Browsing by Subject "Entorhinal cortex"

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    Ageing of the human entorhinal cortex and subicular complex
    (Murcia : F. Hernández, 1992) Trillo, L.; Gonzalo, L. M.
    Age-dependent changes in the entorhinal cortex (EC) and subicular complex (SC) were studied in 30 brains of patients who died between 14 and 86 years of age, without CNS impairment, as determined by macro- and microscopic examination. The brains were fixed in 10% formalin and embedded in paraffin. Three series of corona1 EC and SC sections (7 pm) were stained by Nissl, PAS or hematoxylin-eosin. Using neuronal count and Kariometry, age-dependent modifications were studied in layers 11, 111 and V of the lateral area of the EC; in the pyramidal layer of the subiculum (S), and in layer 11 of the presubiculum (PS). Al1 EC layers studied presented a slight (11-20%) although significant reduction up to 35 years, but from 35 to 75 years the decrease was not significant. After 75 years the neuronal loss increased slightly. The nuclear area decreased up to the age of 40-45 years, (10-18%) and augmented from this age up to 75 years (10-14%). During the last period of life, the nuclear area did not change. From 30-60 years, pyramidal layer in the S showed a significant neuronal loss (30%), thereafter, neuronal reduction was less. At early years, the nuclear area decreased insignificantly (15%), and from 35 years up to the most advanced age studied, it increased significantly (13%). In the PS, layer 11 manifested a cell loss throughout the lifespan (32.9%) and the changes in the nuclear area did not reach statistical significance due to the dispersions of its values. These results lead to the conclusion that the neuronal loss in EC is notably less than in S and PS and, in general, than in other centres. The sequence of neuronal loss is also different in the EC and in the S. While in EC the maximal loss occurs up to 35 years of age, in S the most pronounced loss begins precisely after this age.
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    Radial derivatives of the mouse ventral pallium traced with Dbx1-LacZ reporters
    (Elsevier, 2015-12-31) Puelles, Luis; Medina, Loreta; Borello, Ugo; Teissier, Anne; Pierani, Alessandra; Rubenstein, John L.R.; Legaz Pérez, Isabel; Ciencias Sociosanitarias
    The progeny of Dbx1-expressing progenitors was studied in the developing mouse pallium, using two transgenic mouse lines: (1) Dbx1nlslacZ mice, in which the gene of the β-galactosidase reporter (LacZ) is inserted directly under the control of the Dbx1 promoter, allowing short-term lineage tracing of Dbx1-derived cells; and (2) Dbx1CRE mice crossed with a Cre-dependent reporter strain (ROSA26loxP-stop-loxP-LacZ), in which the Dbx1-derived cells result permanently labeled (Bielle et al., 2005). We thus examined in detail the derivatives of the postulated longitudinal ventral pallium (VPall) sector, which has been defined among other features by its selective ventricular zone expression of Dbx1 (the recent ascription by Puelles, 2014 of the whole olfactory cortex primordium to the VPall was tested). Earlier notions about a gradiental caudorostral reduction of Dbx1 signal were corroborated, so that virtually no signal was found at the olfactory bulb and the anterior olfactory area. The piriform cortex was increasingly labeled caudalwards. The only endopiriform grisea labeled were the ventral endopiriform nucleus and the bed nucleus of the external capsule. Anterior and basolateral parts of the whole pallial amygdala also were densely marked, in contrast to the negative posterior parts of these pallial amygdalar nuclei (leaving apart medial amygdalar parts ascribed to subpallial or extratelencephalic sources of Dbx1-derived GABAergic and non-GABAergic neurons). Alternative tentative interpretations are discussed to explain the partial labeling obtained of both olfactory and amygdaloid structures. This includes the hypothesis of an as yet undefined part of the pallium, potentially responsible for the posterior amygdala, or the hypothesis that the VPall may not be wholly characterized by Dbx1 expression (this gene not being necessary for VPall molecular distinctness and histogenetic potency), which would leave a dorsal Dbx1-negative VPall subdomain of variable size that might contribute partially to olfactory and posterior amygdalar structures.