Thus, these findings represent the first demonstration of impaired context-dependent memory following stress.”
“The chemical alpha-asarone is an important active substance of the Acori graminei rhizome (AGR). It has pharmacological

effects that include antihyperlipidemic, antiinflammatory, and antioxidant activity. Our aim was to study the effects alpha-asarone on nitric oxide (NO) levels in the hippocampus and temporal cortex of click here the rat after injection of the fraction 25-35 from amyloid-beta (A beta((25-35))). In addition we examined the working spatial memory in an eight-arm radial maze. Our results showed a significant increase of nitrites in the hippocampus and temporal cortex of A beta((25-35))-treated rats. Other evidence of neuronal damage was the expression of a glial-fibrillar-acid protein

and a silver staining. There were impairments in the spatial memory evaluated in the eight-arm radial maze. We wanted to determine whether alpha-asarone improves the memory correlated with NO overproduction and neuronal damage caused by the injection of A beta((25-35)) into rats. Then animals received a 16-day treatment of alpha-asarone before the A beta((25-35)) injection. Our results show a significant decrease of nitrite levels in the hippocampus and temporal cortex, without astrocytosis and silver-staining cells, which correlates with memory improvement in the alpha-asarone-treated group. Our results suggest that alpha-asarone may protect neurons against A 3-MA chemical structure beta((25-35))-caused Adenosine triphosphate neurotoxicity by inhibiting the effects of NO overproduction in the hippocampus and temporal cortex. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Both odor-preference and odor-aversion learning occur in perinatal pups before the maturation

of brain structures that support this learning in adults. To characterize the development of odor learning, we compared three learning paradigms: (1) odor-LiCl (0.3M; 1% body weight, ip) and (2) odor-1.2-mA shock (hindlimb, 1sec)-both of which consistently produce odor-aversion learning throughout life and (3) odor-0.5-mA shock, which produces an odor preference in early life but an odor avoidance as pups mature. Pups were trained at postnatal day (PN) 7-8, 12-13, or 23-24, using odor-LiCl and two odor-shock conditioning paradigms of odor-0.5-mA shock and odor-1.2-mA shock. Here we show that in the youngest pups (PN7-8), odor-preference learning was associated with activity in the anterior piriform (olfactory) cortex, while odor-aversion learning was associated with activity in the posterior piriform cortex. At PN12-13, when all conditioning paradigms produced an odor aversion, the odor-0.5-mA shock, odor-1.2-mA shock, and odor-LiCl all continued producing learning-associated changes in the posterior piriform cortex. However, only odor-0.5-mA shock induced learning-associated changes within the basolateral amygdala.