatment subjects caused a significant decrease in the number of neurogenesis makers, as compared to the control group. The neurogenesis markers (Ki-67 and DCX) could be somewhat reversed, while NeuN did not show any significant increase in the CBD group. Our findings demonstrated that CBD can induce neuroprotective effects by modulating neurogenesis. Therefore, it can provide a promising therapeutic approach to improve cognitive performance following chronic exposure to psychostimulant drugs, including meth.

scholarly journals Cannabidiol Modulates the Expression of Neurotrophin Signaling Pathway in Chronic Exposure Methamphetamine Rats During Abstinence Period

2021 ◽  
pp. 1-23
Author(s):  
Yasaman Razavi ◽  
◽  
Mohammad Najafi ◽  
Abbas Haghparast ◽  
Fariborz Keyhanfar ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Signaling Pathway ◽  
Chronic Exposure ◽  
Mrna Level ◽  
Neuropsychiatric Disorders ◽  
Control Group ◽  
Hippocampal Damage ◽  
Neuroprotective Effects ◽  
Neurotrophin Signaling ◽  
Abstinence Period

Several neuropsychiatric disorders such as addiction have indicated variations in the levels of neurotrophic factors. As an extremely addictive stimulant, Methamphetamine (METH) is associated with rising levels of abuse on a global scale. We have recently demonstrated that repeated intracerebroventricular (ICV) of cannabidiol (CBD), the most important non-psychotomimetic compound, can lead to diminished impairing memory and hippocampal damage caused by chronic exposure METH (CEM) in rats over the abstinence period. Furthermore, the results indicated a possible contribution of the neurotrophin signaling pathway (NSP) in regulating neurogenesis and survival. The next study was intended to evaluate whether these remained effects as measured in molecular pathway after abstinence period. In this regard, animals were given 2 mg/kg METH twice daily for a 10-day period. Then, we adopted real-time polymerase chain reaction (PCR) throughout the 10-day abstinence period for assessing the CBD’s effect (10 and 50 μg/5 μl) on the levels of the mRNA expression of the NSP. The findings suggested that CEM, compared with the control group in the hippocampus, downregulated mRNA expression of NSP. Moreover, a dosage of 50 μg/5μl CBD may possibly enhance the mRNA expression level of BDNF/TrkB and NGF/TrkA in the hippocampus. Besides, the expression raf-1 mRNA level could be reversed significantly by both doses of CBD. According to our results, CBD may partly bring about the neuroprotective effects by modulating the NSP. These findings set forth solid evidence demonstrating that CBD is a protection factor attributed to neuropsychiatric disorders such as METH addiction.

scholarly journals Sevoflurane Preconditioning against Focal Cerebral Ischemia

2009 ◽  
Vol 110 (6) ◽  
pp. 1271-1278 ◽  
Author(s):  
Jean-Laurent Codaccioni ◽  
Lionel J. Velly ◽  
Chahrazad Moubarik ◽  
Nicolas J. Bruder ◽  
Pascale S. Pisano ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Cerebral Injury ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Sprague Dawley ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Sevoflurane Preconditioning

Background Preconditioning the brain with volatile anesthetics seems to be a viable option for reducing ischemic cerebral injury. However, it is uncertain whether this preconditioning effect extends over a longer period of time. The purpose of this study was to determine if sevoflurane preconditioning offers durable neuroprotection against cerebral ischemia. Methods Rats (Sprague-Dawley) were randomly allocated to two groups: nonpreconditioned control group (n = 44) and preconditioned group (n = 45) exposed to 2.7 vol% sevoflurane (45 min) 60 min before surgery. Animals in both groups were anesthetized with 3.0 vol% sevoflurane and subjected to transient middle cerebral artery occlusion. After 60 min of awake focal ischemia, the filament was removed. Functional neurologic outcome (range 0-18; 0 = no deficit), cerebral infarct size (Nissl staining), and apoptosis (Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling; cleaved caspase-3 staining) were evaluated at 3, 7, and 14 days after ischemia. Results Sevoflurane preconditioning significantly improved functional outcome and reduced infarct volume (109 +/- 43 vs. 148 +/- 56 mm(3)) 3 days after ischemia compared to the control group. However, after 7- and 14-day recovery periods, no significant differences were observed between groups. The number of apoptotic cells was significantly lower in the preconditioned group than in the control group after 3- and 7-day recovery periods. Fourteen days after ischemia, no differences were observed between groups. Conclusion In this model of transient focal cerebral ischemia, sevoflurane preconditioning induced effective but transient neuroprotective effects. Sevoflurane preconditioning also decreased ischemia-induced apoptosis in a more sustained way because it was observed up to 7 days after injury.

