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Biomedical subjects

J C Louis

Publications and source records attributed to J C Louis.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effect of naftidrofuryl on metabolism and survival of cultured neurons.

The direct influence of Naftidrofuryl, a drug widely used for the treatment of cerebrovascular diseases, on the metabolism and survival of neurons was investigated in 8-day-old chick embryo forebrain cultures. Interaction of Naftidrofuryl with neurons resulted in the increase of the intracellular cyclic AMP levels. Naftidrofuryl stimulated deoxyglucose uptake and lactate production in a time- and dose-dependent fashion. These effects were observed after a few minutes following the beginning of the treatment with Naftidrofuryl. In parallel to the action on the metabolic activities, Naftidrofuryl was able to increase the survival rate of a significant proportion of the neuronal population. These data support the notion that Naftidrofuryl may act as a neuroprotective agent.

Animals↗
PubMed1989

Antidepressant effect of lithium: a neurochemical study on neuronal uptake of norepinephrine and serotonin.

1. The effect of lithium chloride on neuronal uptake of norepinephrine and serotonin was explored on a pure culture of chicken neurons. While an acute lithium treatment (25 minutes) proves ineffective, a long-term treatment (7 days) decreases the uptake of serotonin and increases the uptake of norepinephrine. 2. The combined administration of lithium (7 days) and clomipramine (25 minutes) appears to have a greater effect on the uptake of serotonin than a treatment limited to only one of the two products. 3. The clinical implications of these results are discussed while emphasizing the interest of lithium in the treatment of depression.

Animals↗
PubMed1989

Ca2+ regulates hormone secretion and proopiomelanocortin gene expression in melanotrope cells via the calmodulin and the protein kinase C pathways.

The mechanism by which Ca2+ regulates proopiomelanocortin (POMC)-derived peptide secretion and POMC mRNA levels was investigated in primary cultures of porcine intermediate lobe (IL) cells maintained in serum-free medium. POMC gene expression was evaluated by the dot blot hybridization assay with a 32P-labeled DNA probe complementary to the full-length sequence of porcine POMC mRNA. Treatment of IL cells for 24 h with the calmodulin (CAM) antagonists W7 and W13 reduced POMC mRNA levels by a maximum of 50% in a dose-dependent manner (ED50 approximately 10(-8) M). Accumulation of alpha-melanocyte-stimulating hormone (alpha-MSH) in the medium was also depressed by 50% after 8 h of treatment. The role of protein kinase C (PKC) was investigated by depleting the IL cell PKC content with phorbol ester treatment. Phorbol 12-myristate 13-acetate (PMA) at 5 X 10(-8) M induced a rapid translocation of cytoplasmic PKC activity toward the membrane. After 12 h of PMA treatment, PKC activity was undetectable in either the cytoplasmic or the particulate fractions. The same dose of PMA induced a time-dependent decrease in POMC mRNA levels (50% inhibition after 24 h). The same effect was seen with the phorbol ester phorbol 12,13-dibutyrate at 5 X 10(-8) M, whereas the inactive phorbol ester 4 alpha-phorbol at 5 X 10(-8) M was without effect after 24 h of treatment. PMA treatment had a biphasic effect on alpha-MSH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Protein kinase C alterations in the fetal rat brain after global ischemia.

Marked changes in the intracellular localization of brain protein kinase C are evident after global ischemia generated by the restriction of the placental blood flow in the near-term rat embryo. A rapid (5 min) ischemia-dependent translocation of the enzyme from the cytosol to the particulate membrane fraction, which is completely reversible upon reperfusion, is observed. After 30 min of ischemia, substantial losses in protein kinase C activity and content as measured by [3H]phorbol dibutyrate binding are apparent. This is accompanied by a marked increase of a Ca2+-phosphatidylserine-independent kinase activity, already evident after 5 min of ischemia. By 15 or 30 min the total activity of the latter enzyme is equally distributed between the particulate and the cytosol fractions and is more than 3-fold higher in ischemic in comparison to naive animals. Activation and possible deregulation of protein kinase C are proposed to represent an initial step in the pathophysiology of brain ischemia.

