Folial White Matter Research Articles

Cerebellar oligodendroglial cells have a mesencephalic origin

While the origin of oligodendroglia in the prosencephalon and spinal cord has been extensively studied and accurately described, the origin of this cell type in the cerebellum is largely unknown. To investigate where cerebellar oligodendrocytes generate and which migratory pathways they follow to reach their final destination in the adult, in ovo transplants were performed using the quail/chick chimeric system. The chimeric embryos were developed up to HH43-49 (17-19 days of incubation) to map the location of donor cells and analyze their phenotype by immunohistochemistry. As a result, mesencephalic homotopic and homochronic transplants generated cellular migratory streams moving from the grafted epithelium into the host cerebellum, crossing the isthmus mainly through the velum medullare and invading the central white matter. From here, these mesencephalic cells invaded all the layers of the cerebellar cortex except the granular layer. The majority of the cells were detected in the central and folial white matter, as well as in superficial regions of the internal granular layer, surrounding the Purkinje cells. In the latter case, the donor cells presented a Bergmann glial morphology and were Vimentin positive, while in other areas they were PLP and Olig2-positive, indicating an oligodendroglial fate. The combinatory analysis of the different grafts allowed us to propose the fate map of chick cerebellar oligodendroglia at the neural tube stage. As a result, the majority of the cerebellar oligodendrocytes originate from the parabasal plate of the mesencephalon.

The genesis of cerebellar GABAergic interneurons

Event Abstract Back to Event The genesis of cerebellar GABAergic interneurons Ferdinando Rossi1* 1 University of Torino, Rita Levi Montalcini Centre for Brain Repair, Department of Neuroscience, Italy The local GABAergic network in the cerebellum is composed by different types of cortical and deep nuclear inhibitory interneurons, generated from late embryonic to early postnatal life, according to an inside-out sequence. Unlike other cerebellar cell types which derive from faterestricted progenitors, precursors of inhibitory interneurons share a common lineage and maintain their multipotency up to late phases of postnatal development.However, the mechanisms giving rise to the different interneuron classes remain unknown. Namely, it is not clear whether mature interneuron phenotypes are specified in germinal zones or at their final destination sites in the cortex or nuclei. In order to clarify this point, we analysed the proliferation and the migratory pathways of interneuron precursors in wild type and transgenic Pax2-GFP and GAD67-GFP mice that finely characterize this cell population during earlier and later stages of development, respectively. We found that inhibitory interneuron precursors exclusively proliferate in the periventricular zone and along the folial white matter tracts of postnatal cerebellum, migrating to the cortex as postmitotic cells. To ask whether transplanted precursors entrain in the same developmental mechanisms we considered their behaviour at short time-intervals after graft in hosts of different ages. Donor cells integrate in the host proliferative sites and follow the usual migratory routes of the local inhibitory interneurons, joining a final layer position, which is strictly dependent on the host age. In particular, grafted interneurons consistently acquire positions and phenotypes that match those adopted by host interneurons born on the day of transplantation. Interestingly, donor cells acquire host-specific identities even when grafted as postmitotic neurons, indicating that fate specification of cerebellar interneurons occurs after the progenitors have left the cell cycle. Overall, our results indicate that grafted interneuron precursors fully integrate into the host neurogenic mechanisms in which different phenotypes are generated by temporally patterned signals acting on cells that remain multipotent even after leaving the cell cycle. Conference: 3rd Mediterranean Conference of Neuroscience , Alexandria, Egypt, 13 Dec - 16 Dec, 2009. Presentation Type: Oral Presentation Topic: Symposium 11 – Development of the cerebellum: from neurogenesis to axon guidance and dendritic differentiation Citation: Rossi F (2009). The genesis of cerebellar GABAergic interneurons. Front. Neurosci. Conference Abstract: 3rd Mediterranean Conference of Neuroscience . doi: 10.3389/conf.neuro.01.2009.16.053 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Nov 2009; Published Online: 19 Nov 2009. * Correspondence: Ferdinando Rossi, University of Torino, Rita Levi Montalcini Centre for Brain Repair, Department of Neuroscience, Torino, Italy, 335186@frontiersin.org Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ferdinando Rossi Google Ferdinando Rossi Google Scholar Ferdinando Rossi PubMed Ferdinando Rossi Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Lesions in the brains of three cattle resembling the lesions of enterotoxaemia in lambs

