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A M Goffinet

Publications and source records attributed to A M Goffinet.

At least 73 records · Page 4Linked to original sources
PubMed1989

Online brain attenuation correction in PET: towards a fully automated data handling in a clinical environment.

We have improved the calculation of the brain attenuation correction in positron emission tomography (PET) and set up a procedure which allows the clinician to get a fully corrected image in a single reconstruction step, without human intervention. By using a general object description scheme based on polygonal contour trees we are able to calculate the attenuation correction for brain tissue, bone and head holder. The head contour is generated from the emission sinogram. On a set of 15 adult patients, the emission values obtained using this calculated attenuation compare favorably with those obtained with an attenuation resulting from a transmission measurement. Residual discrepancies are attributed to incomplete scatter compensation between emission and transmission. The robustness of the algorithm has been tested on more than 100 brain fluorodeoxyglucose (18FDG) studies in adult patients, including pathological cases. Its applicability for 18FDG studies in children and for other tracers such as water (H2 15O) and fluoroethylspiperone (18FESP) is also presented.

Adult↗
PubMed1988

Immunohistological localization of cell adhesion molecules L1, J1, N-CAM and their common carbohydrate L2 in the embryonic cortex of normal and reeler mice.

The expression of the cell adhesion molecules L1, J1 and N-CAM and their shared carbohydrate L2 was studied in the embryonic cerebral cortex of normal and reeler mutant mice using light and electron microscopic immunocytochemistry. Apart from a general delay in their appearance in the reeler cortex, the 4 antigens were present with a cellular distribution in both genotypes reflecting the anatomical characteristics of normal and mutant phenotypes. The cell surface glycoprotein L1 was exclusively expressed by neurons, particularly axons, but was never detected at sites of neuron-glia contact. L1 was accumulated in the marginal zone and subplate of the normal cortex and in the homologous layers of the reeler cortex. The secreted glycoprotein J1 was found on glia and neurons. Although initially present in regions of fiber outgrowth, J1 became characteristically excluded from the large fiber tracts at later stages. J1 mapped in the marginal zone and subcortical plate of the normal cortex and in the corresponding layers of the mutant cortex. N-CAM had a more ubiquitous distribution and was present in ventricular zones, particularly at early stages, as well as on glia and neurons and large fiber tracts at later developmental stages. The distribution of the L2 epitope was quite similar to that of the J1 molecule but remained present on large fiber tracts, like N-CAM and L1, also at later developmental stages. These comparative observations in normal and reeler mutant mice lend support to previous suggestions that L1, together with N-CAM, may play a role in the aggregation of neuronal cell bodies after migration and in the fasciculation of developing fiber bundles. They also point to a possible function of the extracellular matrix component J1 in the guidance or support of fiber outgrowth in large fiber tracts.

Animals↗
PubMed1988

Brain glucose utilization in childhood Huntington's disease studied with positron emission tomography (PET).

Brain glucose metabolism was measured in two children with early-onset Huntington's disease, using positron emission tomography with fluorodeoxyglucose (FDG) as the tracer. A marked (48%) hypometabolism was found at the level of the caudate nuclei, but other areas of the brain, particularly the cerebral cortex, were not significantly affected. Despite its different clinical presentation, Huntington's disease in children is characterized by brain metabolic alterations similar to those found in adult patients.

Adolescent↗
PubMed1988

Brain glucose metabolism in thalamic syndrome.

Regional brain glucose metabolism was studied in a case of postischaemic thalamic syndrome. Despite a normal density of the thalamus on MRI and CT images, a 17% relative hypometabolism was found in the posterior thalamus on the affected side. This observation of functional anomalies in the posterior thalamic complex in case of thalamic syndrome is compatible with a deregulated processing of pain-related information at this level.

Blood Glucose↗
PubMed1988

Effect of D-penicillamine treatment on brain metabolism in Wilson's disease: a case study.

Sequential measurements of brain glucose metabolism were carried out in a patient with Wilson's disease, before and after successful treatment with D-penicillamine. They demonstrate an evolution of regional metabolism consistent with clinical improvement. The first study showed marked hypometabolism in the putamen on both sides. The second analysis showed bilateral improvement, with predominant residual deficits in the right putamen, while clinical symptoms of striatal dysfunction persisted on the left side. This observation suggests that positron emission tomography is able to follow the neurological evolution in cases of Wilson's disease.