scholarly journals Pneumococcal Cell Wall-Induced Meningitis Impairs Adult Hippocampal Neurogenesis

2007 ◽  
Vol 75 (9) ◽  
pp. 4289-4297 ◽  
Author(s):  
Olaf Hoffmann ◽  
Cordula Mahrhofer ◽  
Nina Rueter ◽  
Dorette Freyer ◽  
Bettina Bert ◽  
...  
Keyword(s):  
Bacterial Meningitis ◽  
Dentate Gyrus ◽  
Adult Neurogenesis ◽  
Neuronal Degeneration ◽  
Continuous Process ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
High Rate ◽  
Induction Treatment ◽  
The Impact

ABSTRACT Bacterial meningitis is a major infectious cause of neuronal degeneration in the hippocampus. Neurogenesis, a continuous process in the adult hippocampus, could ameliorate such loss. Yet the high rate of sequelae from meningitis suggests that this repair mechanism is inefficient. Here we used a mouse model of nonreplicative bacterial meningitis to determine the impact of transient intracranial inflammation on adult neurogenesis. Experimental meningitis resulted in a net loss of neurons, diminished volume, and impaired neurogenesis in the dentate gyrus for weeks following recovery from the insult. Inducible nitric oxide synthase (iNOS) immunoreactivity was prominent in microglia in nonproliferating areas of the dentate gyrus and hilus region after meningitis induction. Treatment with the specific iNOS inhibitor N6-(1-iminoethyl)-l-lysine restored neurogenesis in experimental meningitis. These data suggest that local central nervous system inflammation in and of itself suppresses adult neurogenesis by affecting both proliferation and neuronal differentiation. Repair of cognitive dysfunction following meningitis could be improved by intervention to interrupt these actively suppressive effects.

scholarly journals NEUROPROTECTIVE EFFECTS OF POMEGRANATE JUICE ON LEAD INDUCED NEUROTOXICITY IN MICE

2017 ◽  
Vol 9 (2) ◽  
pp. 207
Author(s):  
Leila Gadouche ◽  
Noureddine Djebli ◽  
Khayra Zerrouki
Keyword(s):  
Drinking Water ◽  
Cerebral Cortex ◽  
Lead Acetate ◽  
Neuronal Degeneration ◽  
Neuroprotective Effect ◽  
Pomegranate Juice ◽  
Total Phenolic ◽  
Control Group ◽  
Histological Structure ◽  
Neuroprotective Effects

<p><strong>Objective: </strong>This study evaluates the potential neuroprotective of the pomegranate juice against chronic intoxication with lead acetate for 3<strong> </strong>months.</p><p><strong>Methods: </strong>Twenty-one female Swiss mice divided into 3 groups were employed in the present investigation. Control group: received drinking water for 90 days, neurotoxic group were exposed to 1000 ppm of lead acetate in the drinking water for 12 weeks, and neurotoxic treated group represents the mice received treatment with juice pomegranate diluted with distilled water (v/v) orally for 4 h / day followed by lead acetate at a dose of 1000 ppm orally for 20 h / day for 90 days. After cessation of treatment, neurobehavioral studies using the open field test, black and white test box and swimming test were made. In the next phase, brain injury was assessed histologically with hematoxylin-eosin staining.</p><p><strong>Results:</strong> Chronic exposure to lead led to significant increase in the level of anxiety, depression and the locomotor activity (P &lt; 0.05). It was confirmed by histopathological alterations in many areas of the cerebral cortex and hippocampus including neuronal degeneration and decrease cell density. Treatment with the juice significantly improve the level of depression, locomotor function (P &lt; 005) and anxiety (P &gt; 0.05) in mice exposed to lead as well as restored the histological structure in cerebral cortex and hippocampus of mice. The total phenolic and flavonoids content in juice of pomegranate was found to be 3809. 8±29.404 mg GAE/l; 2109. 57±18.936 mg QE /l of juice.</p><p><strong>Conclusion: </strong>This finding suggests that phenolic compounds found in pomegranate juice provide a neuroprotective effect on behavioural impairments and histopathological change induced by lead.</p>

