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M Schorderet

Publications and source records attributed to M Schorderet.

At least 19 recordsLinked to original sources
PubMed2000

Transgenic Arabidopsis plants expressing a fungal cutinase show alterations in the structure and properties of the cuticle and postgenital organ fusions.

A major structural component of the cuticle of plants is cutin. Analysis of the function of cutin in vivo has been limited because no mutants with specific defects in cutin have been characterized. Therefore, transgenic Arabidopsis plants were generated that express and secrete a cutinase from Fusarium solani f sp pisi. Arabidopsis plants expressing the cutinase in the extracellular space showed an altered ultrastructure of the cuticle and an enhanced permeability of the cuticle to solutes. In addition, pollen could germinate on fully differentiated leaves of cutinase-expressing plants but not on control leaves. These differences coincided with strong postgenital organ fusions. The junctions of the fusions contained pectic polysaccharides. As fused organs grew apart from each other, organ deformations and protrusions of epidermal cells developed at positions with high mechanical stress. These results demonstrate that an intact cutin layer not only is important for plant-environment interactions but also prevents fusions between different plant organs and is therefore necessary for normal epidermal differentiation and organ formation.

Arabidopsis↗
PubMed1998

Protective effect of neurotrophic factors, neuropoietic cytokines and dibutyryl cyclic AMP on hydrogen peroxide-induced cytotoxicity on PC12 cells: a possible link with the state of differentiation.

We present evidence that the survival of PC12 cells exposed to hydroxyl radicals generated by hydrogen peroxide applied for 30 min at 1 mM was effective when they were differentiated in response to Nerve Growth Factor (NGF) and/or other inducers of neurite outgrowth such as basic-fibroblast growth factor and dibutyryl cyclic AMP. The time- and dose-dependent differentiation triggered by NGF was (1) markedly increased by basic fibroblast growth factor, interleukin-6 or dibutyryl cyclic AMP; (2) diminished by leukemia inhibitory factor or ciliary neurotrophic factor; (3) not potentiated by insulin-like growth factor I or progesterone. The influence of these various factors and agents on PC12 cells was evaluated by the estimation of neurite outgrowth, whereas their possible protective effects were assessed by the measurement of cell survival. Our results would indicate that the factors and agents that induced differentiation were also able to protect the cells against an oxidative stress.

Animals↗
PubMed1997

Structural cell-wall proteins in protoxylem development: evidence for a repair process mediated by a glycine-rich protein.

Polyclonal antibodies were used to localize structural cell-wall proteins in differentiating protoxylem elements in etiolated bean and soybean hypocotyls at the light- and electron-microscopic level. A proline-rich protein was localized in the lignified secondary walls, but not in the primary walls of protoxylem elements, which remain unlignified, as shown with lignin-specific antibodies. Secretion of the proline-rich protein was observed during lignification in different cell types. A glycine-rich protein (GRP1.8) was specifically localized in the modified primary walls of mature protoxylem elements and in cell corners between xylem elements and xylem parenchyma cells. The protein was secreted by Golgi bodies both in protoxylem cells after the lignification of their secondary walls and in the surrounding xylem parenchyma cells. The modified primary walls of protoxylem elements were visualized under the light microscope as filaments or sheets staining distinctly with the protein stain Coomassie blue. Electron micrographs of these walls show that they are composed of an amorphous material of moderate electron-density and of polysaccharide microfibrils. These materials form a three-dimensional network, interconnecting the ring- or spiral-shaped secondary wall thickenings of protoxylem elements and xylem parenchyma cells. The results demonstrate that the modified primary walls of protoxylem cells are not simply breakdown products due to partial hydrolysis and passive elongation, as believed until now. Extensive repair processes produces cell walls with unique staining properties. It is concluded that these walls are unusually rich in protein and therefore have special chemical and physical properties.

Antibodies↗
PubMed1995

Alzheimer's disease: fundamental and therapeutic aspects.

