Entorhinal Cortex Layer III input to the hippocampus is crucial for temporal association Memory.
Science
Science. 2011 Dec 9; 334(6061): 1415-20
Suh J, Rivest AJ, Nakashiba T, Tominaga T, Tonegawa S.
Abstract:
Associating temporally discontinuous elements is crucial for the formation of episodic and working memories that depend on the hippocampal-entorhinal network. However, the neural circuits subserving these associations have remained unknown. The layer III inputs of the entorhinal cortex to the hippocampus may contribute to this process. To test this hypothesis, we generated a transgenic mouse in which these inputs are specifically inhibited. The mutant mice displayed significant impairments in spatial working-memory tasks and in the encoding phase of trace fear-conditioning. These results indicate a critical role of the entorhinal cortex layer III inputs to the hippocampus in temporal association memory.
News Links About this Article:
Australian Broadcasting Corporation "Brain Circuit Helps Order Memories"
Characterization of Beta Amyloid Assemblies in Drusen: The Deposits Associated with Aging and Age-Related Macular Degeneration.
Exp Eye Research
Exp Eye Res. 2004 Feb;78(2): 243-56
Anderson DH, Talaga KC, Rivest AJ, Barron E, Hageman GS, Johnson LV.
Purpose: Recent studies strongly suggest that drusen, the extracellular deposits associated with age-related macular degeneration (AMD), are a manifestation of local inflammatory events. New evidence indicates that substructural elements within drusen contain activated complement components as well as amyloid beta (Abeta), a major pro-inflammatory compoents of Alzheimer's disease plaques. We characterized the ultrastructural organization and histochemical staining properties of these Abeta-containing elements in order to further assess their significance in drusen formation and AMD pathogenesis.
The Alzheimer's A Beta-Peptide is deposited at sites of complement activation in pathologic deposits associated with aging and age-related macular degeneration.
PNAS
Proc Natl Acad Sci USA. 2002 Sep 3;99(18): 11830-5
Johnson LV, Leitner WP, Rivest AJ, Staples MK, Radeke MJ, Anderson DH .
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss in older individuals worldwide. The disease is characterized by abnormal extracellular deposits, known as drusen, that accumulate along the basal surface of the retinal pigmented epithelium. Although drusen deposition is commin in older individuals, large numbers of drusen and/or extensive areas of confluent drusen represent a significant risk factor for AMD. Widespread srusen deposition is associated with retinal pigmented epithelial cell dysfunction and degeneration of the photoreceptors cells of the neural retina. Recent studies have shown that drusen contain a variety of immunomodulatory molecules, suggesting that teh process of drusen formation involves local inflammatory events, including activation of the complement cascade. Similar observations in Alzheimer's disease (AD) have lead to the hypothesis that chronic localized inflammation is an important element of AD pathogenesis, with significant neurodegenerative consequences. Accordingly, the amyloid beta (A beta) peptide, a major constituent of the neuritic plaques in AD, has been inplicated as a primary activator of the complelent in AD. Here we show that A beta is associated with a substructural vesicular component within drusen. A beta cololcalizes with activated complement components in these "amyloid vesicles," thereby identifying them as potential primary sites of complement activation. Thus, A beta deposition could be an important component of the local inflammatory events that contribute to atrophy of the retinal pigmented epithelium, drusen biogenesis, and the pathogenesis of AMD.