Adult↗
PubMed1988

Regional brain glucose utilization in adenylosuccinase-deficient patients measured by positron emission tomography.

Regional brain glucose utilization was investigated by positron emission tomography with fluorodeoxyglucose in three children with adenylosuccinase deficiency. A consistent pattern was found in the three patients, namely a marked decrease of fluorodeoxyglucose uptake in all gray structures, with the exception of the cerebellum, which was minimally affected. Anomalies predominated in the cerebral cortex, particularly in the anterior regions; they were less pronounced in thalamus and basal ganglia. The observations suggest that positron emission tomography may be a useful tool for the localization of the deleterious effects of metabolic diseases and for the investigation of their pathophysiologic mechanisms.

Adenylosuccinate Lyase↗
PubMed1987

Brain glucose metabolism in children with the autistic syndrome: positron tomography analysis.

Brain glucose metabolism was measured in 18 autistic children, using high resolution positron emission tomography. Global brain glucose utilization in the autistic population was slightly more elevated than in young adult volunteers but did not differ significantly from that of control children. Regional metabolic maps were also normal, although there was evidence for heterogeneities, particularly at the level of prefrontal and parieto-temporo-occipital association areas: 6 children showed a relative hyperfrontality whilst hypofrontality was found in 2 cases; these heterogeneities were not correlated with clinical symptoms. These data suggest that both the rate and the regional distribution of brain glucose metabolism are normal in autistic children. Variations in terms of relative metabolic rates in association cortex remains to be investigated further.

Adolescent↗
PubMed1986

Autoradiographic localization of beta 1 and alpha 1-adrenoceptors in the midbrain and forebrain of normal and reeler mutant mice.

The distribution of alpha-1 and beta-1 adrenoceptors has been studied in the midbrain and forebrain of normal and reeler mutant mice, using autoradiographic visualization of radioiodinated HEAT and ICYP, respectively. All cortical structures and nuclear groups of the murine forebrain and midbrain bind ICYP and HEAT. For each ligand, there is substantial regional variation in binding density and these variations tend to observe boundaries between nuclei or cortical regions or the stratification of cortical regions. Regional variations in binding densities are generally different for ICYP and HEAT. Binding sites for ICYP are distributed densely throughout all fields of the neocortex (particularly, layers I-III greater than VI) and paleocortex, the striatum, pallidum, substantia nigra and superficial strata of the superior colliculus. Dense concentrations of binding sites for HEAT in cortical structures, by contrast, are limited to frontal (all layers except IV) and anterior cingulate regions of the neocortex and, as with ICYP, the stratum lacunosum-moleculaire of the regio superior of the hippocampal formation. In subcortical structures, again in contrast to the pattern with ICYP, binding density is greatest in the principal nuclei of the dorsal thalamus and the septal nuclei. The regional binding patterns of both ICYP and HEAT in the reeler brain are identical to those in the normal animal. Differential laminar binding patterns within the neocortex are approximately inverted in the two genotypes, however. Thus, binding of ICYP is densest in an inner zone of the mutant, but in the outer 3 layers of the normal neocortex. Binding of this ligand is of relatively lower density in an outer zone of the mutant and in the inner 3 layers of the normal neocortex. Similar inversions are characteristic of the laminar binding patterns of HEAT in the frontal, primary sensory and associational cortical regions of the two genotypes where densest binding is encountered superficially in reeler but at deeper levels of the normal neocortex.

Animals↗
PubMed1986

Neurogenesis in reptilian cortical structures: 3H-thymidine autoradiographic analysis.

