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C Faivre-Sarrailh

Publications and source records attributed to C Faivre-Sarrailh.

28 records · Page 2Linked to original sources

F3/F11 cell surface molecule expression in the developing mouse cerebellum is polarized at synaptic sites and within granule cells.

The distribution of the F3/F11 neuronal cell surface molecule was investigated in the developing and adult mouse cerebellum by immunocytochemistry at the light and electron microscopic levels. F3/F11 was confined to subsets of neuronal types, since the Purkinje cell body and dendritic arborization as well as the stellate cells were not immunoreactive. In the young developing cerebellum, the granule cell axons strongly express F3/F11 as soon as they begin to grow, consistent with a functional role in promoting directional outgrowth of neuronal processes. In 10-d-old and adult cerebella, the granule cell bodies and dendrites were not immunoreactive whereas the parallel fibers, which are the granule cell axons, were labeled including in their presynaptic varicosities. By contrast, dendrites, cell bodies, and axons of Golgi cells were labeled by anti-F3 antibodies. Hence, F3/F11 can either be expressed throughout the cell or be polarized to the axons. This raises the question of how segregation of the glypiated F3/F11 molecule between different subcellular compartments depending on the type of neuron is achieved. F3/F11 was found to be present at three types of synaptic sites, suggesting that it might play a role in the formation and maintenance of synapses. However, in each type of synpase, F3/F11 was present at only the pre- or postsynaptic site, never at both: the parallel fiber varicosities contained F3/F11 whereas the postsynaptic compartment in contact, that is, the Purkinje cell dendritic spines, did not. The granule cell dendrites were unlabeled while the mossy fiber terminals contacting them were immunoreactive, and finally, the Golgi cell dendrites and dendritic spines were labeled while the presynaptic compartment contacting them was not. If F3/F11 functions as an adhesion molecule in vivo as indicated by in vitro assays, F3/F11-mediated adhesion is likely to be heterophilic.

Animals↗

Effect of thyroid deficiency on glial fibrillary acidic protein (GFAP) and GFAP-mRNA in the cerebellum and hippocampal formation of the developing rat.

The concentrations of glial fibrillary acidic protein (GFAP) and its encoding mRNA in the cerebellum and hippocampal formation were assayed during the development of normal and hypothyroid rats. Neonatal hypothyroidism induced a significant reduction in the GFAP concentration in both regions from day 14. The reduction was especially marked on day 35 in the cerebellum (-43%) and the hippocampal formation (-55%). The immunocytochemical study of vimentin showed that the developmental disappearance of this protein from the Bergmann and internal astrocytes is greatly delayed in the cerebellum of the hypothyroid rats. The reduction in GFAP concentration together with the delayed vimentin-GFAP transition could explain how astrocyte morphogenesis is impaired by neonatal thyroid deficiency. The GFAP-mRNA concentration in the hippocampal formation was reduced throughout the development of thyroid-deficient rats, while the GFAP-mRNA concentration in the cerebellum first increased between birth and day 14 to reach a peak well above the normal value (+78%) and decreased thereafter to reach 53% of the normal value by day 35. This transient increase in the cerebellar GFAP-mRNA concentration may be related to the astroglial hyperplasia that occurs in these animals. The difference between the developmental profile of GFAP and its encoding mRNA, especially under pathological conditions, indicates that two distinct mechanisms control the synthesis or stability of the protein and its messenger RNA, as was previously found in the forebrain of the developing normal rat.

Animals↗

Actin-depolymerizing factor (ADF) in the cerebellum of the developing rat: a quantitative and immunocytochemical study.

