Odor-context effects in free recall after a short retention interval: a new methodology for controlling adaptation.

The present study investigated context effects of incidental odors in free recall after a short retention interval (5 min). With a short retention interval, the results are not confounded by extraneous odors or encounters with the experimental odor and possible rehearsal during a long retention interval. A short study time condition (4 s per item), predicted not to be affected by adaptation to the odor, and a long study time condition (8 s per item) were used. Additionally, we introduced a new method for recovery from adaptation, where a dissimilar odor was briefly presented at the beginning of the retention interval, and we demonstrated the effectiveness of this technique. An incidental learning paradigm was used to prevent overshadowing from confounding the results. In three experiments, undergraduates (N = 200) incidentally studied words presented one-by-one and received a free recall test. Two pairs of odors and a third odor having different semantic-differential characteristics were selected from 14 familiar odors. One of the odors was presented during encoding, and during the test, the same odor (same-context condition) or the other odor within the pair (different-context condition) was presented. Without using a recovery-from-adaptation method, a significant odor-context effect appeared in the 4-s/item condition, but not in the 8-s/item condition. Using the recovery-from-adaptation method, context effects were found for both the 8- and the 4-s/item conditions. The size of the recovered odor-context effect did not change with study time. There were no serial position effects. Implications of the present findings are discussed.

Akt plays a central role in the anti-apoptotic effect of estrogen in endothelial cells.

Estrogen has been reported to inhibit apoptosis in vascular endothelial cells. However, its precise mechanism still remains to be elucidated. Here we determined the role of Akt in the anti-apoptotic effect of estrogen. 17Beta-estradiol prevented the apoptosis induced by TNF-alpha in bovine aortic endothelial cells, as evaluated by double staining with fluorescein isothiocyanate-conjugated annexin V and propidium iodide. Introducing a dominant negative mutant of Akt by using a cell-penetrating peptide of Tat protein inhibited the anti-apoptotic effect of estrogen in a concentration-dependent manner, and resulted in the complete inhibition of the anti-apoptotic effect of 17beta-estradiol at 1nM and higher concentrations. The dominant negative mutant without the cell-penetrating peptide and Tat peptide-conjugated protein A had no effect. The intracellular protein transduction was confirmed by immunoblot analysis. Our observations thus provide first direct evidence that Akt plays a central role in the anti-apoptotic effect of estrogen in vascular endothelial cells.

Endothelium-dependent and independent enhancement of vascular contractility in the ovariectomized rabbit.

OBJECTIVE: Estrogen suppresses contractile response and increases vasodilator response, partly by modulating endothelial function. However, the effect of estrogen on the contractility of vascular smooth muscle remains to be elucidated. We investigated the effect of a long-term estrogen deficiency on vascular contractility and the Ca(2+) sensitivity of the contractile apparatus in arterial smooth muscle. METHODS: Female rabbits were divided into the following three groups: control group, an ovariectomized group (OVX), and a group supplemented with 17beta-estradiol after ovariectomy (OVX+E2). Twelve weeks later, the mesenteric artery was isolated, and the vascular contractility was evaluated. RESULTS: In OVX, the contractile responses to phenylephrine and 118 mM potassium were enhanced, and the basal release of nitric oxide decreased in the strips with endothelium compared with either OVX+E2 or control. An enhancement of contraction was also observed in the strips without endothelium. However, the extent of enhancement was smaller than that observed in the presence of endothelium. The simultaneous measurement of calcium ([Ca(2+)](i)) and tension revealed no significant difference in the [Ca(2+)](i) elevations induced by phenylephrine among the three groups. In the alpha-toxin permeabilized strips, the Ca(2+)-tension relationships obtained both with and without phenylephrine and guanosine triphosphate were similar among the three groups. No difference in the myosin expression and the histology of vascular tissue was observed among the three groups. CONCLUSION: Long-term estrogen deficiency increased the vascular tone mainly by enhancing smooth muscle contractility. Endothelial dysfunction is considered to play a minor role in the augmentation of vascular tone.