Electrophysiological and behavioral evidence for attentional up-regulation, but not down-regulation, when encoding pictures into long-term memory.

Visual long-term memory allows us to store a virtually infinite amount of visual information (Brady, Konkle, Alvarez, & Oliva in Proceedings of the National Academy of Sciences of the United States of America, 105(38), 14325-14329, 2008; Standing in Quarterly Journal of Experimental Psychology, 25(2), 207-222, 1973). However, our ability to encode new visual information fluctuates from moment to moment. In Experiment 1, we tested the hypothesis that we have voluntary control over these periodic fluctuations in our ability to encode representations into visual long-term memory using a precueing paradigm combined with behavioral and electrophysiological indices of memory encoding. We found that visual memory encoding can be up-regulated, but it was much more difficult, if not impossible, to down-regulate encoding on a trial-by-trial basis. In Experiment 2, we tested the hypothesis that voluntary up-regulation of visual memory encoding for an item incurs a cost to memory encoding of other items by manipulating the cueing probability. Here, we found that, although the cueing benefit was constant for both low (20%) and high (50%) cueing probabilities, the benefit in the high cueing probability condition came with the overall impairment of memory encoding. Taken together, our findings demonstrate that top-down control of visual long-term memory encoding may be primarily to prioritize certain memories, but this prioritization has a cost and should not be overused to avoid its negative consequences.

Luteinizing hormone acts at the hippocampus to dampen spatial memory.

Luteinizing hormone (LH) rises dramatically during and after menopause, and has been correlated with an increased incidence of Alzheimer's disease and decreased memory performance in humans and animal models. To test whether LH acts directly on the dorsal hippocampus to affect memory, ovariectomized female rats were infused with either the LH-homologue human chorionic gonadotropin (hCG) or the LH receptor antagonist deglycosylated-hCG (dg-hCG). Infusion of hCG into either the lateral ventricle or the dorsal hippocampus caused significant memory impairments in ovariectomized estradiol-treated females. Consistent with this, infusion of the LH antagonist dg-hCG into the dorsal hippocampus caused an amelioration of memory deficits in ovariectomized females. Furthermore, the gonadotropin-releasing hormone antagonist Antide, failed to act in the hippocampus to affect memory. These findings demonstrate a significant role for LH action in the dorsal hippocampus in spatial memory dysfunction.