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Amelioration of learning and memory deficits by willughbeia cochinchinensis in mice

Objectives: To study effects of willughbela cochinchinensis (WC) on learning and memory deficits in experimental animals. Subjects and methods: 50 Swiss mice were randomly separated into 5 experimental groups, 10 mice for each group. | Journal of military pharmaco-medicine No7-2017 AMELIORATION OF LEARNING AND MEMORY DEFICITS BY WILLUGHBEIA COCHINCHINENSIS IN MICE Nguyen Thi Hoa*; Le Van Quan*; Can Van Mao* SUMMARY Objectives: To study effects of willughbela cochinchinensis (WC) on learning and memory deficits in experimental animals. Subjects and methods: 50 Swiss mice were randomly separated into 5 experimental groups, 10 mice for each group. Group 1: mice were intraperitoneally (i.p) injected and orally (p.o) administered saline at dose 0.1 mL/10 g; group 2: mice were injected i.p 1.5 mg/kg scopolamin and p.o 0.1 mL/10 g saline; group 3, group 4 and group 5: mice were injected i.p 1.5 mg/kg scopolamin and p.o 100 mg/kg, 150 mg/kg and 200 mg/kg WC, respectively. 60 minutes after drug injections, animals performed a passive avoidance test which includes two phases: training phase: animals were placed in the light compartment and if they moved to the dark compartment, they were given electrical foot shocks for 3 seconds; test phase: animals were also placed in the light compartment but they were not given any electrical foot shocks at the dark compartment. Results: In test phase, mean latency to entry dark compartment in group 2 was shorter than that in group 1 and the latencies in group 4 and 5 were longer than that in group 2. Conclusion: Our results provided an evidence for effective treatment of WC in memory deficits animal model. * Keyword: Willughbela cochinchinensis; Learning and memory deficits; Mice. INTRODUCTION Alzheimer’s disease (AD) accounts for 60 - 80% of cases of dementia in older people [1]. Mechanism of AD has been suggested to be involved in neurodegeneration and formations of plaques and neurofibrillary tangles in brains which cause atrophied cortex and enlarged ventricles [2]. Following these damages in brains, patients with AD develop deficits in memory, recognition and behavioral controlling [3]. If they don’t receive any treatments, these disorders will be worse and .