Alzheimer's disease is the most common type of progressive and debilitating dementia affecting aged people. In some early--as well as late--onset familial cases, a genetic linkage with chromosomes 14, 21 (early-onset) or 19 (late-onset) has been indicated. Furthermore, a direct or indirect role has been attributed to normal or structurally altered amyloid beta-protein (concentrated in senile plaques) and/or excessively phosphorylated tau protein (located in neurofibrillary tangles). Degeneration of cholinergic neurons and concomitant impairment of cortical and hippocampal neurotransmission lead to cognitive and memory deficits. Several compounds are being tested in attempts to prevent and/or cure Alzheimer's disease, including tacrine, which has very modest efficacy in a sub-group of patients, and new acetylcholinesterase inhibitors. Pilot experiments have also been launched using nerve growth factor (NGF) to prevent or stabilize the processes of cholinergic pathway degeneration. Alternatively, antioxidants, free radical scavengers and/or non steroidal anti-inflammatory agents may be screened as potential therapies for neurodegenerative diseases induced by multiple endogenous and/or exogenous factors. The recent use of transgenic mice, in parallel with other genetic, biochemical and neurobiological systems, in vivo and/or in vitro (cell cultures), should accelerate the discovery and development of specific drugs for the treatment of Alzheimer's disease.

Alzheimer Disease↗
PubMed1995

Okadaic acid modulates exocytotic and transporter-dependent release of dopamine in bovine retina in vitro.

Bovine retinas were isolated for the study of the modulation of exocytotic and transporter-dependent release of dopamine (DA) in vitro. Endogenous DA was measured in the medium using HPLC with electrochemical detection under successive incubations with transfers in fresh medium every 30 min. As expected, potassium caused a calcium-dependent exocytotic liberation of DA. Amphetamine or tyramine induced a calcium-independent release by reversing DA transport across the plasma membrane. Okadaic acid, a specific inhibitor of phosphatases 1 and 2A, induced a slight but significant DA release in the absence of calcium. Furthermore, the toxin increased potassium-, amphetamine- or tyramine-induced DA release independently of extracellular calcium. In addition, okadaic acid completely annulled the ability of a calcium-free extracellular environment to inhibit the potassium-induced DA release. Finally, the toxin prevented the time-dependent decline in the efficacies of amphetamine or tyramine to release DA. In agreement with proposed schemes described for rat striatum, the results of the present study confirmed the existence of distinct release modes of DA in bovine retina. The results obtained with okadaic acid suggest that phosphatase 1 and/or phosphatase 2A constitute part of a direct or indirect mechanism to inhibit both exocytotic and transporter-dependent DA release.

Animals↗
PubMed1995

Effects of YM 435 and A 77636 on dopamine D-1 receptors in bovine retina in vitro.

1. Homogenates of bovine retinas were used to study the capacities of two new dopamine (DA) receptor agonists, e.g. YM 435 and A 77636, to interact with D1 receptors. 2. Adenylate cyclase experiments. YM 435 and A 77636 enhanced cAMP accumulation, with EC50 values of 1.97 microM and 22.9 nM, respectively. The receptor-mediated nature of the effects of these two novel D1 agonists was shown by the abilities of both SCH 23390 or (+)-butaclamol to inhibit the agonist-induced increase of cAMP formation. 3. Binding experiments. The same agonists were also tested for competition with 3H-SCH 23390 for binding to D1 receptors. IC50 values for YM 435 and A 77636 were 8.15 microM and 6.15 nM, respectively. 4. The results of the present report demonstrate the suitability of bovine retina in vitro to evaluate the specificity of new DA D1 agonists at the receptor level.

Adamantane↗
PubMed1994

Nitric oxide modulates endogenous dopamine release in bovine retina.

A study of the possible modulation by nitric oxide (NO) of endogenous dopamine (DA) release was performed in bovine retina in vitro. NO synthase activity was measured in retinal homogenates and totally blocked by L-nitroarginine methyl ester (L-NA). Intact retinas were also exposed to hydroxylamine, an NO-generator which significantly decreased both basal and potassium-induced liberation of DA. In contrast, dibutyryl cGMP was ineffective. Furthermore, L-NA was able to increase basal DA release, its effects being potentiated in calcium free medium. Taken together, these results suggest that endogenous NO regulates DA release via cGMP independent mechanisms.

