PubMed · 3311070
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J Mancilla-Ramírez, R S Rodríguez-Suárez, J I Santos-Preciado. 1987. [Neonatal necrotizing enterocolitis].. https://pubmed.ncbi.nlm.nih.gov/3311070/
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The distribution of neurons expressing immunoreactivity for the protein Bcl-2 was studied in the brain of squirrel monkeys (Saimiri sciureus) of various ages. Several subsets of small and intensely immunoreactive neurons displaying an immature appearance were disclosed in the amygdala and piriform cortex. The piriform cortex exhibited clusters of various forms in which Bcl-2+ neurons appeared linked to one another by their own neurites. The subventricular zone, which is known to harbor the largest population of rapidly and constitutively proliferating cells in the adult rat brain, was intensely stained, particularly at the basis of the lateral ventricle. A long and dorsoventrally oriented Bcl-2+ fiber fascicle was seen to emerge from the subventricular zone, together with numerous Bcl-2+ cells that formed a densely packed column directed at the olfactory tubercle. In adult and aged monkeys, the small and intensely labeled neurons were progressively replaced by larger and more weakly stained neurons in the amygdala and piriform cortex. In contrast, Bcl-2 immunostaining did not change with age in the subventricular zone and olfactory tubercle, the islands of Calleja of which were markedly enriched with Bcl-2. The dentate gyrus contained only a few layers of intensely labeled granule cells in juvenile monkeys, but the number of these layers increased markedly in adult and aged monkeys. These findings suggest that Bcl-2 can serve as a marker of both proliferating and differentiating neurons and indicate that such immature neurons may be much more widespread than previously thought in postnatal primate brain.
The activity-dependent immediate early gene protein Krox-24, expressed in the neocortex at high basal levels, decreases rapidly upon neuronal deactivation (Chaudhuri et al. [1995] Vis. Neurosci. 12:35-50). In infant marmosets, as in most primates, the geniculo-cortical terminations segregate into eye-specific anatomical ocular dominance columns (ODCs), which disappear, however, during adolescence (Spatz [1989] Brain Res. 488:376-380), resulting in balanced inputs from the two eyes (Sengpiel et al. [1996] Vis. Neurosci. 13:145-160). Nevertheless, we found, in adult marmosets, 24 hours after monocular retinal activity blockade by tetrodotoxin, distinct alternating compartments of potentiated and depressed Krox-24-like immunoreactivity (Krox-IR) in layer IV of area 17. This pattern of Krox-IR disappeared at 10 days of retinal silencing, but was still present at this survival time in stains for cytochrome oxidase or NADPH-diaphorase. After 20 days of retinal silencing, the pattern was not demonstrable with any of the three stains. We term these compartments physiological ODCs, in contrast to the anatomical ODCs of most primates. If the anatomical ODCs of infant marmosets disappear by collateral sprouting into the inappropriate ODCs, then the collateral geniculo-cortical synapses might differ slightly in their properties from the original ones. We silenced the sets of original and collateral synapses of the one ocularity. This apparently transiently initiated, at the synapses driven by the intact eye, two different complex processes leading to molecular potentiation at the original synapses and to molecular depression at the collateral synapses.
Here, we report on the analysis of keratin 18 null mice. Unlike the ablation of K8, which together with K18 is expressed in embryonic and simple adult epithelia, K18 null mice are viable, fertile, and show a normal lifespan. In young K18 null mice, hepatocytes were completely devoid of keratin filaments. Nevertheless, typical desmosomes were formed and maintained. Old K18 null mice, however, developed a distinctive liver pathology with abnormal hepatocytes containing K8-positive aggregates. These stained positively for ubiquitin and MM120-1 and were identified as Mallory bodies, one hallmark of human alcoholic hepatitis. This is the first demonstration that the ablation of one keratin leads to the accumulation of its single partner. Another striking finding was the absence or drastic down regulation of K7 in several tissues despite its ongoing transcription. Moreover, K18 null mice revealed new insights in the filament-forming capacity of the tail-less K19 in vivo. Due to the unexpected secondary loss of K7, only K8/19 are expressed in the uterine epithelium of K18 null mice. Immunoelectron microscopy of this tissue demonstrated the presence of typical K8/19 IF, thus highlighting in vivo that K19 is a fully competent partner for K8.