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1.
Psychopharmacology (Berl) ; 240(4): 951-967, 2023 Apr.
Article in English | MEDLINE | ID: mdl-36811650

ABSTRACT

RATIONALE: Aging is the major risk factor for Alzheimer's disease (AD), and cognitive and memory impairments are common among the elderly. Interestingly, coenzyme Q10 (Q10) levels decline in the brain of aging animals. Q10 is a substantial antioxidant substance, which has an important role in the mitochondria. OBJECTIVE: We assessed the possible effects of Q10 on learning and memory and synaptic plasticity in aged ß-amyloid (Aß)-induced AD rats. METHODS: In this study, 40 Wistar rats (24-36 months old; 360-450 g) were randomly assigned to four groups (n = 10 rats/group)-group I: control, group II: Aß, group III: Q10; 50 mg/kg, and group IV: Q10+Aß. Q10 was administered orally by gavage daily for 4 weeks before the Aß injection. The cognitive function and learning and memory of the rats were measured by the novel object recognition (NOR), Morris water maze (MWM), and passive avoidance learning (PAL) tests. Finally, malondialdehyde (MDA), total antioxidant capacity (TAC), total thiol group (TTG), and total oxidant status (TOS) were measured. RESULTS: Q10 improved the Aß-related decrease in the discrimination index in the NOR test, spatial learning and memory in the MWM test, passive avoidance learning and memory in the PAL test, and long-term potentiation (LTP) impairment in the hippocampal PP-DG pathway in aged rats. In addition, Aß injection significantly increased serum MDA and TOS levels. Q10, however, significantly reversed these parameters and also increased TAC and TTG levels in the Aß+Q10 group. CONCLUSIONS: Our experimental findings suggest that Q10 supplementation can suppress the progression of neurodegeneration that otherwise impairs learning and memory and reduces synaptic plasticity in our experimental animals. Therefore, similar supplemental Q10 treatment given to humans with AD could possibly provide them a better quality of life.


Subject(s)
Alzheimer Disease , Humans , Rats , Animals , Aged , Child, Preschool , Alzheimer Disease/metabolism , Antioxidants/pharmacology , Rats, Wistar , Quality of Life , Neuronal Plasticity , Long-Term Potentiation , Amyloid beta-Peptides/metabolism , Hippocampus , Memory Disorders/etiology , Disease Models, Animal , Maze Learning
2.
Neurochem Int ; 155: 105304, 2022 05.
Article in English | MEDLINE | ID: mdl-35176438

ABSTRACT

Various impacts of exercise on brain performance following the induction of morphine dependence have been documented; however, the underlying neuronal mechanisms are still unclear. The present research was done to investigate the impact of different exercise training modes on apoptosis, neuronal maturation, and synaptic plasticity in the perforant pathway (PP)-dentate gyrus (DG) synapses in the morphine-dependent rats. Five groups, including a control group (Con, ten healthy rats) and forty morphine-dependent rats were considered as follows (n = 10/group): 1) sedentary-dependent (Sed-D); 2) endurance exercise-dependent (En-D); 3) strength exercise-dependent (St-D); and 4) concurrent exercise-dependent (Co-D). The exercise training groups were subjected to endurance, strength, and concurrent training five days a week for ten weeks. After training sessions, the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude in the DG were determined in response to high-frequency stimulation (HFS) of the PP. For assessing neurogenesis and apoptosis, NeuroD and Caspase-3 expression levels were evaluated after all experiments. Concurrent training increased PS amplitude and EPSP compared to the control group. NeuroD in the morphine-dependent rats significantly decreased, but concurrent training returned the NeuroD to its levels in healthy rats. Furthermore, Caspase-3 expression levels in morphine-dependent rats remarkably increased and concurrent training significantly reduced Caspase-3 expression levels compared to the Sed-D group. Concurrent training can ameliorate synaptic plasticity impairment in morphine-dependent rats through neurogenesis promotion and apoptosis reduction. According to the results, concurrent training can be an appropriate novel candidate for treating opioid addiction.