scholarly journals Ventilation With Argon Improves Survival With Good Neurological Recovery After Prolonged Untreated Cardiac Arrest in Pigs

2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Francesca Fumagalli ◽  
Davide Olivari ◽  
Antonio Boccardo ◽  
Daria De Giorgio ◽  
Roberta Affatato ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Neuronal Degeneration ◽  
Left Ventricular ◽  
Neurological Recovery ◽  
Control Treatment ◽  
Control Group ◽  
Neuroprotective Effects ◽  
Reactive Microglia ◽  
In Vivo Models

Background Ventilation with the noble gas argon (Ar) has shown neuroprotective and cardioprotective properties in different in vitro and in vivo models. Hence, the neuroprotective effects of Ar were investigated in a severe, preclinically relevant porcine model of cardiac arrest. Methods and Results Cardiac arrest was ischemically induced in 36 pigs and left untreated for 12 minutes before starting cardiopulmonary resuscitation. Animals were randomized to 4‐hour post‐resuscitation ventilation with: 70% nitrogen–30% oxygen (control); 50% Ar–20% nitrogen–30% oxygen (Ar 50%); and 70% Ar–30% oxygen (Ar 70%). Hemodynamic parameters and myocardial function were monitored and serial blood samples taken. Pigs were observed up to 96 hours for survival and neurological recovery. Heart and brain were harvested for histopathology. Ten animals in each group were successfully resuscitated. Ninety‐six‐hour survival was 60%, 70%, and 90%, for the control, Ar 50%, and Ar 70% groups, respectively. In the Ar 50% and Ar 70% groups, 60% and 80%, respectively, achieved good neurological recovery, in contrast to only 30% in the control group ( P <0.0001). Histology showed less neuronal degeneration in the cortex ( P <0.05) but not in the hippocampus, and less reactive microglia activation in the hippocampus ( P =0.007), after Ar compared with control treatment. A lower increase in circulating biomarkers of brain injury, together with less kynurenine pathway activation ( P <0.05), were present in Ar‐treated animals compared with controls. Ar 70% pigs also had complete left ventricular function recovery and smaller infarct and cardiac troponin release ( P <0.01). Conclusions Post‐resuscitation ventilation with Ar significantly improves neurologic recovery and ameliorates brain injury after cardiac arrest with long no‐flow duration. Benefits are greater after Ar 70% than Ar 50%.

scholarly journals Cannabidiol promotes neurogenesis in the dentate gyrus during an abstinence period in rats following chronic exposure to methamphetamine

2021 ◽  
Author(s):  
Yasaman Razavi ◽  
Fariborz Keyhanfar ◽  
Abbas Haghparast ◽  
Ronak Shabani ◽  
Mehdi Mehdizadeh
Keyword(s):  
Dentate Gyrus ◽  
Chronic Exposure ◽  
Abstinence Period

scholarly journals Chrysin Protects against Memory and Hippocampal Neurogenesis Depletion in D-Galactose-Induced Aging in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1100
Author(s):  
Ram Prajit ◽  
Nataya Sritawan ◽  
Kornrawee Suwannakot ◽  
Salinee Naewla ◽  
Anusara Aranarochana ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Survival ◽  
Brain Aging ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Hippocampal Neurogenesis ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Novel Object ◽  
Immature Neurons

