Visualization of S100B‐positive neurons and glia in the central nervous system of EGFP transgenic mice

Abstract

S100B, the EF-hand Ca(++)-binding protein with gliotrophic and neurotrophic properties implicated in the pathogenesis of Alzheimer's disease, is coined as a glial marker, despite its documented presence in rodent brain neurons. We have generated a transgenic mouse whose EGFP reporter, controlled by the -1,669/+3,106 sequence of the murine S100B gene, allows the direct microscopic observation of most S100B-expressing cells in the central nervous system (CNS). From embryonic day 13 onward, EGFP expression was targeted to selected neuroepithelial, glial, and neuronal cells, indicating that cell-specific expression of S100B is regulated at the transcriptional level during development. In adult mice, the highest level of EGFP expression was found in ependymocytes; astrocytes; and spinal, medullar, pontine, and deep cerebellar S100B neurons. Our results, thus, agree with earlier reports suggesting that S100B is not a CNS glial-specific marker. In addition, we detected EGFP and S100B in forebrain neurons previously thought not to express S100B in the mouse, including neurons of primary motor and somatosensory neocortical areas, the ventral pallidum and prerubral field. Another interesting finding was the selected EGFP targeting to neonatal S100B oligodendrocytes and adult NG2 progenitors as opposed to mature S100B oligodendrocytes. This finding suggests that, except for oligodendrocytes at the last stage of myelin maturation, the -1,669/+3,106 sequence of the S100B gene is a useful reagent for driving expression of transgenes in most S100B-expressing cells of mouse brain.

Fluorescent Proteins Expressed in Mouse Transgenic Lines Mark Subsets of Glia, Neurons, Macrophages, and Dendritic Cells for Vital Examination

“…In many of the lines, expression occurs in the same cells in which the S100B protein itself is reportedly present, i.e., in Schwann cells, dendritic cells of the immune system, astrocytes, microglia, adipocytes, and some neurons in the brainstem. These results mirror some findings in a previous report in which 4.8 kb of mouse S100B regulatory sequence was used to drive expression of GFP (Vives et al, 2003). They also complement findings in which other promoters were used to drive transgenic expression of FPs in glial cells (Zhuo et al, 1997;Fuss et al, 2000;Nolte et al, 2001).…”

Dynamic distribution and stem cell characteristics of Sox1-expressing cells in the cerebellar cortex

“…This suggests a migration path of Sox1-expressing cells, from the ventricular zone toward the cortical layers, which is consistent with that of Bergmann glia precursors during cerebellar formation [13,20], although the possibility of Sox1 expression being sequentially turned off and on in different populations during development cannot be formally excluded at this stage. Although an earlier report proposed that Sox1 expression marked a neuronal population [19], the results presented here show that the Sox1-positive cells express Sox9, BLBP and S100, a signature recently confirmed to be associated with Bergmann glia progenitors [12,21]. These observations suggest that Sox1/Sox2/Sox9 expression, typically associated with NSCs in the CNS, is also a characteristic of Bergmann The pattern of Sox1-expressing cells observed at P7 would explain the apparent contradiction between the presence of a stem cell-like population located in the white matter of the immature cerebellum, as reported by Lee et al [9], and recent evidence that expression of the stem cell markers Sox1/Sox2/Sox9 is specifically found in the PCL in the adult [10].…”

Radial glia and neural stem cells

“…Among these features (summarized in Fig. 2), there is the expression of genes typical of mature or reactive astrocytes, like the lipid-binding protein BLBP (Feng et al 1994;Hartfuss et al 2001), the astrocytic glutamate transporter GLAST (Hartfuss et al 2001;Malatesta et al 2000;Shibata et al 1997), the adhesion molecule TN-C (Bartsch et al 1992;Gotz et al 1997), the enzyme glutamine synthase (Akimoto et al 1993), the calcium-binding protein S100β (Vives et al 2003), the intermediate filament vimentin (Schnitzer et al 1981) and, in some species (but not in rodents), GFAP (Levitt and Rakic 1980;Sancho-Tello et al 1995). Moreover, glycogen granules start to accumulate in the radial glia cytoplasm, which becomes electron-lucent, another characteristic of astrocytes (Choi 1981).…”