Subject(s)
Morphine Dependence , Animals , Dentate Gyrus , Long-Term Potentiation , Morphine/pharmacology , Morphine Dependence/metabolism , Neuronal Plasticity/physiology , Rats , Rats, Wistar
3.
J Physiol Sci ; 71(1): 14, 2021 Apr 29.
Article in English | MEDLINE | ID: mdl-33926383

ABSTRACT

High-fat diets (HFDs) and obesity can cause serious health problems, such as neurodegenerative diseases and cognitive impairments. Consumption of HFD is associated with reduction in hippocampal synaptic plasticity. Rosa damascena (R. damascena) is traditionally used as a dietary supplement for many disorders. This study was carried out to determine the beneficial effect of hydroalcoholic extract of R. damascena on in vivo hippocampal synaptic plasticity (long-term potentiation, LTP) in the perforant pathway (PP)-dentate gyrus (DG) pathway in rats fed with an HFD. Male Wistar rats were randomly assigned to four groups: Control, R. damascena extract (1 g/kg bw daily for 30 days), HFD (for 90 days) and HFD + extract. The population spike (PS) amplitude and slope of excitatory post-synaptic potentials (EPSP) were measured in DG area in response to stimulation applied to the PP. Serum oxidative stress biomarkers [total thiol group (TTG) and superoxide dismutase (SOD)] were measured. The results showed the HFD impaired LTP induction in the PP-DG synapses. This conclusion is supported by decreased EPSP slope and PS amplitude of LTP. R. damascena supplementation in HFD animals enhanced EPSP slope and PS amplitude of LTP in the granular cell of DG. Consumption of HFD decreased TTG and SOD. R. damascena extract consumption in the HFD animals enhanced TTG and SOD. These data indicate that R. damascena dietary supplementation can ameliorate HFD-induced alteration of synaptic plasticity, probably through its significant antioxidant effects and activate signalling pathways, which are critical in controlling synaptic plasticity.


Subject(s)
Diet, High-Fat , Hippocampus/drug effects , Long-Term Potentiation/drug effects , Plant Extracts/pharmacology , Rosa/chemistry , Animals , Diet, High-Fat/adverse effects , Hippocampus/physiology , Long-Term Potentiation/physiology , Male , Neural Pathways/drug effects , Neuronal Plasticity/drug effects , Rats , Rats, Wistar
4.
Metab Brain Dis ; 32(4): 1255-1265, 2017 08.
Article in English | MEDLINE | ID: mdl-28536937

ABSTRACT

A high-fat diet (HFD) causes deficits in learning and memory by increasing oxidative stress. Antioxidants are known to improve learning and memory. Since Hypericum scabrum (H. scabrum) extract is rich in antioxidants, the aim of this study was to investigate the effects of the administration of H. scabrum extract on passive avoidance learning (PAL), novel object recognition (NOR), and locomotor activity in male rats on a HFD. Fifty-four male Wistar rats (weighing 220 ± 10 g) were divided into the following six groups: (1) Control (standard diet), (2) Ext100 (standard diet supplemented with 100 mg/kg extract once/day), (3) Ext300 (standard diet supplemented with 300 mg/kg extract once/day), (4) HFD (high-fat diet), (5) HFD + Ext100, and (6) HFD + Ext300. Rats in these groups were maintained on their respective diets for 3 months. In the PAL test, the step-through latencies in the retention test (STLr) were significantly higher in the HFD + extract group than in the HFD group. The time spent in the dark compartment (TDC) was significantly lesser and the time spent in exploring the novel object was significantly greater in the HFD + extract group than in the HFD group. In the HFD-fed rats, the activity of catalase had significantly decreased, and level of malondialdehyde had significantly increased; H. scabrum extract administration significantly reversed these changes. In conclusion, these results suggested that the administration of H. scabrum extract and its strong antioxidant properties enhanced learning and memory and reversed the memory impairment induced by chronic HFD consumption.