The interruption of hippocampal neurogenesis due to aging impairs memory. The accumulation of D-galactose (D-gal), a monosaccharide, induces brain aging by causing oxidative stress and inflammation, resulting in neuronal cell damage and memory loss. Chrysin, an extracted flavonoid, has neuroprotective effects on memory. The present study aimed to investigate the effect of chrysin on memory and hippocampal neurogenesis in brains aged using D-gal. Male Sprague-Dawley rats received either D-gal (50 mg/kg) by i.p. injection, chrysin (10 or 30 mg/kg) by oral gavage, or D-gal (50 mg/kg) and chrysin (10 or 30 mg/kg) for 8 weeks. Memory was evaluated using novel object location (NOL) and novel object recognition (NOR) tests. Hippocampal neurogenesis was evaluated using Ki-67, 5-bromo-2′-deoxyuridine (BrdU), and doublecortin (DCX) immunofluorescence staining to determine cell proliferation, cell survival, and number of immature neurons, respectively. We found that D-gal administration resulted in memory impairment as measured by NOL and NOR tests and in depletions in cell proliferation, cell survival, and immature neurons. However, co-treatment with chrysin (10 or 30 mg/kg) attenuated these impairments. These results suggest that chrysin could potentially minimize memory and hippocampal neurogenesis depletions brought on by aging.

scholarly journals Active constituent of Polygala tenuifolia attenuates cognitive deficits by rescuing hippocampal neurogenesis in APP/PS1 transgenic mice

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiao-feng Wang ◽  
Hong-he Xiao ◽  
Yu-tong Wu ◽  
Liang Kong ◽  
Ji-cong Chen ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Cell Model ◽  
Hippocampal Neurogenesis ◽  
Brdu Incorporation ◽  
Active Constituent ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Polygala Tenuifolia ◽  
Proliferation And Differentiation

Abstract Background Alzheimer’s disease (AD) is the most common dementia worldwide, and there is still no satisfactory drug or therapeutic strategy. Polygala tenuifolia is a traditional Chinese medicine with multiple neuroprotective effects. In present study, we investigated the effects of three active constituents [3,6′-disinapoyl sucrose (DISS), onjisaponin B (OB) and tenuifolin (TEN)] of Polygala tenuifolia (PT) on the proliferation and differentiation of neural stem cells (NSCs) to identify the potential active constituent of PT promoting hippocampal neurogenesis. Methods NSCs were isolated from hippocampi of newborn C57BL/6 mice, and transfected with mutant amyloid precursor protein (APP) gene to establish an AD cell model (APP-NSCs). 3-(4,5- Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays were performed, and the proliferation and differentiation of NSCs were assessed by neurosphere formation assay, 5-bromo-2′-deoxyuridine (BrdU) incorporation assay and immunofluorescence (IF) staining analysis. APP/PS1 transgenic mice were administrated with the potential active constituent DISS for 4 weeks. Morris water maze (MWM), Nissl staining assay and IF staining assays were carried out to evaluate the cognitive function, neural damages and hippocampal neurogenesis, respectively. Results DISS exerted the optimal ability to strengthen APP-NSCs proliferation and neuronal differentiation, followed by OB and TEN. Furthermore, DISS treatment for 4 weeks strikingly rescued the cognitive deficits, neuronal injures, and neurogenesis disorder in adult APP/PS1 transgenic mice. Conclusions Our findings demonstrated that DISS is the constituent of PT that triggers the most potent increase of hippocampal neurogenesis in our mouse model of AD.

scholarly journals Neuroprotective Effects of Berberine Hydrochloride on Cognitive Dysfunction-Induced by Methamphetamine: Immunohistochemical and Behavioral Studies in Rats

2021 ◽  
Author(s):  
Leila Rezaeian ◽  
◽  
Mehdi Khaksari ◽  
Raheleh Rafaiee ◽  
Hamid Kalalian Moghaddam ◽  
...  
Keyword(s):  
Treated Group ◽  
Control Group ◽  
Self Administration ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Berberine Hydrochloride ◽  
Behavioral Studies ◽  
Gfap Expression ◽  
Male Wistar Rats ◽  
The Impact

