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Background: Terpenoids possess antidepressant, memory enhancer, neuroprotective and other Central Nervous System (CNS) actions. Eucalyptus tereticornis is a rich source of terpenoids. Aim and Objectives: The aim of the present study is to evaluate anti-depressant and anti-cataleptic effect of Eucalyptus tereticornis. Molecular docking studies were also employed to study the mechanism of action. Material and Methods: Locomotor activity and muscle coordination was studied by using actophotometer and rotarod apparatus in rats. The evaluation of anti-depressant activity was studied by forced swimming and tail suspension test in mice. Haloperidol induced catalepsy model was used to evaluate anti-cataleptic effect. Different phytoconstituents present in Eucalyptus tereticornis like citronellal, geranyl acetate and terpine-4-ol were screened through computational assessment with the Lipinski's rule of 5, ADMET properties and molecular docking studies. Computational docking analysis was performed by AutoDock Vina 4.2.6 version. Results: Eucalyptus tereticornis significantly increases the locomotor activity and improves motor coordination. At 100 mg/kg hydroalcoholic extract of Eucalyptus tereticornis significantly shows anti-depressant and anti-cataleptic activity. Phytoconstituents like citronellal, geranyl acetate and terpinen-4-ol exhibit nonselective Monoamine Oxidase (MAO) inhibition activity. Conclusion: Hydroalcoholic extract of Eucalyptus tereticornis may possess anti-depressant and anti-cataleptic activity with efficient CNS stimulant action which may be attributed to non-selective MAOinhibition activity of its phytoconstituents like geranyl acetate, citronellal and terpinen-4-ol.

Alzheimer's disease (AD) is a common neurodegenerative disorder. Aluminium chloride induces AD like pathology in rats. Renin angiotensin system plays a significant role in the pathogenesis and occurrence of Alzheimer's disease. In the present study we evaluated and compared the effect of Captopril and Perindopril against aluminium chloride induced amyloidogenesis and cognitive dysfunction in rats. Wistar rats of both sex were divided randomly into four groups i.e. Group I was served as normal control and treated with normal saline, Group II was administered with AlCl3 (100 mg/kg, p. o.) and Group III and IV received Captopril (30 mg/kg, p. o.) and Perindopril (5 mg/kg, p. o.) respectively 1hr prior to administration of AlCl3. All the doses were given once daily for 42 days. The evaluation of memory function was carried out in Y-maze (spontaneous alternation), radial arm maze (number of correct responses) and elevated plus maze (transfer latency). After behavioral studies, estimation of antioxidant status (brain and serum), amyloid-β content (brain) and histopathology of brain hippocampus region was done. Administration of AlCl3 for 42 days impaired cognitive dysfunction. Captopril and Perindopril prevented AlCl3 induced cognitive dysfunction by improving spontaneous alternation behavior, number of correct responses and reducing transfer latency. They also increase the antioxidant status, reduce the Aβ42 content in the brain and reverse the histopathological changes caused by AlCl3 in hippocampal region. Both Captopril and Perindopril protects against aluminium chloride induced amyloidogenesis and AD like pathology. Captopril is found to be more effective than Perindopril.