Histogenesis was studied in forebrain cortical areas of two reptiles, Emys orbicularis and Lacerta trilineata, by using tritiated thymidine autoradiography. Four areas were considered: the dorsomedial, the general (dorsal), and the lateral cortices, and the dorsal ventricular ridge (DVR). The bulk of neurogenesis in these four pallial fields proceeds within a short period of 8-9 days, between developmental stages 15 and 18 in Emys and stages 32-34 in Lacerta. Lateral-to-medial as well as anterior-to-posterior tangential gradients of histogenesis are present in both species. Radial neurogenetic gradients are directed from outside to inside, except in the medial cortex of lizards, where no radial gradient is seen. This pattern of histogenesis in the cortex of turtles and lizards is comparable to that in mammals in terms of timing and tangential, areal variations. It might represent a "common denominator" of cortical histogenesis. However, in contrast to the mammalian cortex, which develops according to an inside to outside, "inverted" pattern, radial neurogenesis in the cortex of turtles and lizards follows an outside-to-inside gradient. These observations suggest that the inside-out gradient of cortical neurogenesis has been acquired during evolution of the synapsid radiation from stem reptiles to mammals, and that it may be related to the development of radial cortical architectonics.

Animals↗
PubMed1986

Autoradiographic study of beta 1-adrenergic receptor development in the mouse forebrain.

The development of beta 1-adrenergic receptors has been studied in the mouse forebrain from embryonic day 14 (E14) to adulthood, using autoradiographic visualization of [125I]iodocyanopindolol (ICYP) binding sites. From E14, ICYP binding sites are detected in moderate amounts in the striatum and basal forebrain and in very low concentration in the cortical plate. At E17, binding sites have increased in number in the deep layers of the embryonic cortex and extend over the whole thickness of the cortical ribbon at birth. On postnatal day 4 (P4), ICYP binding sites are more abundant in the superficial than in the inner cortex. By P10 the adult pattern of ICYP binding site distribution is achieved, namely: a high concentration in ventral pallidum, striatum and cortical layers I, II and III, a moderate concentration in layers V and VI and a lower density in septal areas and in cortical layer IV. It is well established that norepinephrine fibers arrive in the embryonic cortex early in development. The present results show that the development of norepinephrine fiber and beta 1 receptor systems are coincident in the mouse.

Animals↗
PubMed1986

[Leukotriene C4 binding sites in the mouse forebrain: autoradiographic demonstration].

The presence of binding sites for leukotriene C4 (LTC4) is demonstrated in the mouse forebrain, by using autoradiography of sections incubated with tritiated LTC4. The binding of LTC4 is inhibited by an excess of cold LTC4, but unaffected by the presence of a large excess of LTD4, which differs from LTC4 by the absence of a glutamic acid residue. The density of binding sites is minimal on fiber bundles and on choroid plexuses, maximal at the level of granule cell-rich structures such as the dentate gyrus and entorhinal area, and high in the cerebral cortex, thalamic relay nuclei and the caudoputamen. These data suggest that leukotrienes and their receptors might play a role as regulators of central neural activity, a hypothesis which was recently proposed by Lindgren et al.

Animals↗
PubMed1984

Events governing organization of postmigratory neurons: studies on brain development in normal and reeler mice.

The purpose of the present work is to examine some of the mechanisms responsible for the early architectonic differentiation of the central nervous system, as well as for the abnormal development which occurs in certain hereditary malformations. In order to approach these questions, the embryonic development of the cerebral cortex, the cerebellum, the inferior olivary complex and the facial nerve nucleus has been studied in normal and reeler mutant mice, using morphological methods. The adult reeler phenotype is characterized not only by extreme laminar abnormalities of cell positioning in the telencephalic and cerebellar cortices, but also by relatively less extreme, though distinct abnormal architectonics in non-cortical structures such as the inferior olive and the facial nerve nucleus. Study of the embryonic development of these structures reveals that neurons are generated at the normal time and migrate along normal pathways. Moreover, the processes of directional axonal growth, differentiation of class specific features of neurons and glia, and synaptogenesis appear similar in both genotypes and are probably not directly affected by the reeler mutation. However, in all instances, the early architectonic organization achieved by reeler cortical, Purkinje, olivary or facial neurons at the end of their migration is consistently less regular than in normal embryos. In addition, these anomalies become amplified during the later developmental period. This evidence for the early appearance of abnormalities in reeler embryos indicates that the disposition of neurons at maturity cannot be exclusively regarded as secondary to the maturation of cells, neurites and connections, but is contingent upon a specific mechanism. One may infer that the presence of a normal allele at the reeler locus is necessary for the normal completion of this histogenetic step, which consequently is submitted to genetic control. Although the factor(s) responsible for the stable configuration of the early architectonics is unknown, various hypotheses are considered. Several lines of evidence are presented which argue against a major role being played by diffusible factors, mesodermal components and afferent fiber systems. Two mechanisms are considered particularly worth evaluating: (1) a diminution of relative adhesivity between neurons and radial glial fibers at the end of migration, and (2) a stabilization of neuronal configuration by selective recognition-adhesion among postmigratory neurons. The reeler gene could, directly or indirectly, affect these cell-cell interactions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Architectonic and hodological organization of the cerebellum in reeler mutant mice.

