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Biomedical subjects

J Legrand

Publications and source records attributed to J Legrand.

At least 55 records · Page 3Linked to original sources
PubMed1977

Effects of undernutrition on cell formation in the rat brain and specially on cellular composition of the cerebellum.

In 35-day-old rats which were undernourished by quantitative restriction of the mother's diet from the 6th day of gestation, the wet weight and the DNA content of the cerebellum were slightly more decreased than those of the cerebrum. Cell growth (estimated from the DNA concentration and form the ratios of RNA and protein to DNA) was significantly affected by food deprivation only in the cerebellum. In the cerebullar cortex, the number of Purkinje, Golgi and stellate cells were unchanged. The numbers of other cell tyes were affected to various extents: there were significantly less granules and basket cells per Purkinje cell, and a still more marked hypoplasia of glia involving the glial cells of the molecular layer, as well as the astrocytes of the internal granular layer and the Bergmann cells of the Purkinje cell layer. Finally, the total number of glial cells within the cortex was decreased by 44% against 13% for neurones. These effects of undernutrition on cell acquisition within the brain, and on the cellular composition of the cerebellum, contrast with those of thyroid deficiency.

Animals↗
PubMed1977

Effects of thyroid dysfunction on the development of the rat cerebellum, with special reference to cell death within the internal granular layer.

The increased cell death within the internal granular layer of the cerebellar cortex, previously demonstrated by other investigators in 12-day-old rats treated with propylthiouracil, was found again in 10-, 14- and 21-day-old similarly treated young rats. In thyroid-deficient as well as in normal animals, cell death was maximal at 10 days. In hypothyroid rats, the greatest difference with the normal animals was at 14 days, when there was an increase by a factor of 20 of the number of dying cells. On day 13, the ratio of free to total N-acetyl-beta-D-glucosaminidase activities was also increased by 34%. Cell death predominantly occurred in the lower part of the internal granular layer at 10 days, in the middle part at 14 days and the upper part at 21 days. The increase in thickness of the molecular layer, which reflects the development of the Purkinje cell dendritic arborizations, was also more retarded than the acquisition of a normal ratio of granule cells to Purkinje cells. Administration of a daily dose of 0.10 mug thyroxine to thyroid-deficient animals was sufficient (and a lower dose insufficient) to return to normal the number of dying cells as well as the development of the molecular layer and the evolution of the ratio of granule cells to Purkinje cells. A daily dose of T4 as low as 0.20 or 0.25 mug already induced a marked hyperthyroid state resulting in a decrease in granule cells formation without increased cell death. Indeed, an increased cell death seemed to occur only when the normal synchronism between the development of the Purkinje cell arborizations and the laying down of granule cells was suppressed, as is the case in thyroid deficiency but not in neonatal hyperthyroidism.

Acetylglucosaminidase↗
PubMed1977

Effects of methylazoxymethanol given at different stages of postnatal life on development of the rat brain. Comparison with those of thyroid deficiency.

Newborn rats were treated at different stages of their development with low doses of methylazoxymethanol acetate. The postnatal increase of the DNA content of the cerebrum did not differ from that of controls. In the cerebellum, the DNA content was transitorily reduced, but later, the external granular layer became thicker and DNA deposition increased in comparison with controls; finally, the cerebellar DNA returned to a normal value. Morphological abnormalities of the cerebellum, abnormal orientation of migrating cells, scattering of Purkinje cell bodies within the internal granule cells and specially striking abnormalities of the morphology and orientation of Purkinje cell dendrites were noted in rats treated with MAM from birth to day 3. The effects of the Purkinje cell morphogenesis persisted but were much less marked when MAM was given from 4 to 7 or from 8 to 11 days. Neonatal thyroid deficiency, as MAM-treatment between days 0 and 3, leads to an abnormal position of Purkinje cell bodies within the cerebellar cortex; it also leads to morphological abnormalities of their dendritic arborization which closely resemble those observed after MAM-treatment during the second postnatal week. It also alters the cell formation in the cerebellum. Thyroid deficiency probably exerts its effect on cell formation earlier than previous biochemical studied have shown. On another hand, the morphological abnormalities of Purkinje cell arborizations in the thyroid-deficient animals may be partly due to the perturbations of cell formation which persist later in the cerebellum.

Animals↗
PubMed1976

Thyroid hormone and cell formation in the developing rat cerebellum.

