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A Gelot

Publications and source records attributed to A Gelot.

34 records · Page 2Linked to original sources
PubMed1998

[Histogenesis of the corpus callosum].

The corpus callosum results from neocortical commissural axon fasciculation. Its development reflects the interhemispheric circuitry and then follows the successive steps of synaptogenesis. The first stage consists of callosal neuron differentiation, which allows the extention of the future callosal axon; this is an early event that occurs while neuronal migration to the cortical plate is still ongoing. Callosal axon guidance towards its specific target is the second step which includes reaching and crossing the midline and further target recognition with formation of initial synapses. This period extends from 12 to 22 post-conceptional weeks and corresponds to the following histological features: i) progressive invasion by callosal growth cones of the dorsal part of lamina reuniens through a preformed glial pathway; ii) appearence of the three parts of corpus callosum, namely truncus, rostrum and lastly the splenium. Both these stages are genetically controlled either directly by developmental gene expression (neurogenesis genes) or indirectly by the establishment of cue maps (spatial expression of extra-cellular matrix proteins). The third step is that of synapse remodeling by synaptic activity, giving rise to axonal elimination, macroscopically revealed by a transitory thinning of corpus callosum. This perinatal event contributes to the corpus callosum acquiring a mature topography. Finally, analysis of corpus callosum ontogenesis appears as a striking model of synaptogenesis study and provides physiopathological assumptions for a understanding of the corpus callosum agenesis.

Animals↗
PubMed1998

[Agenesis of the corpus callosum. Neuropathologic study and physiopathologic hypotheses].

The neuropathological study of corpus callosum agenesis requires a two-phase approach: first it should analyze the putative causal factors, i.e. absence of callosal neurons, commissuration inability or synapse remodelling defect; secondly it has to detect any morphogenetic effects stemming from the absence of commissure such as nonregression of archicortical structures, ventricular enlargement or possible invasion of the remaining telencephaplic commissure by callosal neurons. Absence of callosal neurons due to abnormal corticogenesis gives rise to corpus callosum agenesis without callosal axon, that is without Probst's bundles. Conversely, corpus callosum agenesis occurring secondary to a commissuration default is associated with the presence of callosal axons which travel along the midline instead of crossing, that leads to the formation of Probst's bundles. This inability to cross the midline could be secondary to an obstacle, such as lipoma or as interhemispheric cysts, or primitive due to axonal guidance disturbance. In the latter situation, the commissural defect could affect the other cerebral commissures i.e. anterior or hippocampal commissures, or could become integrated into a more diffuse midline pathology involving both cerebral and extracerebral structures. Finally, it could be assumed that a synapse remodelling defect could lead to atrophy or hypertrophy of the commissure, that occurs in the absence of white matter pathology.

Agenesis of Corpus Callosum↗
PubMed1997

[Prenatal MRI of the brain. Retrospective study apropos of 34 tests].

We performed 34 antenatal MRI, in utero in 29 foetuses with cerebral malformations depicted by US. For five patients, a second antenatal MRI was performed because of a technical failure or of diagnosis doubt. We considered that MRI is a valuable imaging method. We have observed 2 false negatives (myelomeningocele, gyration abnormality) on MR study (n = 34). MRI is more contributive that US for the etiological diagnosis of ventricular enlargement: 83% versus 46%. MRI depicted corpus callosum agenesis misdiagnosed in 5 patients by US. MR results modified the therapeutic procedure in 37% of our patients. We think that the optimal term to perform MRI study is after 28 weeks gestational age because of the size of the fetus and for the timing of cerebral development. Ventricular dilatation (criteria: occipital horn size more that one centimeter at 25 weeks of term) is the main indication of MR study.

Brain↗
PubMed1996

Alpha-brain spectrin mRNA belongs to the population of intradendritically transported mRNAs.

Brain spectrin is a cytoskeletal protein involved in neuronal polarization and differentiation. We have studied the intraneuronal expression of non-erythroid (NE) alpha-spectrin mRNA in the rat brain during the development of the CA3 pyramidal cells, and compared it with alpha-tubulin mRNA expression. In contrast to alpha-tubulin expression, which remains located in the neuronal somata, NE alpha-spectrin mRNA was present in the dendritic compartment during the first 2 weeks of life. NE alpha-Brain spectrin mRNA transport into the dendrites coincides with critical development events, including dendritic arborization, growth and synaptogenesis, and could be dependent on the appearance of synaptic activity at the mossy fibre/CA3 synapse.

Animals↗
PubMed1996

[MRI and computer-assisted tomography in Kufs disease. Apropos of a familial form].

Kufs disease is the adult form of ceroid neurolipofuscinosis, and an uncommon cause of degenerative nervous system disease affecting young adults. We present here 4 cases of family form revealed by a demential syndrome. In all 4 patients MRI showed diffuse cortical atrophy predominant in the parietal regions. In 3 of these 4 patients MRI also exhibited a low signal in T2-weighted sequences on the putamens. There was no abnormality of the white matter. Diagnosis was made by cerebral biopsy in one case and by rectal biopsy in all other cases. Although the MRI images are not specific, they must be used when the diagnosis of Kufs disease is suspected in young patients with demential syndrome.