The architectonic and hodologic organization of the reeler cerebellum has been studied by means of immunohistochemistry, general cell and fiber stains and by horseradish peroxidase and autoradiographic tracing methods. Malposition of Purkinje cells, which varies in degree, is the most salient architectonic anomaly of the mutant cerebellum. Mapping the distribution of Purkinje cells is facilitated by a monoclonal antibody which selectively stains neurons of this class in the cerebellum. Although some Purkinje cells form a normal monolayer, most lie in heterotopic positions within or below the granule cell layer. The major contingent is segregated in subcortical masses in the depths of the cerebellum. Fiber bundles continuous with the cerebellar peduncles run in septa between the subcortical Purkinje cell masses. The distribution of Purkinje cell masses as well as the roof nuclei and areas of normal cortex and fiber bundles are identical from animal to animal. These consistent architectonic variations serve to partition the reeler cerebellum into 7 sagittally oriented compartments: one medial, two intermediate, two lateral and two additional lateral lobular appendages which may correspond to paraflocculus and/or flocculus of the normal cerebellum. The topography of the reeler olivocerebellar, or climbing fiber, system is normal in that the caudal-to-rostral axis of the olivary complex maps onto the medial-to-lateral axis of the contralateral hemicerebellum. The climbing fiber projection in reeler, like that of the normal animal, appears to be organized in parasagittal strips. In the mutant, mossy fibers from the pons and spinal cord project respectively to the lateral and medial cerebellar fields, and overlap in the intermediate compartment. They thus invest different and to a large extent complementary cerebellar territories, which approximate the architectonic divisions. This segregation of the two principal mossy fiber systems is not so marked in the normal cerebellum. In terms of laminar distribution, the pontine projection is distributed principally to the granule cell stratum in the mutant. The reeler spinocerebellar afferents, by contrast, project not only to the granule cell layer but also to the heterotopic Purkinje cells. The present observations suggest that the primary defect in the reeler cerebellum is malposition of Purkinje cells. As appears to be the case during development of the forebrain in reeler, the mutation may affect the terminal phase of migration of Purkinje cells in the cerebellum.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Abnormal development of the facial nerve nucleus in reeler mutant mice.

The architectonics and development of the facial nerve nucleus have been compared in reeler and normal mice. In both genotypes neurons were generated at E10, and their axons entered the facial nerve at E11. Cell bodies migrated radially at E12-E13, possibly along radial neuroepithelial fibres. From the end of migration, the reeler nucleus was less superficially located and less clearly organised than the normal nucleus. The normal adult architectonic divisions were present in the mutant, but less distinct than in the normal nucleus. These observations have been related to other data on the developmental biology of the reeler brain. It is suggested that the reeler gene could affect an interaction between neurons or between neurons and radial fibres at the end of migration.

Animals↗
PubMed1983

The embryonic development of the inferior olivary complex in normal and reeler (rlORL) mutant mice.