Introduction: Methamphetamine (MA) as an addictive psychostimulant drug affects the central nervous system. The present research aimed at evaluating the impact of Berberine-hydrochloride on cognitive function Improvement and neuroprotective effects in MA Addicted Rats. Methods: In this study, 27 Male Wistar rats were randomly assigned to three groups, including Control, MA addiction and MA addiction with Berberine Hydrochloride (100 mg/kg/day) per oral during the three-week period of withdrawal. Two groups received inhaled MA self-administration for two weeks (up to 10 mg/kg). Following the experimental procedures, Morris Water Maze (MWM) and shuttle box were used to assess memory and hippocampal sections from the animals were examined for caspase-3, ki-67 and GFAP expression. Results: The obtained results from MWM showed that Berberine Hydrochloride decreases (p<0.01) the distance moved and spent time to reach the hidden platform in four-day learning trails phase and there were significant differences in the distance moved, spent time and frequency of motion in target quadrant on probe test day between groups. Berberine Hydrochloride reduced also the latency to enter animals into the dark chamber in the treated group in comparison with the control group (p<0.05). A significant decrease in activation of caspases-3, higher percentages of Ki67 expression and increase in GFAP expression of cells in Addicted group was found to compare with Berberine-treated and control groups (p<0.05). Conclusions: Berberine Hydrochloride administration for 3 weeks improves cognition function in MA addiction and it has a potential for neuroprotective efficacy.

scholarly journals Melatonin Protects Against the Side-Effects of 5-Fluorouracil on Hippocampal Neurogenesis and Ameliorates Antioxidant Activity in an Adult Rat Hippocampus and Prefrontal Cortex

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 615
Author(s):  
Kornrawee Suwannakot ◽  
Nataya Sritawan ◽  
Ram Prajit ◽  
Anusara Aranarochana ◽  
Apiwat Sirichoat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Working Memory ◽  
Prefrontal Cortex ◽  
Protein Expression ◽  
Dentate Gyrus ◽  
Antioxidant Enzyme ◽  
Hippocampal Neurogenesis ◽  
Rat Hippocampus ◽  
Related Factor ◽  
Neuroprotective Effects

Melatonin is an endogenous hormone that exhibits antioxidant functions and neuroprotective effects. The hippocampus and the prefrontal cortex (PFC) play an important role linked to working memory. 5-fluorouracil (5-FU) can induce oxidative stress and reduce neurogenesis in the subgranular zone (SGZ) of the dentate gyrus in a rat hippocampus and these alterations are related to working memory deficits. This study aimed to determine the effect of melatonin on 5-FU-induced oxidative stress that interferes with the antioxidant enzymes and protein expression levels in a rat hippocampus and PFC. A total of 68 male Sprague Dawley rats were divided into four groups: vehicle, 5-FU, melatonin and melatonin+5-FU groups. Rats were administered 5-FU (25 mg/kg, i.v.) on days 9, 12, 15, 18 and 21 and received melatonin (8 mg/kg, i.p.) at 19:00 from day 1 to day 21 of the experiment. Lipid peroxidation was assessed by measuring malondialdehyde (MDA) levels. Antioxidant enzyme levels including glutathione peroxidase (GPX), catalase (CAT) and superoxide dismutase (SOD) were determined. p21 immunofluorescence staining and Western blotting were used to detect the cell cycle arrest and protein expression of the nuclear factor erythroid 2-related factor 2 (Nrf2), doublecortin (DCX) and brain derived neurotrophic factor (BDNF), respectively. The results showed that melatonin reduced the number of p21-positive cells in the SGZ of the dentate gyrus and increased Nrf2, DCX and BDNF protein expression in rats treated with 5-FU. Moreover, melatonin restored antioxidant enzyme levels and reduced oxidative stress in the hippocampus and PFC caused by 5-FU. These findings reveal a mechanism of the neuroprotective properties of melatonin against 5-FU in a rat hippocampus and PFC.

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