Adult↗
PubMed1995

Developmental aspects of type II lissencephaly. Comparative study of dysplastic lesions in fetal and post-natal brains.

We report neuropathological studies of five cases of type II lissencephaly from three fetuses and two infants. This comparative study allowed us to determine the developmental course of the cerebral lesions. Two distinct developmental events seem to generate this type of brain malformation: firstly, an early disturbance in cortex formation, which results both from a disorder of radial migration and a pial barrier disruption; secondly, a late perturbation of cerebral surface organization, resulting in fusion of the cerebral surface. All these features can be related to a primitive meningeal pathology, and more generally, to a neurocristopathy. Accordingly to our observations, this brain malformation appears during both migrational and post-migrational stages and may be considered more like a polymicrogyria than a lissencephaly.

Abnormalities, Multiple↗
PubMed1995

Central effects of neuropeptide FF on intestinal motility in naive and morphine-dependent rats.

The effects on intestinal myoelectric activity of (1DME)Y8Fa (D-Tyr-D-Leu[N-Me]-Phe-Gln-Pro-Gln-Arg-Phe-NH2), a synthetic analog of the neuropeptide FF (Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2) were examined in rats after central (i.c.v.) administration performed before acute morphine and after chronic morphine treatment. The acute administration of morphine sulphate (5 mg/kg s.c.) inhibited the occurrence of intestinal migrating myoelectric complexes (MMC) for 46.0 +/- 15.2 min and increased the number of contractions on the proximal colon (13.5 +/- 2.9 vs 8.1 +/- 0.6/10 min). The duration of the MMC disruption was significantly (P < 0.05) reduced (19.0 +/- 5.6 min) by central administration of naloxone (100 micrograms/kg) but not of (1DME)Y8Fa. In rats rendered tolerant to morphine by injections of a slow-release emulsion containing morphine (75 mg/rat over 48 h), intestinal MMC were disrupted and replaced by a continuous irregular activity. Central administration of naloxone (100 micrograms/kg) restored MMC after having induced for 38.3 +/- 7.3 min a motor pattern typical of the diarrhoeal state, termed minute rhythm. No change in colonic motility was observed despite the occurrence of dirrahoea. The effects of naloxone were reproduced by (1DME)Y8Fa (100 micrograms/kg) that induced a pattern of minute rhythm for 48.9 +/- 15.7 min. These features indicate that neuropeptide FF has no action on the acute effects of morphine on intestinal motility but exerts anti-opioid activities in digestive motor alterations associated to morphine withdrawal.

Amino Acid Sequence↗
PubMed1995

[Nervous microangiopathy and POEMS syndrome].

The authors report the case of a 40 year-old man with POEMS syndrome (peripheral neuropathy, organomegaly, endocrinopathy, M-protein and skin changes). Pathological studies of the peroneal nerve showed a microangiopathy of the vasa nervorum. Several authors have already reported microvascular abnormalities that could be responsible for some systemic manifestations of the POEMS syndrome, involving the skin, the kidney and the peripheral nerves. This new case enhances this hypothesis. The relation between microangiopathy and plasma cell dyscrasia is unknown.

Adult↗
PubMed1995

Non-Hodgkin malignant lymphomas and peripheral neuropathies--13 cases.

Non-Hodgkin's malignant lymphomas (NHML) are malignant lymphoid proliferations which may be of B or T cell type. Thirteen observations of an association between peripheral neuropathy and B type NHML are reported. None of the cases had evidence of meningeal propagation or neurotoxicity from chemotherapy. The NHML were classified according to the Working Formulation and Kiel classifications. The various mechanisms of peripheral neuropathy in these cases were split into four broad groups. Group I consisted of four cases in which the peripheral nerve lesions were directly linked to a propagation of malignant cells into the peripheral nervous system; this was revealed by autopsy and/or nerve biopsy. Malignant B cell proliferation was demonstrated in three out of four of these cases by immunolabelling of the infiltrates. Group II included three patients whose serum contained a monoclonal immunoglobulin (IgM) with antimyelin activity, and two who had pathological IgM deposits in endoneurial connective tissue. Group III comprised two cases. The immune dysfunction of the NHML was responsible for a Guillain-Barré syndrome in one, and for a chronic inflammatory demyelinating polyneuropathy in the other. Group IV included two patients in whom the mechanism of the peripheral neuropathy, although almost certainly directly related to the NHML, could not be determined beyond doubt. The peripheral neuropathy might have been a result of a paraneoplasic process or, possibly, an undetected lymphomatous invasion of nervous tissue. All these cases of clinically diverse peripheral neuropathy, which either occurred before the discovery of the haemopathy or arose as complications of it, are discussed along with similar observations reported in the literature. Immunolabelling of lymphomatous proliferations and nerves is now of considerable value for classifying and indicating the exact aetiology of the peripheral neuropathy. It can also detect pathogenic consequences of any associated monoclonal dysglobulinemia. In any event, a direct link between the peripheral neuropathy and NHML represents an indication for intensification of specific chemotherapy, which in some of our patients led to significant regression of the peripheral neuropathy. Nonetheless, in some cases, the link between peripheral neuropathy and NHML could not be established with certainty. Long-term follow-up is essential in such cases. The present results show the importance of a case by case study of patients with NHML and peripheral neuropathy.

