Background: The cognitive and motor effects of sub-anesthetic doses of ketamine remain controversial. The aim of this study was to investigate the effects of ketamine administration under anesthesia on cognitive function and motor responses in Wistar rats. Methods: Twenty-five Wistar rats were randomized into five groups of five rats each (n=5): group 1 (normal control), group 2 (1mg/kg ketamine), group 3 (2mg/kg ketamine), group 4 (3mg/kg ketamine) and group 5 (0.5ml/100g celecoxib). Treatment for each group lasted 3 weeks. Rats from each group were subjected to a total of nine (9) trials of cognitive-motor tests, including; the Barnes maze test (memory based on visual scenes), hand grip test (motor response to foreleg strength), rotarod test (coordination ability). The neurobehavioral ability displayed by the animals was recorded and analyzed using analysis of variance (ANOVA). Results: Observations from the cognitive function study showed a significant improvement (p<0.05) from week 1 to week 3. The quality of motor task performance also improved from week 1 to week 3 compared to control and celecoxib-treated groups. Conclusions: Sub-anesthetic doses of ketamine improved cognitive function and motor responses in Wistar rats.

Cyclophosphamide (CP) has appreciably improved survival rate in cancer patients, but the occurrence of hepatotoxicity may undermine its use. This study assessed the potential of dexamethasone (DEXA) to prevent CP-induced hepatotoxicity in albino rats. Thirty-six adult male albino rats were randomised in to six groups of n = 6. Group I (Control) was treated with a dose of normal saline (0.3mL) intraperitoneally (i.p.) for 24 hr. Group II was treated with a dose of DEXA (1mg/kg) ip for 24 hr. Group III was treated with a dose of CP (150mg/kg) i.p for 24 hr. Group IV was treated i.p with a dose of CP (150 mg/kg) for 24hr before treatment with a dose of DEXA (1mg/kg) for 24 hr. Group V was co-treated with a dose of DEXA (1mg/kg) and a dose of CP (150mg/kg) i.p for 24hr. Group VI was pre-treated with a dose of DEXA (1mg/kg/ day) for 24 hr before treatment with a dose of CP (150mg/kg) ip for 24 hr. The rats were anesthetized after treatment; liver samples were excised and evaluated for histology and biochemical markers. Sera were obtained from blood samples and assessed for liver function markers. Liver glutathione, catalase, superoxide dismutase and glutathione peroxidase levels were decreased significantly (p < 0.001) whereas malondialdehyde levels were increased significantly (p < 0.001) in CP-treated rats when compared to control. Significant (p < 0.001) elevations in serum and liver aminotransferases, alkaline phosphatase, gamma-glutamyl transferase, conjugated bilirubin, lactate dehydrogenase and total bilirubin levels occurred in CP-treated rats when compared to control. The liver of CP-treated rats showed hepatocyte necrosis. Interestingly, the aforementioned alterations were significantly reversed in rats post-treated (p < 0.05), co-treated (p < 0.01) and pre-treated (p < 0.001) with DEXA when compared to CP. DEXA may be re-purposed as treatment for CP associated hepatotoxicity.