A specific antiserum against actin-depolymerizing factor (ADF) was used in a quantitative and immunocytochemical study of ADF in the cerebellum of developing rats. The Triton-soluble ADF concentration remained stable throughout development. Light and electron microscopic immunocytochemistry showed that ADF was not detected in all cerebellar cells. ADF immunoreactivity was found in Purkinje cells, but not in granule cells. It was found in the Bergmann astrocytes and the astrocytes of the white matter, but not in the oligodendrocytes. The cell bodies and dendrites of Purkinje cells were immunoreactive for ADF but the axons were not. In contrast, the other axons of the white matter (mossy and climbing fibres) were labeled. Thus, ADF was not restricted to either the dendritic or axonal compartments. However, dendritic spines and postsynaptic densities were immunoreactive, whereas presynaptic varicosities were unlabeled. The immunoreactivities for ADF and actin were compared. ADF staining was uniformly distributed throughout the entire dendritic arborization of the Purkinje cell, while filamentous actin is highly concentrated in the dendritic spines, indicating that ADF activity might vary according to its cellular localization.

Actin Depolymerizing Factors↗

Profilin and profilin mRNA in the cerebellum of the developing rat.

Profilin and profilin mRNA concentrations were determined in the cerebellum of the developing rat. Profilin represented nearly 0.1% of total Triton-soluble protein both at birth and at the end of the developmental period. During brain maturation, the profilin concentration was regulated at the transcriptional level. A transient increase of profilin mRNA and profilin was observed at the end of the first postnatal week, a period of intense cell proliferation, neuritic outgrowth and synaptogenesis. We propose that profilin may act by forming, during the critical period of cerebellar development, a reserve pool of monomeric actin that can easily be mobilized in cell regions such as growth cones or synaptic junctions where filamentous actin is highly concentrated.

Actins↗

Effects of hypothyroidism on the detyrosylation of alpha-tubulin in the parallel fibers of the developing rat cerebellar cortex.

The immunocytochemical staining of tyrosylated alpha-tubulin using the specific monoclonal antibody YL 1/2 decreases dramatically in the parallel fibers of the rat cerebellum during development. Detyrosylation starts at 14 days in the deeper part of the molecular layer and then spreads over the entire molecular layer within a week. Thyroid deficiency induces a marked delay in alpha-tubulin detyrosylation in the parallel fibers. Detyrosylation begins only at the age of 28 days in hypothyroid animals. Immunobinding assays of detyrosylated and tyrosylated alpha-tubulin concentrations in the cerebellar supernatant of developing rats confirm that thyroid deficiency increases the tyrosylated alpha-tubulin content at 21 and 35 days. Short-term thyroxine treatment (daily from day 8, 10 or 12, to day 14) do not induce the normal pattern of tubulin detyrosylation starting at 14 days, although they do induce parallel fiber lengthening. Daily treatment from birth is required to produce the alpha-tubulin modification found in normal rats. We propose that the microtubule detyrosylation which occurs during axonal maturation is not a prerequisite for axon growth and synaptic differentiation, but may rather be implicated in the stabilization of microtubules in the mature axons.

Aging↗

Effect of thyroid deficiency on actin mRNA content in the developing rat cerebellum.

The actin mRNA content of the cerebellum was determined in normal and hypothyroid developing rats using RNA dot hybridization with a beta-actin cDNA probe. The decline in actin mRNA content occurring during the second postnatal week in normal development was delayed by about 1 week in hypothyroid rats. Since this effect coincides exactly with the delay in actin filament formation recently reported in thyroid-deficient rats, it strengthens the hypothesis of an inverse relationship in the developing brain between the polymerization state of actin and the production of actin mRNA.

Actins↗

Expression of tropomyosin genes during the development of the rat cerebellum.

The expression of the tropomyosin genes in the rat nervous system was examined during the postnatal development of the cerebellum, using human-specific alpha-, beta-, gamma-, and delta-tropomyosin cDNA probes and rat-specific alpha-, beta-, and delta-tropomyosin oligonucleotide probes. The beta- and gamma-genes do not seem to be expressed in the rat brain. The delta-tropomyosin gene produces two mRNAs: a major one of 2.4 kb, which is highly concentrated during the first postnatal week and then decreases fourfold in level until the age of 35 days, and a minor one of 2 kb, with the same developmental profile as the 2.4-kb mRNA. A 3-kb mRNA is expressed by the alpha-tropomyosin gene and is characteristic of the mature rat. The expression of the tropomyosin genes during the development of the rat cerebellum does not seem to be regulated through alternative splicing but rather implies the differential expression of two different isogenes. The multiple isoforms of tropomyosin produced during neuronal differentiation may be intimately involved in the regulation of the organization and function of actin microfilaments.