CASE HISTORY: A 3-month-old female Angus calf was found dead, and two adult Friesian dairy cows died soon after developing nervous signs. PATHOLOGICAL FINDINGS: Grossly, bilateral and mostly symmetrical areas of haemorrhage were evident that mainly involved areas of grey matter in the brainstem from the level of the caudal colliculi to the thalamus and, in one, the internal capsule and caudate nucleus. In the occipital and caudal parietal cortex, there was extensive oedema of white matter. Histologically, in addition to haemorrhage, there was protein-rich oedema around arterioles and venules in the cerebrum, hippocampus, internal capsule, thalamus, midbrain, dorsal medulla, and central cerebellar and cerebellar folial white matter. The calf's brain had bilateral and symmetrical oedema and necrosis affecting several brainstem nuclei and the occipital grey matter overlying areas of oedema of the corona radiata. DIAGNOSIS: Although the cause was not established, the perivascular lesions resembled those produced in calves by the intravenous administration of epsilon toxin. CLINICAL RELEVANCE: It is possible that epsilon toxin-induced enterotoxaemia occurs naturally in cattle, and where bilateral haemorrhage is recognised in the brains of cattle, small intestinal contents should be collected for analysis of epsilon toxin.

MRI in Lhermitte-Duclos disease.

Lhermitte-Duclos disease (LDD) is a disorder sometimes referred to as a dysplastic gangliocytoma of the cerebellum. This is a focally indolent growth of the cerebellar cortex in which the folia enlarge due to a profusion of dysplastic cortical neurons and a thickening of the molecular layer. Loss of Purkinje cells and thinning of medullary white matter results. The enlarged folia lose their secondary foldings and asymmetrically expand the cerebellar hemisphere. These morphologic features produce a characteristic pattern on some CTs and all MRIs, affording an opportunity for a preoperative diagnosis. MRI of a pathologic specimen suggested that the abnormal T1 and T2 signals corresponded to the atrophic folial white matter, thickened granule cell layer, and outer molecular layer. Because of inherent Hounsfield artifact in posterior fossa with CT, MRI is the imaging modality of choice, with better visualized striated pattern. The uniqueness of these imaging features obviates the need for an obligatory biopsy for asymptomatic patients and either permits more definitive planning for surgical decompression or, in restricted lesions, guides more assuredly complete excision of the cerebellar mass.

Prominent location of a K + channel containing the α subunit K V 1.2 in the basket cell nerve terminals of rat cerebellum

A panel of monoclonal antibodies specific for a family of voltage-dependent, fast-activating K + channels, raised against α-dendrotoxin acceptors purified from bovine brain, were used to probe the distribution of these important proteins in rat cerebellum. All the antibodies reacted with their antigens in the folial white matter, the granular cell layer and the basket cell nerve termini within the Purkinje cell layer. However, a very intense staining pattern was exhibited by only one monoclonal that reacts exclusively with K v 1.2 α subunit, the predominant isoform present in α-dendrotoxin sensitive K + channels. Double-labelling procedures with neuronal and glial markers were used to verify this discrete antibody staining of the basket cell terminals that synapse with the base of Purkinje cell bodies in a readily recognizable and characteristic fashion. This is the first direct demonstration, using a monoclonal antibody, of a presynaptic location for a voltage-activated K + channel; its discrete distribution in the basket cell pinceau suggests that it could control release of the inhibitory transmitter GABA and, thereby, influence excitability of Purkinje cells in the cerebellum.

Anterograde tracing of the rat olivocerebellar system with Phaseolus vulgaris leucoagglutinin (PHA-L). Demonstration of climbing fiber collateral innervation of the cerebellar nuclei.