Subject(s)
Antioxidants/pharmacology , Avoidance Learning/drug effects , Memory/drug effects , Oxidative Stress/drug effects , Plant Extracts/pharmacology , Recognition, Psychology/drug effects , Animals , Body Weight/drug effects , Catalase/blood , Diet, High-Fat , Hypericum , Lipid Peroxidation/drug effects , Male , Malondialdehyde/blood , Motor Activity/drug effects , Rats , Rats, Wistar
5.
Can J Physiol Pharmacol ; 95(4): 382-387, 2017 Apr.
Article in English | MEDLINE | ID: mdl-28112976

ABSTRACT

Despite previous findings on the effects of cannabinoid and vanilloid systems on learning and memory, the effects of the combined stimulation of these 2 systems on learning and memory have not been studied. Therefore, in this study, we tested the interactive effects of cannabinoid and vanilloid systems on learning and memory in rats by using passive avoidance learning (PAL) tests. Forty male Wistar rats were divided into the following 4 groups: (1) control (DMSO+saline), (2) WIN55,212-2, (3) capsaicin, and (4) WIN55,212-2 + capsaicin. On test day, capsaicin, a vanilloid receptor type 1 (TRPV1) agonist, or WIN55,212-2, a cannabinoid receptor (CB1/CB2) agonist, or both substances were injected intraperitoneally. Compared to the control group, the group treated with capsaicin (TRPV1 agonist) had better scores in the PAL acquisition and retention test, whereas treatment with WIN55,212-2 (CB1/CB2 agonist) decreased the test scores. Capsaicin partly reduced the effects of WIN55,212-2 on PAL and memory. We conclude that the acute administration of a TRPV1 agonist improves the rats' cognitive performance in PAL tasks and that a vanilloid-related mechanism may underlie the agonistic effect of WIN55,212-2 on learning and memory.


Subject(s)
Avoidance Learning/drug effects , Benzoxazines/pharmacology , Cannabinoid Receptor Agonists/pharmacology , Capsaicin/pharmacology , Cognition/drug effects , Memory/drug effects , Morpholines/pharmacology , Naphthalenes/pharmacology , TRPV Cation Channels/agonists , Animals , Benzoxazines/administration & dosage , Calcium Channel Blockers/pharmacology , Cannabinoids , Capsaicin/administration & dosage , Injections, Intraperitoneal , Male , Morpholines/administration & dosage , Naphthalenes/administration & dosage , Rats , Rats, Wistar , Sensory System Agents/pharmacology
6.
Brain Res ; 1629: 270-81, 2015 Dec 10.
Article in English | MEDLINE | ID: mdl-26462654

ABSTRACT

Lead (Pb) exposure during development is associated with impaired cognitive function and long-term potentiation (LTP). Vitamin E (VE) is an antioxidant that could have protective effects against Pb intoxication. In this study, we examined the protective effects of vitamin E against Pb-induced LTP impairments. Forty-six adult male Wistar rats were randomly divided into 6 treatment groups: (1) control; (2) Pb exposure; (3) VE; (4) Pb +VE; (5) Pb exposure followed by VE 2 months after exposure; (6) VE followed by Pb exposure 1 month after treatment. Rats were exposed to Pb through daily consumption of Pb-contaminated distilled water; VE was administered by daily gavage for 3 months. After this period, the population spike (PS) amplitudes and the slopes of excitatory postsynaptic potentials (EPSPs) were measured in the dentate gyrus (DG) area of the hippocampus in adult rats in response to electrical stimulation applied to the perforant pathway in vivo. Blood samples were also collected to evaluate malondialdehyde (MDA) levels, total antioxidant capacity (TAC), and total oxidant status (TOS). Biochemical analyses demonstrated significant increases in plasma MDA and TOS levels in the Pb-exposed group compared to the control group. VE-protected groups revealed significant increases in TAC levels. Our results demonstrate that Pb decreased EPSP slopes and PS amplitudes compared to the control group, whereas VE increased these parameters compared to the control group. Co-administration of VE with Pb exposure inhibited Pb-induced effects. These findings suggest that VE via its antioxidant activity reverses Pb-induced impairments of synaptic plasticity in the DG.


Subject(s)
Excitatory Postsynaptic Potentials/drug effects , Hippocampus/drug effects , Lead/toxicity , Neuronal Plasticity/drug effects , Vitamin E/pharmacology , Animals , Antioxidants/pharmacology , Antioxidants/therapeutic use , Cognition Disorders/chemically induced , Cognition Disorders/drug therapy , Cognition Disorders/physiopathology , Excitatory Postsynaptic Potentials/physiology , Hippocampus/pathology , Hippocampus/physiology , Lipid Peroxidation/drug effects , Lipid Peroxidation/physiology , Male , Neuronal Plasticity/physiology , Rats , Rats, Wistar , Treatment Outcome , Vitamin E/therapeutic use
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