Aluminum and ethanol induce alterations in superoxide and peroxide handling capacity (SPHC) in frontal and temporal cortex.

Aluminum is an omnipresent neurotoxicant and has been associated with several neuropathological disorders. Cerebrum and cerebellum have been shown to face augmented oxidative stress when animals are exposed to aluminum and high doses of ethanol. To establish the link between oxidative stress and neurobehavioral alterations, the present study was conducted to determine the extent of oxidative stress in low levels of pro-oxidant (ethanol exposure) status of the functionally discrete regions of the cerebrum. Male Wistar rats were exposed to aluminum (10 mg/kg body wt) and ethanol (0.2-0.6 g/kg body wt) for 4 weeks. Spontaneous motor activity (SMA) and Rota-Rod performances (RRP) were recorded weekly during the period of exposure. At the end of 4th week, oxidative stress parameters were determined from the homogenized cerebral tissue. GSH-independent superoxide peroxide handling capacity (GI-SPHC) and GSH-dependent superoxide peroxide handling capacity (GD-SPHC) were determined for FC and TC upon exposure to ethanol in the absence and presence of aluminum exposure. Aluminum was found to augment the oxidative stress at higher doses (0.6 g Ethanol/kg body wt) of ethanol, particularly in FC. The SPHC of FC was also found to be compromised significantly in aluminum-ethanol co-exposed animals. It was concluded that even though the manifestation of oxidative stress was not observed as revealed by assaying the widely used oxidative stress biochemical markers (indices), aluminum and ethanol (low doses) exposure induced alterations in the handling capacity of oxidant imbalance that could be recognized by studying the SPHC of FC. Comparison of GD-SPHC and GI-SPHC offered a possible mechanism of compromised SPHC in FC. This observation is likely to offer insights into the mechanism of association between aluminium exposure and behavioral changes in neurodegenerative disorders towards therapeutic strategies for these disorders.

Potential of Pandanus odoratissimus as a CNS depressant in Swiss albino mice / Potencial de Pandanus odoratissimus como um depressor do sistema nervoso central em camundongos Swiss albinos

In this study, several neuropharmacological effects of methanolic leaf extract of Pandanus odoratissimus (PO) (family; Pandanaceae) were studied in albino mice using various experimental models. The effect of PO on the CNS was studied by using different neuropharmacological paradigms including spontaneous motor activity, rota-rod performance and potentiation of Pentobarbital sodium sleeping time in albino mice. Preliminary phytochemical evaluation and acute toxicity studies were also carried out where LD50 >2000 mg/kg was considered non-toxic through acute exposure in rats by the oral route. The methanolic leaf extract (50,100 and 200 mg/kg i. p.) produced a reduction in spontaneous motor activity, motor coordination and prolonged Pentobarbital sodium sleeping time. Preliminary qualitative chemical studies indicated the presence of steroids, saponins, terpinoids, glycosides, tannins, flavonoids and phenolics in the extract. These observations suggest that the leaf of Pandanus odoratissimus contains some active principles which possess potential CNS-depressant action.

Estudaram-se alguns efeitos neurofarmacológicos do extrato metanólico de Pandanus odoratissimus (PO) (família Pandanaceae) em camundongos albinos, usando vários modelos experimentais. O efeito do PO no SNC foi estudado por meio de diferentes paradigmas neurofarmacológicos, como atividade motora espontânea, desempenho na haste rotatória e a potenciação do tempo de sono em camundongos albinos pelo pentobarbital sódico. A avaliação fitoquímica preliminar e os estudos de toxicidade aguda foram realizados e a DL50 >2000 mg/kg é considerada não tóxica, por meio da exposição aguda, por via oral, em ratos. O extrato metanólico de folha (50,100 e 200 mg/kg i. p.) produziu redução da atividade motora espontânea, da coordenação motora e tempo prolongado de sono pelo pentobarbital sódico. Estudos químicos qualitativos preliminares indicaram a presença de esteróide, saponinas, terpenóides, glicosídios, taninos, flavonóides e fenólicos no extrato. As observações sugerem que a folha de Pandanus odoratissimus contém alguns princípios ativos com atividade potencial como depressores do SNC.

Evaluation of antianxiety and sedative effects of essential oil of Ducrosia anethifolia in mice

INTRODUCTION: We investigated the antianxiety and sedative effects of the essential oil of Ducrosia anethifolia. Boiss. (Apiaceae). METHODS: We used elevated plus maze, spontaneous motor activity and ketamine-induced sleep tests in mice. In addition, the essential oil was analyzed by GC/MS. Twenty compounds were identified, and n-decanal (70.1 percent) and alpha-pinene (12.4 percent) constituted the major components. RESULTS: In elevated plus maze, Ducrosia anethifolia essential oil at doses of 25-200 mg/kg increased the percentage of open arm time and entries. Unlike diazepam, ducrosia anethifolia essential oil could not suppress spontaneous motor activity and did not alter ketamine-induced sleep parameters. These results are indicative of antianxiety effect of Ducrosia anethifolia essential oil without sedative effect.

The Effect of Fluoxetine on Behaviors in Transient Forebrain Ischemic Gerbil / 대한정신약물학회지

OBJECTIVE: This study aims to explore the effect of fluoxetine on memory, locomotor and depressive behavior in transient forebrain ischemic model of gerbil. METHODS: Doses of fluoxetine (10, 40 mg/kg) or vehicle were intraperitoneally administered once 30 min before ischemic surgery in gerbil. Novel object recognition test, spontaneous motor activity, learned helplessness test were performed 4 days, 8 days, or 9 days, respectively, after sham or ischemic surgery. RESULTS: Fluoxetine treatment (40 mg/kg) significantly reduced recognition memory in sham operated gerbil. However, fluoxetine (10, 40 mg/kg) did not affect ischemia-induced impairment in recognition memory. The treatment of fluoxetine (10, 40 mg/kg) significantly inhibited locomotor hyperactivity induced by transient ischemia even though fluoxetine (40 mg/kg) did not affect spontaneous motor activity in the sham operated gerbils. Fluoxetine did not affect depressive behavior in sham and ischemic gerbils. CONCLUSION: The treatment of fluoxetine inhibited ischemia-induced hyperactivity, but did not affect memory and depressive behavior in transient forebrain ischemic gerbils.