The olivocerebellar climbing fiber system was investigated in the rat with anterograde Phaseolus vulgaris leucoagglutinin (PHA-L) tracing. The specific objective of the study was to find morphological evidence of climbing fiber collaterals innervating the cerebellar nuclei. Small iontophoretic injections of PHA-L were placed in different parts of the inferior olivary complex, and labelled olivocerebellar fibers could be traced to their termination as climbing fibers in sagittal zones of the contralateral cerebellar cortex. Reaching the cerebellum via the restiform body, the labelled olivocerebellar axons entered the deep cerebellar white matter anterior to the cerebellar nuclei. Most of these thicker, nonterminal axons continued dorsally around the nuclei, but some ran through them. Bundles of fibers could be followed into the folial white matter toward their cortical zones of termination. Depending on which part of the olivary complex that was injected with PHA-L, labelled axons were seen to converge on different regions of the cerebellar nuclei, where dense plexuses of thin varicose terminal fibers appeared. Quantitative estimates of the innervation ranged from 1.7 to 4.3 million boutons per mm3 in the fastigial (FN), interposed, and main parts of the lateral cerebellar (LCN) nuclei, whereas the parvicellular portion of LCN demonstrated 15-20 million varicosities per mm3. Frequently, thicker olivocerebellar axons, which seemed directed toward the cerebellar cortex, were seen to send a fine collateral branch toward these areas of nuclear innervation. As controls, PHA-L was injected into the degenerated olivary complex of 3-acetylpyridine-treated rats. Neither cortical climbing fiber terminals nor nerve terminal plexuses in the nuclei appeared in these experiments. In cases with injection sites extending into the reticular formation, substantial mossy fiber labelling was present bilaterally in the cortex, but the cerebellar nuclei were devoid of labelled innervation or demonstrated only a few larger diameter fibers. The projection of the inferior olivary complex to the cerebellar nuclei was strictly topographically organized and agreed in principle with the organization described in the cat by Groenewegen et al. ('79). The caudal medial accessory olive (MAO) projected to FN, the rostral MAO to the posterior interposed nucleus (NIP), the rostral part of the dorsal accessory olive (DAO) to the anterior interposed nucleus (NIA), and the principal olive (PO) to LCN.(ABSTRACT TRUNCATED AT 400 WORDS)

Cerebellar degeneration in the rat following rapid correction of hyponatremia.

Degenerative lesions in the superior vermis of the cerebellum were produced in 8 of 14 rats that were first made hyponatremic for three days with vasopressin and water and then given hypertonic saline. Within the superior vermis, lesions were predominantly localized to the crests of the folia. These lesions were characterized by demyelination of folial white matter and necrosis of granule cells at the junction with the white matter. In severe degeneration, the entire width of the granule cell layer was involved and Purkinje cell necrosis was found as well. Hyponatremia alone or administration of hypertonic saline to normonatremic rats did not result in lesions. Because of the topographical and histopathological similarity of these lesions to those of alcoholic cerebellar degeneration, our findings raise the possibility of a contribution of electrolyte-induced injury to the pathogenesis of alcoholic cerebellar degeneration.

EM-autoradiography of cerebellar nucleocortical terminals in the cat.

The findings from the present EM-autoradiography experiments identify the cerebellar nucleocortical projection as a mossy fiber-type pathway. In these studies orthogradely labelled axons and terminals were observed in the folial white matter and granule cell layer, with only background levels of silver grains over the Purkinje cell and molecular layers. Most nucleocortical axons synapsed within cerebellar glomeruli either at en passant contacts along dilated segments of unmyelinated axons or at multilobulated (terminal) expansions of the axons. Typically these synaptic junctions were of the asymmetrical type containing clear round vesicles. Usually, each labelled mossy fiber rosette synapsed on a large number of small terminal dendrites of granule cells; however, occasionally a series of 4-8 asymmetric contacts were noted on a single large dendrite. Labelled nucleocortical terminals were occasionally present in the nonglomerular neuropil between granule cell bodies where they contacted large dendrites of Golgi cells.

THE MODE OF TERMINATION AND TEMPORAL COURSE OF DEGENERATION OF CORTICAL ASSOCIATION PATHWAYS IN THE CEREBELLUM OF THE CAT.

AbstractThe Nauta‐Laidlaw silver degeneration technique was used to study the mode of termination and temporal course of degeneration of cerebellar cortical association pathways in the cat. All associational pathways examined appeared to terminate identically in their respective folia of termination. Two specific cerebellar cortical areas were chosen for detailed discussion and illustration. In the vermis lobules (V and VI), fibers pass from one folium to the adjacent caudal two or three folia, and these pathways can be studied conveniently in the sagittal plane. Long connections extend from anterior lobe paravermal cortex (lobule V) to caudal hemispheral folia of the same side, and these terminations could be examined at a site some distance from the lesion.Projections of associational pathways displayed a rather strict localization, with terminal areas corresponding in size and location to the area of damaged cortex giving rise to the pathway.Terminal degeneration was found distributed at Purkinje cell levels and in basal portions of the molecular layer. Some of the degenerated fibers in the molecular layer showed relationships with Purkinje cell dendrites, suggesting that they might be climbing fibers.Early degenerative changes occurred at two days postoperatively. Maximal fine fiber degeneration occurred at eight days. Fragments of large degenerated fibers were stainable in terminal areas and in folial white matter for as long as 41 days postoperatively.