Animals↗
PubMed1986

Separation from protein kinase C--a calcium-independent TPA-activated phosphorylating system.

A calcium-independent but 12-O-tetradecanoylphorbol-13-acetate (TPA)- or diacylglycerol-activated phospholipid-dependent phosphorylating activity has been separated from protein kinase C. This has been made possible by employing calcium-dependent hydrophobic interaction chromatography. The material bound to phenyl-Sepharose in the presence of calcium at low ionic strength was eluted with EGTA and was protein kinase C. While the unbound material passing through the phenyl-Sepharose column showed no appreciable protein kinase C activity, instead it had a high phosphorylating activity manifested in the absence of calcium and in the presence of TPA plus phospholipid. The identification of this phosphorylating activity, distinct from protein kinase C, leads to important clues to cellular responses monitored by TPA in the absence of calcium.

Animals↗
PubMed1986

[Neurotropic action of adrenocorticotropic hormone].

The adrenocorticotropic hormone (ACTH) is produced within the cell body of hypothalamic neurons by proteolytic cleavage of its large precursor molecule, pro-opiomelanocortin. These neurons distribute ACTH-containing nerve endings throughout the central nervous system. ACTH is able to evoke motor and behavioural responses and to modify neuronal metabolism. Since ACTH has been shown to regulate glucose uptake and utilization, its implication in the adaptative response to stress situations, such as cerebral hypoxia, deserves further investigations.

Adrenocorticotropic Hormone↗
PubMed1985

Regulation of cyclic AMP and cyclic GMP levels by adrenocorticotropic hormone in cultured neurons.

The effect of adrenocorticotropic hormone (ACTH) on the intracellular concentration of cyclic nucleotides was studied in cultures of neurons from embryonic chick cerebral hemispheres. Incubation of neurons with ACTH(1-24) in the presence of phosphodiesterase inhibitor isobutylmethylxanthine resulted in a sustained increase in cyclic AMP while rise in cyclic GMP level was transient. The values obtained for half-maximal stimulation were 0.5 microM and 0.03 nM for cyclic AMP and cyclic GMP respectively. Concomitantly, ACTH(1-24) stimulated guanylate cyclase activity (half-maximal stimulation at 0.02 nM). These results suggest the existence of two distinct populations of ACTH receptors in neurons and provide the first evidence that cyclic GMP does mediate the action of ACTH in neurons.

Adrenocorticotropic Hormone↗
PubMed1985

Regulation of deoxyglucose uptake by adrenocorticotropic hormone in cultured neurons.

The influence of ACTH and some of its N-terminal related peptides was investigated on the uptake of (3H)-2-deoxy-D-glucose in pure cultures of neurons from chick embryo cerebral hemispheres. ACTH influences deoxyglucose uptake in a time and dose-dependent fashion. The stimulation of deoxyglucose uptake is observed after a delay of 6-8 h and requires active protein synthesis. ACTH does not affect deoxyglucose in non-neuronal cells (astroglial cells, hepatocytes, myoblasts, fibroblasts). The effect of various peptide hormones, neuropeptides and growth factors, active in the central nervous system or other tissues, has also been examined. None of these were able to stimulate deoxyglucose uptake, suggesting that the regulation of hexose uptake in neurons is specific for the ACTH-related peptides.

Adrenocorticotropic Hormone↗
PubMed1983

Long-term culture of neurones from human cerebral cortex in serum-free medium.

A method for cultivating neurones from the fetal human central nervous system in the absence of glial cells is described. Brain cells from 15-18-week-old human fetuses are plated on polylysine-coated surfaces and grown in a serum-free hormonally-defined medium. About 98% of the cells were identified as neurones using tetanus toxin as a marker. The cultures survive for up to 7 weeks and develop an extremely complex network of neurites.

