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, WistarABSTRACT
Diabetes mellitus (DM) is associated with impaired hippocampal synaptic plasticity. Coenzyme Q10 (CoQ10) acts as an antioxidant and exerts neuroprotective effects. Accordingly, this study aimed at evaluating the effects of CoQ10 on hippocampal long-term potentiation (LTP) and paired-pulse facilitation (PPF) in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were randomly divided into six groups (nâ¯=â¯8 per group) as follows and treated for 90â¯days: the control, controlâ¯+â¯low dose of CoQ10 (100â¯mg/kg), controlâ¯+â¯high dose of CoQ10 (600â¯mg/kg), diabetic, diabeticâ¯+â¯low dose of CoQ10, and diabeticâ¯+â¯high dose of CoQ10 groups. Diabetes was induced by a single intraperitoneal injection of 50â¯mg/kg STZ. The population spike (PS) amplitude and slope of excitatory post synaptic potentials (EPSPs) were measured in dentate gyrus (DG) area in response to the stimulation applied to the perforant path (PP). The results showed that the STZ-induced diabetes impaired LTP induction in the PP-DG synapses. This finding is supported by the decreased EPSP slope and PS amplitude of LTP (Pâ¯<â¯0.05). Both low- and high-dose CoQ10 supplementation in the control and diabetic animals enhanced EPSP slope and PS amplitude of LTP in the granular cells of DG (Pâ¯<â¯0.05). PPF was affected by LTP induction in diabetic animals receiving the high dose of CoQ10 (Pâ¯<â¯0.05). It is suggested that CoQ10 administration could attenuate deteriorative effect of STZ-induced diabetes on in vivo LTP in the DG. The enhanced transmitter release can be partly one of the possible underlying mechanism(s) responsible for the LTP induction in the diabetic animals treated with CoQ10.
Subject(s)
Antioxidants/administration & dosage , Dentate Gyrus/drug effects , Diabetes Mellitus/physiopathology , Long-Term Potentiation/drug effects , Neurons/drug effects , Neuroprotective Agents/administration & dosage , Ubiquinone/analogs & derivatives , Animals , Dentate Gyrus/physiology , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus, Experimental/physiopathology , Male , Neurons/physiology , Rats, Wistar , Streptozocin/administration & dosage , Ubiquinone/administration & dosageABSTRACT
The main objective of current work was to determine the effects of low and high dose supplementation with coenzyme Q10 (CoQ10) on spatial learning and memory in rats with streptozotocin (STZ)-induced diabetes. Male Wistar rats (weighing 220 ± 10) were randomly divided into six groups: (i) Control (Con, n = 8); (ii) Control+ Low dose of CoQ10 (100 mg/kg) (CLD, n = 10); (iii) Control+ high dose of CoQ10 (600 mg/kg) (CHD, n = 10); (iv) Diabetic (D, n = 10); (v) Diabetic + Low dose of CoQ10 (100 mg/kg) (DLD, n = 10); (vi) Diabetic + high dose of CoQ10 (600 mg/kg) (DHD, n = 10). Diabetes was induced by a single intraperitoneal injection of 50 mg/kg STZ. CoQ10 was administered intragastrically by gavage once a day for 90 days. After 90 days, Morris water maze (MWM) task was used to evaluate the spatial learning and memory in rats. Diabetic animals showed a slower rate of acquisition with respect to the control animals [F (1, 51) = 92.81, P < 0.0001, two-way ANOVA]. High dose (but no low dose) supplementation with CoQ10 could attenuate deteriorative effect of diabetes on memory acquisition. Diabetic animals which received CoQ10 (600 mg/kg) show a considerable decrease in escape latency and traveled distance compared to diabetic animals (p < 0.05, two-way ANOVA,). The present study has shown that low dose supplementation with CoQ10 in diabetic rats failed to improve deficits in cognitive function but high dose supplementation with CoQ10 reversed diabetes-related declines in spatial learning.
Subject(s)
Cognition/drug effects , Diabetes Mellitus, Experimental/drug therapy , Memory/drug effects , Ubiquinone/analogs & derivatives , Animals , Antioxidants/pharmacology , Glutathione/metabolism , Lipid Peroxidation/drug effects , Male , Memory Disorders/drug therapy , Oxidative Stress/drug effects , Rats, Wistar , Ubiquinone/chemistry , Ubiquinone/pharmacologyABSTRACT
The objective of this study was to determine the relation between the chronic consumption of garlic powder in combination with high-fat diet (HFD) on long term potentiation (LTP) in the dentate gyrus (DG) of rat hippocampus. Male rats were divided to 4 groups, control with the standard diet, control with a standard diet plus garlic, high-fat diet (HFD) group and high-fat diet with garlic. Following 6 months of controlled dietary in each experimental group, the rats were anesthetized with i.p. injection of ketamine and xylazin (100 and 2.5 mg/kg, respectively), and placed into a stereotaxic apparatus for surgery, electrode implantation and field potential recording. The population spike (PS) amplitude and slope of excitatory post synaptic potentials (EPSP) were measured in the DG area of adult rats in response to stimulation applied to the perforant path (PP) (by 400 Hz tetanization). The results showed that garlic increased EPSP slope and PS amplitude respect to HFD group. It was suggested that the garlic powder administration could attenuate the deteriorating effect of HFD on in vivo hippocampal LTP in the granular cells of the DG.
Subject(s)
Diet, High-Fat , Garlic , Hippocampus/drug effects , Long-Term Potentiation/drug effects , Animals , Antioxidants/pharmacology , Electric Stimulation/methods , Excitatory Postsynaptic Potentials/drug effects , Male , Rats, WistarABSTRACT
Cognitive function is impaired by imbalanced diet consumption. High-fat diet (HFD) induces oxidative stress and metabolic disorders, which results in neuronal damage and interferes with synaptic transmission and neurogenesis; hence, a decline in learning and memory. Antioxidants are believed to have positive effects on cognitive function. The objective of this study was to determine the relation between the chronic consumption of a HFD and antioxidants on passive avoidance learning (PAL) in male rats. Wistar rats were randomly assigned into the following five groups (N=6-8): Control group-consumed an ordinary diet; HFD group-received high-fat diets only; ANO group-received HFD plus antioxidants (vitamins C and E and astaxanthin (ASX)); RHFD group-received the restricted HFD (30% less than the HFD group); and RANO group-received restricted HFD plus antioxidants (30% less than the ANO group). Following 6months of controlled dietary condition as mentioned above, in each experimental group, the PAL was assessed using shuttle box apparatus. Our results showed that HFD caused a decrease in step through latency in the retention test (STLr) and increased the time spent in the dark compartment in the retention test (TDC) when compared to the control group. Antioxidant supplementation caused an increase in STLr and decrease in TDC when compared to the control group. Furthermore, RHFD and RANO had no significant effect on STLr and TDC compared with the control group. According to our results, HFD impairs PAL and the combination of vitamins C and E and astaxanthin improves PAL deficits in the HFD group.