Aged↗
PubMed1994

Developmental change of alpha-spectrin mRNA in the rat brain.

Spectrin is a cytoskeletal protein considered to be a major component of intracellular cohesion. Using an in situ hybridization approach, we have investigated the developmental expression of the mRNA encoding the alpha-subunit of rat brain spectrins, from birth to adulthood. alpha-Subunit mRNA is detectable at birth, in brain areas with perinatal neurogenesis, such as the cerebral cortex, hippocampus, thalamus, and olfactory bulb. alpha-Brain-spectrin mRNA increases gradually during the first postnatal days to reach a plateau between the second and the third week of life. In the young adult brain, the level of alpha-brain spectrin mRNA decreased globally. This spacio-temporal distribution argues for the involvement of the mRNA in the synthesis of both the erythroid and non-erythroid brain spectrin isoforms. We have focused our attention on the hippocampal formation and the cerebellum. In both regions, in situ hybridization signal variations are superimposable with neuronal maturation gradients. This pattern of variation, coupled with the known interaction of brain spectrins with other cytoskeletal proteins, agrees with the notion that brain spectrins may be involved in neuronal differentiation by way of the cytoskeletal lattice organization.

Animals↗
PubMed1994

Iatrogenic Creutzfeldt-Jakob disease in three growth hormone recipients: a neuropathological study.

Since 1985, several cases of Creutzfeldt-Jakob disease, occurring after a treatment by human cadaveric hormone have been reported. Three new iatrogenic cases observed in French patients (two children and one young adult) are described here. Neuropathological study displayed the classical aspects of previously reported sporadic cases of Creutzfeldt-Jakob disease in adults, including severe cortical spongiform change with numerous vacuoles within neuronal dendrites, diffuse astrogliosis and neuronal loss. In addition, the iatrogenic cases described here included two more unusual points: (i) they were homozygotic for the PrP gene on codon 129 and therefore a genetic predisposition could be suspected; (ii) numerous kuru plaques were scattered in the cerebral cortex, the subcortical white matter and in the cerebellar cortex. They were decorated with a PrP monoclonal antibody, but not with a beta A4 antibody. This last point underlines the similarities between iatrogenic Creutzfeldt-Jakob disease and kuru.

Adult↗
PubMed1992

Ultrastructural study of the choroid plexus of spontaneously hypertensive rats.

We previously gave an account of an increased ion transport activity in choroid plexus from spontaneously hypertensive rats. We have since examined this organ in scanning and transmission electronic microscopy. In the choroid plexus from young spontaneously hypertensive rats, the epithelial cells showed the following: a partial loss of the brush border and infoldings of basolateral membranes, an increased number of Golgi apparatus, vesicles, and mitochondria, and an activated nucleus. In adult hypertensive rats, the mitochondria had increased in number and tended to fill the cytoplasma while the nuclei had returned to a resting level. These ultrastructural changes furthermore suggest an increased secretory activity in the choroid plexus in spontaneously hypertensive rats.

Aging↗
PubMed1992

Plus-minus lid syndrome.

A patient presented with ipsilateral ptosis and contralateral superior eyelid retraction due to a nuclear third nerve syndrome. The CT brain scan revealed a paramedian mesencephalic lesion contiguous with the oculomotor nucleus, sparing the midbrain tectum and the posterior commissure.

Aged↗
PubMed1989

The effect of cicletanine on cerebrovascular injury in stroke-prone spontaneously hypertensive rats.

The stroke-prone spontaneously hypertensive rat (SHR-SP) is one of the most suitable models for stroke study. The present trial work was undertaken so as to obtain further information concerning the action of a new furopyridine, cicletanine. Forty-six males--SHR-SP/Iffa Credo rats--aged 7 weeks, were divided into three groups. Group 1 was a control group, groups 2 and 3 were orally treated with cicletanine at 30 and 100 mg/kg. Their drinking water contained 1% NaCl. Systolic blood pressure, body weight, and survival were recorded. After 6 weeks, all the rats were sacrificed. Samples of heart, brain, and kidney were fixed for light and ultrastructural examination. We found that cicletanine treatment (30 and 100 mg/kg) had significantly inhibited the incidence of hypertensive cerebral damages as characterized by cerebral infarction and vascular alterations with fibrinoid necrosis. Compared with the control group, the rats treated with the cicletanine had a significantly increased survival rate (P less than .001); the cicletanine also had an important protective effect on tissue. Cicletanine administration prevented the development of hypertensive cerebral vascular damage, probably through direct action on the vascular walls.

Animals↗