Latexin-immunoreactive neurons were distributed in the lower layers of the neocortex and WH-4-023 cell line adjacent ventral mesocortex, as well as in the claustrum/endopiriform formation. There were marked regional and laminar differences in density and distribution of latexin-immunoreactive neurons in the cerebral cortex. The density followed a roughly lateral-to-medial decreasing gradient: it was high in lateral cortical regions, which included the insular, second somatosensory, and anterior sylvian areas, and in the temporal auditory field; moderate in laterodorsal cortical regions, which

included the primary and second auditory fields; and low in dorsal cortical regions, which included visual areas 18 and 19. Latexin-immunoreactive neurons

were absent in medial cortical regions, which included the motor, premotor, prefrontal, prelimbic, cingulate, and retrosplenial areas. The lateral-to-medial gradient was apparent even within a single cytoarchitectonic area in certain cortical regions. The allocortex was devoid of latexin-immunoreactive neurons, with the exception of the anteroventral part of the dentate gyrus. The majority of cortical latexin-immunoreactive neurons were localized in layers V and VI and appeared to correspond to the “”modified pyramidal cells in the infragranular layers.”" The remaining latexin-immunoreactive neurons were localized in layer IV, as well as in lower layer III and in the white matter. There were no latexin-immunoreactive neurons from layer I through upper layer Ill. Latexin-immunoreactive Lonafarnib neurons were present in telencephalic structures outside the cerebral cortex, with particularly high density in the claustrum/endopiriform formation. All these features, with the exception of that detected

in the archicortex, are compatible with the features observed previously in the rat telencephalon. The similar pattern of distribution of latexin-immunoreactive check details neurons in several mammalian species from different orders suggests that latexin plays an important role in a specific cortical network. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The GluA1 AMPA receptor subunit is a key mediator of hippocampal synaptic plasticity and is especially important for a rapidly-induced, short-lasting form of potentiation. GluA1 gene deletion impairs hippocampus-dependent, spatial working memory, but spares hippocampus-dependent spatial reference memory. These findings may reflect the necessity of GluA1-dependent synaptic plasticity for short-term memory of recently visited places, but not for the ability to form long-term associations between a particular spatial location and an outcome. This hypothesis is in concordance with the theory that short-term and long-term memory depend on dissociable psychological processes.