Biomedical subjects

Valérie Coronas

Publications and source records attributed to Valérie Coronas.

4 recordsLinked to original sources

PubMed2006

Neurogenesis and neural stem cells in the dorsal vagal complex of adult rat brain: new vistas about autonomic regulations--a review.

The dorsal vagal complex (DVC) of the brainstem is the major reflex center of autonomic nervous system. Several neuroplasticity effectors have been identified in the DVC of adult rat, such as PSA-NCAM, GAP-43, BDNF and its receptor TrkB; moreover, acute vagal stimulation was found to induce c-fos and to down-regulate western-blot-assayed tissular concentration of PSA-NCAM. Adult neurogenesis was first shown in rat DVC by BrdU incorporation combined with phenotypic labelling in situ; new neurons are generated in equal proportions with new astrocytes and at a lower rate than in olfactory bulb or hippocampus. Intrinsic proliferative cells were then detected within the DVC of adult rat by means of Ki-67 immunohistochemistry and western-blot of D-cyclins. The presence of neural stem cells within DVC was directly demonstrated by applying the in vitro neurosphere assay on microdissected adult DVC explants; DVC-derived neurospheres display lower proliferation rate and neurogenic potential than forebrain ones. Vagotomy in adult promotes massive and transient increase of neurogenic and microglial proliferations within DVC, the kinetics and location of which were analyzed by Ki-67 immunohistochemistry and cyclin D western blot. These mechanisms shed light on so far unknown plasticity potential in DVC, which brings novel cues about physiological adaptations of autonomic reflexes in adult mammals.

Animals↗

PubMed2006

Endogenous factors derived from embryonic cortex regulate proliferation and neuronal differentiation of postnatal subventricular zone cell cultures.

In rodents, the subventricular zone (SVZ) harbours neural stem cells that proliferate and produce neurons throughout life. Previous studies showed that factors released by the developing cortex promote neurogenesis in the embryonic ventricular zone. In the present report, we studied in the rat the possible involvement of endogenous factors derived from the embryonic cortex in the regulation of the development of postnatal SVZ cells. To this end, SVZ neurospheres were maintained with explants or conditioned media (CM) prepared from embryonic day (E) 13, E16 or early postnatal cortex. We demonstrate that early postnatal cortex-derived factors have no significant effect on SVZ cell proliferation or differentiation. In contrast, E13 and E16 cortex release diffusible, heat-labile factors that promote SVZ cell expansion through increased proliferation and reduced cell death. In addition, E16 cortex-derived factors stimulate neuronal differentiation in both early postnatal and adult SVZ cultures. Fibroblast growth factor (FGF)-2- but not epidermal growth factor (EGF)-immunodepletion drastically reduces the mitogenic effect of E16 cortex CM, hence suggesting a major role of endogenous FGF-2 released by E16 cortex in the stimulation of SVZ cell proliferation. The evidence we provide here for the regulation of SVZ cell proliferation and neuronal differentiation by endogenous factors released from embryonic cortex may be of major importance for brain repair research.

Age Factors↗

PubMed2004

Neurogenic and intact or apoptotic non-neurogenic areas of adult brain release diffusible molecules that differentially modulate the development of subventricular zone cell cultures.

Abstract In the adult mammalian brain, neurogenic activity is maintained in the subventricular zone (SVZ). Damage to non-neurogenic areas can stimulate SVZ cell proliferation and trigger addition of new neurons in the affected areas. We therefore examined the possible control exerted by specific microenvironment cues on SVZ neurogenic activity. To this end, neonatal SVZ neurospheres were maintained in the presence of diffusible signals derived from the adult neurogenic SVZ or from the non-neurogenic cerebral cortex either previously treated (apoptotic cortex) or not (untreated cortex) with staurosporine, a known apoptosis inducer. To restrict interactions to soluble signals, the explants were separated from the SVZ neurospheres by a microporous membrane. The results indicated that molecules released by the SVZ itself promoted the expansion of SVZ cell population through increased proliferation and reduced apoptosis. In contrast, untreated cortex factors reduced the expansion of SVZ cell population by decreasing proliferation. In addition, SVZ or untreated cortex factors, respectively, promoted or inhibited neuronal differentiation. Following apoptotic damage, cortex factors no longer inhibited and instead promoted the expansion of the SVZ cell population by increasing proliferation. These effects on cell numbers were replicated following use of culture media conditioned with the different explants but were no longer present following heat inactivation, which indicates that proteins were involved. These findings indicate that the neurogenic SVZ delivers autocrine/paracrine signals that promote neurogenesis whereas the non-neurogenic cerebral cortex releases signals that inhibit proliferation and neuronal differentiation. Interestingly, this constitutive growth inhibitory effect of the cerebral cortex is inverted following apoptotic lesion.

Animals↗

PubMed2002

Cortical diffusible factors increase MAP-2 immunoreactive neuronal population in thalamic cultures.

Previous experiments have established that grafts of embryonic day (E) 16 frontal cortex placed into the occipital cortex of postnatal day (P) 0-P1 rats selectively attract axons from the ventrolateral and ventromedial (VL/VM) thalamic nuclei (Frappé et al., Exp. Neurol. 169 (2001) 264). The present study was therefore undertaken to identify any possible maturation-promoting activity of the cortex on VL/VM thalamic cells. In a first step, a primary culture of VL/VM thalamic cells taken from P0-P1 rats was developed. Neurons, glial cells and a few immature, nestin immunoreactive cells were identified in the culture. In a second step, VL/VM thalamic cells that had been maintained in vitro for 4-5 days were cultured for 7 additional days in isolation (control condition) or with an E16 or P5 explant of frontal or occipital cortex placed on a microporous membrane. In control conditions, the total cell population and the percentage of MAP-2 immunoreactive neurons were not modified with time. In contrast, the percentage of MAP-2 immunoreactive neurons was increased in E16 cortex co-cultures whereas the total cell population was unchanged and the proliferative activity remained very low. Also, the mean number of neurites per neuron was increased but no effect was found on neuritic length. Similar effects on neuronal maturation were found with E16 frontal or occipital cortex explants, indicating a lack of areal specificity. P5 cortex also produced, but to a lesser extent, an increase in percentage of MAP-2 immunoreactive neurons. Further, P5 cortex had no effect on mean number of neurites per neuron but substantially promoted elongation of neuronal processes. We propose that in addition to their well-established survival promoting effect, diffusible molecules released by embryonic and early postnatal cortex can promote in vitro the maturation of thalamic neurons.

Animals↗