Browsing by Subject "Calcium binding proteins"

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    Dynamic patterns of colocalization of calbindin, parvalbumin and GABA in subpopulations of mouse basolateral amygdalar cells during development
    (Elsevier, 2008-01) Dávila, José Carlos; Olmos, Luis; Legaz Pérez, Isabel; Medina, Loreta; Guirado, Salvador; Real, Mª Angeles; Ciencias Sociosanitarias
    Calbindin cells represent a major interneuron subtype of the cortical/pallial regions, such as the basolateral amygdala, which are often analyzed in studies of tangential migration of interneurons from the subpallial ganglionic eminences to the pallium/cortex. However, previous evidence suggests that during development the calbindin cells may include more than one of the interneuron subtypes found in the adult pallium/cortex. Furthermore, in the adult basolateral amygdala, calbindin cells include a subpopulation of non-GABAergic (non-interneuron) cells. To better characterize these cells throughout development, in the present study we investigated the colocalization of calbindin, parvalbumin and GABA in cells of the mouse basolateral amygdala during late embryonic (E16.5) and several postnatal ages from birth until 4 weeks after birth (P0, P10 and P28). Our results indicate that CB, PV and GABA show a dynamic pattern of colocalization in cells of the mouse basolateral amygdalar nucleus throughout development. From E16.5 through P28, the majority of CB+ neurons and virtually all PV+ neurons are GABAergic. However, after P10, the percentage of GABAergic CB+ cells decline from 96% to 70%. Furthermore, while only 9% of CB+ neurons are PV+ at P10, this percentage raises to 42% at P28. At all postnatal ages studied, the majority of the PV+ cells are CB+, suggesting that PV+ interneurons develop postnatally mainly as a subpopulation within the CB+ cells of the basolateral amygdalar nucleus. These results are important for interpreting data from interneuron migration.
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    Novel features of neurodegeneration in the inner retina of early diabetic rats
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Énzsöly, Anna; Szabó, Arnold; Szabó, Klaudia; Szél, Ágoston; Németh, János; Lukáts, Ákos
    The literature indicates that in diabetes retinal dysfunctions related to neural retinal alterations exist prior to clinically detectable vasculopathy. In a previous report, a detailed description about the alteration of the outer retina was given, where diabetic degeneration preceded apoptotic loss of cells (Enzsöly et al., 2014). Here, we investigated the histopathology of the inner retina in early diabetes using the same specimens. We examined rat retinas with immunohistochemistry and Western blotting, 12 weeks after streptozotocin induction of diabetes. Glial reactivity was observed in all diabetic retinal specimens; however, it was not detectable all over the retina, but appeared in randomly arranged patches, with little or no glia activation in between. Similarly, immunoreactivity of parvalbumin (staining mostly AII amacrine cells) was also decreased only in some regions. We propose that these focal changes appear prior to affecting the whole retina and overt loss of cells. In contrast to these, most other markers used (calretinin, recoverin, tyrosin hydroxylase anti-Brn-3a and also calbindin in the optic part of the retina) did not show any major alterations in the intensity of immunoreactivity or in the number of stained elements. Interestingly, under diabetic conditions, the labeling pattern of PKC-α and calbindin in the ciliary retina showed a clear resemblance to the pattern described during development. This observation is in line with our previous study, reporting an increase in the number of dual cones, coexpressing two photopigments, which is another common feature with developing retinas. These data may indicate a previously uninvestigated regenerative capacity in diabetic retina