Effects of neonatal hyperthyroidism on cell formation in the developing rat cerebellum were reinvestigated. Administration at birth of excessive doses of thyroxine or triiodothyronine led to an early stimulation of cell acquisition, followed by a permanent deficit of cells in the cerebellum. The corrective effects of physiological doses of thyroxine on the troubles of the histological and biochemical development of the cerebellum in thyroid-deficient animals were also studied. As early as 6 days, cell maturation and formation were already retarded in animals treated with propylthiouracil, but, as previously reported, cell formation was prolonged and the final number of cells was normal. Administration to thyroid-deficient animals of progressively increasing doses of thyroxine, nearly equal to the amounts of hormone secreted by the thyroid gland of the developing normal rat, returned the evolution of the cerebellar wet weight and of the cerebellar DNA to normal, as well as the histological maturation of the cerebellum, even if it did not entirely correct the retardation of body growth. These results are consistent with the view that thyroid hormone early stimulates maturation of the cerebellar germinative cells and subsequently interacts with cell formation in the cerebellum, and that this action is physiological.

Animals↗
PubMed1976

Electrophysiological analysis of the circuitry and of the corticonuclear relationships in the agranular cerebellum of irradiated rats.

The cerebellar circuitry and the corticonuclear relationships were studied in the cerebellum of adult rats rendered agranular through 7 successive exposures to X-ray radiations during infancy. Data were obtained through examination of electrical responses induced in Purkinje cells (PC) and in neurons of the lateral vestibular nucleus (LVN) by cerebellar and spinal stimulations. In irradiated rats, PC exhibited antidromic activation with a high axonal threshold and 70% of them also presented typical climbing fiber responses (CFRs). By contrast, they exceptionnally exhibited responses via the mossy fiber (MF)-granule cell pathway, but two other classes of responses were identified: i) short latency single spike responses attributed to a direct excitatory impingement of MF onto PC; ii) atypical CFRs formed of high frequency bursts of simple spikes which were seen in 76% of PC tested. Furthermore, 53% of these cells also presented typical CFRs, strongly suggesting these PC were innervated by more than one CF, thus confirming previous data on the same type of agranular cerebellum. In the LVN neurons of control and irradiated rats, spinal and cerebellar stimulations evoked clear cut IPSPs. On the basis of their shape, latency, and occurrence in animals with or without cerebellum and with or without lesion of the CF pathway, they were interpreted as mediated through direct or synaptic activation of PC or through an extracerebellar pathway. In irradiated rats, the quantitative study of these IPSPs gave further arguments in favor of a multiinnervation of PC by CF and of an important reafferentation of MF onto PC. However, the functional efficiency of this reafferentation appeared very low, as tested by activation of MF originating in the spinal cord. Finally, the intracellular recording of LVN neurons showed that a large majority of PC axons retained normal synaptic connections with nuclear cells in treated animals, indicating that corticonuclear relationships do not markedly depend upon granule cells and normal CF input.

Animals↗
PubMed1975

[Effect of cortisol on the cellular proliferation and maturation in the cerebrum and the cerebellum of the rat: Importance of the age of the animals at the beginning of treatment].

Young rats were given either a single subcutaneous injection (1 mg at 0, 1, 4 or 8 days), or four consecutive daily injections (0.2 mg/day between 0 and 3 days; 0.4 mg/day between 4 and 7 days; 0.6 mg/day between 8 and 11 days) of cortisol acetate in order to test the influence of age on the action of corticosteroids on the biochemical maturation of the cerebrum and cerebellum in terms of their DNA, RNA, and protein contents. The results showed that: 1 The diminution of the DNA content at 35 days was greater in the cerebellum (- 16 to - 32%) than in the cerebrum (- 9 to 20%); the DNA content of the cerebrum was more affected by treatment at birth, whereas that of the cerebellum was more affected by the delayed treatments. Results were different when expressed in terms of reduction of the normal increase: the gain of DNA decreased more in the cerebrum (-70%) than in the cerebellum (-40%); but the most delayed treatment induced a greater effect in both organs. These abnormalities were not always accompanied by a significant decrease of the body weight. 2 Generally, the treatments led to an increase of the mean cell territory, expressed either in terms of decrease of the DNA concentration, or in terms of increase of the organ weight/DNA ratio. Moreover, the increase of the RNA/DNA and the protein/DNA ratios constituted an indication of an accelerated cellular maturation.

Age Factors↗