The development of the inferior olivary complex has been studied comparatively in normal and reeler mutant mice, from embryonic day 14 to birth. In both genotypes, cells migrate tangentially, from the lateral recess of the fourth ventricle, until they reach the ventral rhombencephalon where they enter the olive radially. Some cells also enter the olive laterally, from its external side. In both genotypes, olivary neurons differentiate following the same morphological sequence, both in terms of dendritic deployment and of axonal growth. Olivofugal axons cross the midline as early as E14. Synapses are rare in the inferior olivary complex during the prenatal period. Radial glial cells and the first stages of astrocytogenesis appear similar in both genotypes. The process of olivary maturation begins at E15. In normal embryos, this occurs concurrently with a subdivision of the olivary complex, clearly defined at birth: the principal olive (PO) is "U" shaped and located between the medial accessory olive (MAO) and the dorsal accessory olive (DAO). In reeler mutants, there are abnormalities in the configuration of the inferior olivary complex. Even the earliest lobulated contours are anomalous. The ultimate configuration, though containing the principal elements of the normal complex, is blunted, compact, and very much less "calligraphic" in its undulation than in the normal animal. The reeler dysplasia is mild at E15 and becomes increasingly evident at later developmental stages. These observations show that the reeler gene primarily affects the position of neuronal cells relative to other cellular elements and to fiber strata, while leaving relatively intact the phenomena of cell migration and differentiation. Afferent fibers from spinal and midbrain origin are probably involved in the division of the olivary complex into its components (Martin et al., '80). In addition, the development of the cerebellar cortex could influence the morphogenesis of the olivary nuclei. However, the architectonic malformation of the reeler inferior olive can hardly be exclusively attributed to perturbations of its hodological relationships. It is proposed that the abnormal development of the inferior olive in reeler mutants is largely dependent on a local, intrinsic action of the mutant gene on the olivary primordium.

Animals↗
PubMed1983

The embryonic development of the cortical plate in reptiles: a comparative study in Emys orbicularis and Lacerta agilis.

From the earliest stage of its ontogenesis, the mammalian cerebral cortex displays a remarkable cytoarchitectonic organization, with its neurons oriented radially within the cortical plate (CP). It is not known whether this radial organization of cortical neurons is characteristic of every cerebral cortex or whether it reflects a progressive phylogenetic acquisition. In order to study this question, the embryonic development of the cortex has been examined in reptiles, where it is the most primitive. Two species, Emys orbicularis and Lacerta agilis, representative of the two principal reptilian orders (chelonians and squamates), have been studied with histological methods. Golgi impregnation, and electron microscopy. Very similar patterns of cell proliferation, migration, maturation, and synaptogenesis have been observed. However, important species differences are present in the cellular organization of the cortical plate. Whereas in Emys the structure of the cortical plate is rudimentary, in Lacerta it appears well developed and quite reminiscent of its mammalian counterpart. Preliminary comparisons with embryological preparations of Sphenodon and Crocodilus niloticus show that the organization of the cortical plate displays significant variations among the different reptilian groups. The present results suggest that the radial organization of cortical neurons is not an all or nothing phenomenon but has been acquired independently and is thus a case of homoplasy, probably due to convergence (Northcutt, 81). Several possible implications of these findings are discussed and a working hypothesis based on the role of radial glial cells in the formation of cytoarchitectonic patterns (Rakic, '80) is presented.

Animals↗
PubMed1983

The embryonic development of the cerebellum in normal and reeler mutant mice.

The development of the cerebellum has been studied in normal and reeler mice, from embryonic day fourteen, i.e. when morphogenesis begins in this organ, to birth. The cerebellar nuclei develop according to a similar sequence in both genotypes. Their neurons migrate into the rostral field of the cerebellar bud where they condense in a rounded mass, well defined at E14. From E17, this cell contingent spreads transversally and the three roof nuclei become clearly defined. In reeler mutants, there seems to be an abnormal development of the architectonics of the lateral nucleus. The Purkinje cells migrate into the cortex at the same time in both genotypes. In the normal animal, from E14 onward, Purkinje cells are condensed in a clearly defined plate, where they assume a radial organization. By contrast, the mutant Purkinje cells are not arranged in a plate but are scattered in the periphery of the cortex. The neurons of the external granular layer are identical in both genotypes. Radial glial fibers and early Golgi epithelial cells appear to be normally present in the reeler embryo. The foliation of the cerebellar cortex begins at E17 in the normal embryo. From this stage onward, foliation is increasingly deficient in reeler mutants. Based on these observations, it is suggested that, in normal cerebellar development, a specific, genetically determined mechanism is responsible for the organization and the stabilization of postmigratory neurons and that this mechanism is affected by the reeler mutation.

Animals↗