ABSTRACT
ABSTRACT PURPOSE: To evaluated the long-term effect of scopolamine and sesame oil on spatial memory. METHODS: Memory impairment induced by Intracerebroventricular (ICV) injection of scopolamine hydrochloride (10 μg/ rat). Animals were gavaged for 4 weeks with saline, sesame oil (0.5, 1, or 2 mL/kg/day), or 3 weeks with memantine (30 mg/kg/day) in advance to induction of amnesia. Morris water maze (MWM) test was conducted 6 days after microinjection of scopolamine. Then, blood and brain samples were collected and evaluated for the malondialdehyde (MDA) levels, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities, and total antioxidant status (TAS) and ferric reducing ability of plasma (FRAP). RESULTS: Scopolamine significantly decreased traveled distance and time spent in target quadrant in probe test. Pretreatment of rats with sesame oil (0.5 mg/kg) mitigated scopolamine-induced behavioral alterations. Measurement of MDA, SOD, and GPX in brain tissue, and FRAP and TAS in blood showed little changes in animals which had received scopolamine or sesame oil. CONCLUSIONS: Intracerebroventricular injection of scopolamine has a residual effect on memory after six days. Sesame oil has an improving effect on spatial memory; however this effect is possibly mediated by mechanisms other than antioxidant effect of sesame oil.
Subject(s)
Animals , Male , Rats , Scopolamine/adverse effects , Sesame Oil/administration & dosage , Amnesia/drug therapy , Adjuvants, Anesthesia/adverse effects , Antioxidants/administration & dosage , Superoxide Dismutase/chemistry , Ferric Compounds/chemistry , Rats, Wistar , Oxidative Stress/drug effects , Maze Learning , Disease Models, Animal , Alzheimer Disease/prevention & control , Glutathione Peroxidase/chemistry , Amnesia/chemically induced , Injections, Intraventricular , Memory/drug effects , Antioxidants/chemistryABSTRACT
Chronic administration of aged garlic extract has been shown to prevent memory impairment in mice. Acute and chronic (21 days) effects of marketed formulation of crude garlic extract (Lasuna) were evaluated on learning and memory in mice using step down latency (SDL) by passive avoidance response and transfer latency (TL) using elevated plus maze. Scopolamine (0.4 mg/kg, ip) was used to induce amnesia in mice and piracetam (200 mg/kg, ip) served as positive control. In the acute study, Lasuna (65 mg/kg, po) partially reversed the scopolamine-induced amnesia but failed to improve learning and memory in untreated animals. Chronic administration of Lasuna (40 mg/kg/day for 21 days) significantly improved learning both in control and scopolamine induced amnesic animals. Influence of Lasuna on central cholinergic activity and its antioxidant properties were also studied by estimating the cortical acetylcholinesterase (AchE) activity and reduced glutathione (GSH) levels respectively. Chronic administration of Lasuna inhibited AchE, while increasing GSH levels. Thus the results indicate that long-term administration of crude garlic extract may improve learning and memory in mice while the underlying mechanism of action may be attributed to the anti-AchE activity and anti-oxidant property of garlic.
Subject(s)
Acetylcholinesterase/metabolism , Amnesia/chemically induced , Amnesia/drug therapy , Amnesia/metabolism , Amnesia/pathology , Animals , Antioxidants/administration & dosage , Antioxidants/chemistry , Avoidance Learning/drug effects , Brain/drug effects , Brain/metabolism , Garlic/chemistry , Glutathione/metabolism , Humans , Learning/drug effects , Maze Learning/drug effects , Memory/drug effects , Mice , Oxidative Stress , Plant Extracts/administration & dosage , Plant Extracts/chemistry , Scopolamine/toxicityABSTRACT
The neuroprotective potential of ethanolic extract of roots of Pseudarthria viscida (L) Wight and Arn (EEPV) was investigated against -amyloid(25-35)-induced amnesia in mice which is a suitable animal model for Alzheimer’s disease (AD). The senile plaques of -amyloid (A) are major constituents accumulated during the progression of AD as a potent neurotoxicant. In our investigation, intracerebroventricular injection of A(25-35) in mice induced the neurodegeneration, exhibited the increased time of escape latency in behavioral pattern using water maze and decreased the levels of antioxidants namley superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and vitamin C with elevated level of acetylcholinesterase enzyme (AChE). The neuroprotective potential of EEPV was determined by behavioral pattern using water maze and biochemical parameters such as SOD, CAT and GPx and vitamin C content as well as AChE. Mice were treated with EEPV at 200 and 400 mg/kg doses for 21 days. Except control, all animals received a single injection of neurotoxicant A(25-35) on 14th day. In behavioural assessment, treatment with ethanolic extract improved the cognitive function in the water maze and attenuated the elevated levels of AChE with increase in antioxidant enzymes, indicating the neuroprotection with increased levels of vitamin C. These findings suggest that ethanolic extract of P. viscida exerts anti-amnesiac effects and enhances cognitive function.
Subject(s)
Acetylcholinesterase/drug effects , Acetylcholinesterase/metabolism , Alzheimer Disease/chemically induced , Alzheimer Disease/drug therapy , Alzheimer Disease/enzymology , Alzheimer Disease/pathology , Amnesia/chemically induced , Amnesia/drug therapy , Amnesia/enzymology , Amnesia/pathology , Amyloid beta-Peptides , Animals , Antioxidants/administration & dosage , Behavior, Animal/drug effects , Catalase/drug effects , Catalase/metabolism , Disease Models, Animal , Glutathione Peroxidase/drug effects , Glutathione Peroxidase/metabolism , Lipid Peroxidation/drug effects , Male , Maze Learning/drug effects , Mice , Neuroprotective Agents/administration & dosage , Plant Extracts/administration & dosage , Superoxide Dismutase/drug effects , Superoxide Dismutase/metabolismABSTRACT
Effect of pre-electroconvulsive shock (ECS) administration of calcium channel blockers (CCBs) like verapamil, diltiazem, nifedipine, nimodipine, flunarizine and cinnarizine on retrograde amnesia induced by ECS was examined using passive avoidance paradigm in rats. The groups (Gr 1-7) of adult, male Wistar rats received true ECS with CCBs (5mg/kg; i.p) or vehicle (10 ml/kg; ip) and other groups (Gr 8-14) received sham ECS with CCBs (5mg/kg; i.p) or vehicle (10 ml/kg; i.p). The anti-amnestic activity of CCBs were evaluated using the passive avoidance paradigm in rats. Results showed that, the baseline latencies for all the groups did not differ significantly. Rats receiving true ECS produced significantly lower latencies. There was increase in the post ECS step through latencies of the rats administered CCBs before ECS. Therefore, pre-ECS administration of calcium channel blockers might reduce retrograde amnesia produced by ECS without altering seizure duration.