Animals↗

Developmental study of factors controlling microtubule in vitro cold-stability in rat cerebrum.

The ability of crude cerebrum supernatant to stabilize, at a low temperature, cold-labile microtubules purified from beef brain was studied during development in the rat. The cold-stabilizing activity of the supernatant was low during the first postnatal week, rose significantly during the second postnatal week, and thereafter continued to increase to the adult level. The partial purification of stable-tubule-only polypeptide (STOP) from the supernatant showed that high amounts of this protein exist at all ages, especially in young animals. The age-related increase in the microtubule cold-stabilizing activity of the cerebrum supernatant resulted from a developmental decrease in factors inhibiting STOP activity. The present study shows that (1) a close temporal correlation exists between the in vitro and in situ acquisition of cold-stable microtubules during brain development, (2) STOP activity may account for this acquisition, and (3) STOP activity is controlled by inhibiting factors that decrease with age, in turn allowing increased stability of the microtubular apparatus, a necessary condition for the development of neuronal processes.

Aging↗

A lower proportion of filamentous to monomeric actin in the developing cerebellum of thyroid-deficient rats.

Using a DNase I inhibition assay, in the presence or the absence of guanidine hydrochloride (which depolymerizes the actin filaments), developmental changes in total and filamentous actin were determined in the cerebellum of normal and hypothyroid rats. The total actin content per mg protein was not modified by hypothyroidism. As in normal animals, it reached a maximum around the age of 8 days and then decreased until adulthood. In contrast, the proportion of filamentous actin, which increased after the first postnatal week during normal development, was significantly reduced in the thyroid-deficient rats, only reaching normal values at 35 days. Thyroxine treatment for at least 4 days returned the filamentous actin content to normal at 14 days. The present study shows that the morphogenetic action of thyroid hormone is exerted not only on the microtubular apparatus, as previously described, but also in part through a control of actin monomer-polymer equilibrium.

Actins↗

Axons containing a prolactin-like peptide project into the perivascular layer of the median eminence: an immunocytochemical light and electron microscope study in adult and infant rats.

A light and electron microscopic immunocytochemical study was undertaken to explore the fine structural organization of prolactin-immunoreactive axons in the rat median eminence. In adult intact males and females and in hypophysectomized females, light microscopic immunocytochemical labeling of the mediobasal hypothalamus revealed a marked concentration of prolactin-like immunoreactive fibers in the perivascular layer throughout the median eminence and the hypophysial stalk. At the electron microscopic level, immunostaining was associated with typical neurosecretory axons located either in the palisade layer where they displayed numerous contacts with tanycyte processes, or in the perivascular layer where they frequently contacted the perivascular space. Within the labeled axonal profiles, immunostaining was essentially located on secretory granules, 90-120 nm in diameter, whereas the microvesicles accumulated in some perivascular profiles constantly remained unlabeled. These data strongly suggest that most prolactin-immunoreactive axons of the median eminence release their content into the hypophysial portal vessels. In 1-day-old infant rats, intensely prolactin-like immunoreactive fibers were similarly localized in the most external layer of the median eminence, in which, contrary to adult animals, very slight if any tyrosine-hydroxylase-immunoreactive fibers were detected. Since earlier studies have provided evidence for a nondopaminergic prolactin-release-inhibiting factor in the hypothalamus of infant rats, and for an inhibitory effect of prolactin on pituitary mammotrophs, we propose that hypothalamic prolactin may contribute, as an additional prolactin-release-inhibiting factor, to the multifactorial control of pituitary mammotrophs.

Aging↗