Cells, Cultured↗
PubMed1983

Influence of adrenocorticotropic hormone on the growth of isolated neurons in culture.

The present study reports the influence of adrenocorticotropic hormone (ACTH) on the development of cultured neurons from chick embryo cerebral hemispheres. Cultures were initiated in serum-supplemented medium and then transferred to serum-free hormonally-defined medium containing various concentrations of ACTH1--24. The effects of ACTH on the light microscopic features, metabolic activity and permeation properties were examined. The results demonstrate that ACTH exerts a trophic action on the neurons.

Adrenocorticotropic Hormone↗
PubMed1983

Presence of somatostatin, enkephalins, and substance P-like peptides in cultured neurons from embryonic chick cerebral hemispheres.

The presence of peptides in pure cultures of neurons from 8-day-old chick embryo cerebral hemispheres has been investigated by means of specific radioimmunoassays and chromatographic purification. Somatostatin, Met-enkephalin, Leu-enkephalin, and substance P immunoreactive substances have been detected in 8-day-old cultures grown in serum-free culture medium. The peptides were present in the cellular extracts, as well as in the culture medium extracts. beta-Endorphin, thyroliberin, luteinizing hormone-releasing hormone, and ACTH could not be detected. The largest amount was accounted by somatostatin (48 +/- 2 ng/mg protein). Some 60% of the somatostatin-immunoreactive material was found in the culture medium. Met-enkephalin, Leu-enkephalin, and substance P were present at lower concentrations: 1.61 +/- 0.27, 0.24 +/- 0.02, and 0.14 +/- 0.005 ng/mg protein, respectively. The identities of somatostatin- and enkephalin-immunoreactive materials were confirmed by high pressure liquid chromatography. The findings suggest that cultured neurons that express dopaminergic and GABAergic properties contain peptides similar, if not identical, to somatostatin, Met-enkephalin, Leu-enkephalin, and substance P.

Animals↗
PubMed1982

Efflux of choline from neurons and glia in culture.

The efflux of radioactive choline from exclusively neuronal or glial cell cultures was dependent upon the concentrations of choline present in the cells and in the incubation medium, suggesting the possible presence of a homoexchange phenomenon between influx and efflux. The ionic dependence of the outward movement of choline from these cells showed that is could be stimulated by high K+ concentrations and by the absence of Ca2+. In glial cells, however, the efflux of choline was increased with a much lower concentration of K+ compared to neurons. The result may suggest that during nerve stimulation the release of K+ from neurons could stimulate, from glia, the efflux of choline which would then be taken up in neurons.

Animals↗
PubMed1982

Possible role of sialocompounds in the uptake of choline into synaptosomes and nerve cell cultures.

Incubation of primary nerve cell cultures and of crude synaptosomal preparations with neuraminidase released sialic acid from both gangliosides and sialoglycoproteins. After this treatment, the pattern of ganglioside distribution was severely modified with a decrease of polysialogangliosides (GD1b, GT1b, Gt1L, GQ1) and a dramatic increase in monosialoganglioside GM1. The choline influx into neuraminidase treated cells and organelles was reduced by 30--50% but the efflux was unmodified. In particular the high affinity mechanism of choline uptake disappeared and the low affinity mechanism was modified in both cases. The disappearance of the high affinity uptake mechanism was not followed by a decreased acetylcholine synthesis as it should be if the current theories on choline uptake and acetylcholine synthesis are correct. Our present data thus confirm our previous hypothesis that choline metabolism regulates choline uptake rather than the other way round as is suggested by the theories most widely accepted at present. Choline uptake was unaffected by pretreatment of cells and organelles with tetanus toxin suggesting that the effect of neuraminidase on the choline uptake were either mediated through glycoproteins or through gangliosides other than those which bind to tetanus toxin (GD1b and GT1b). Several speculative models for explaining the effect of neuraminidase on choline uptake are proposed.

Animals↗