Amino Acid Oxidoreductases↗
PubMed1993

["Cerebro-active" drugs].

The prevention and treatment of age related mental diseases, including cerebrovascular dementia and Alzheimer's disease, are complicated by diagnostic problems and by the lack of specificity of the so-called "cerebroactive" drugs. These agents are frequently prescribed at the patient's or the relatives' request, without clear-cut evidence for their therapeutic efficacy. The economic consequences of these usually long term treatments should also be taken into consideration. A few "cerebroactive" agents may marginally slow down or modulate the progression of the various neuropathological processes: for example "vasoactive" drugs (such as pentoxifylline) in cerebrovascular dementia and "nootropic" drugs (such as co-dergocrine) when advanced and irreversible mental impairment has not yet occurred. There is currently no effective treatment for Alzheimer's disease. The results obtained with neurotransmitter replacement therapy, e.g. with the acetylcholinesterase inhibitor tacrine, have generally been disappointing, even if a small clinical improvement has been observed in a few selected patients.

Aged↗
PubMed1993

Agonist-induced desensitization of dopamine D-1 receptors in bovine retina and rat striatum.

We have investigated agonist-induced desensitization of dopamine (DA) D-1 receptor mediated accumulation of adenosine 3':5'-cyclic monophosphate (cAMP) in bovine retinas and rat striata in vitro. Tissues were exposed to various pharmacological agents for 60 min, washed and homogenized. D-1 agonist-promoted accumulation of cAMP in the presence of adenosine 5'-triphosphate (ATP) and 5'-guanylylimidodiphosphate (GppNHp) was then measured. Retinas and striata incubated with DA or (+) SKF 38393 (100 microM each) displayed diminished capacities to accumulate cAMP when they were re-exposed to the same drugs. As expected, retinas and striata treated wtih (+) SKF 38393 also showed an attenuated formation of cAMP when restimulated with DA. In addition, D-1 receptors in retinas that had been treated with quinpirole, a D-2 agonist, did not become desensitized. Furthermore, 0.2 microM SCH 23390 prevented D-1 receptor subsensitivity caused by 100 microM DA. Interestingly, retinas and striata incubated with forskolin, a direct stimulator of adenylyl cyclase, also displayed a diminished enzymatic response to restimulation by the same agent, as well as by DA. Additionally, retinas incubated with 100 microM DA were refractory to forskolin-induced cAMP formation. Finally, results of 3H-SCH 23390 binding to control and DA-treated retinas indicated that agonist treatment did not induce significant changes in either receptor density or binding affinity. The data indicate that bovine retinas and striatal slices in vitro are suitable to investigate various aspects of the desensitization of neuronal responses to DA D-1 agonists or forskolin.

Adenylyl Cyclases↗
PubMed1991

Dark-induced supersensitivity of dopamine D-1 and D-2 receptors in rat retina.

Light deprivation of rat retina leads to a rapid (within 6 h) development of a state of supersensitivity (upregulation) of dopamine D-1 receptors (positively coupled to adenylate cyclase), which are essentially involved in the modulation by light of the electrical activity and communication between horizontal cells. In contrast, the supersensitivity of D-2 receptors (negatively coupled to cAMP generating system) appears to develop only after 2 days (better after 4 days) of dark adaptation, although these receptors are linked to multiple light-dependent retinal functions. These results suggest the existence of different mechanisms of sensory adaptation for these two subtypes of dopamine receptors.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Retinal dopamine D1 and D2 receptors: characterization by binding or pharmacological studies and physiological functions.

1. In the retinal inner nuclear layer of the majority of species, a dopaminergic neuronal network has been visualized in either amacrine cells or the so-called interplexiform cells. 2. Binding studies of retinal dopamine receptors have revealed the existence of both D1- as well D2-subtypes. The D1-subtype was characterized by labeled SCH 23390 (Kd ranging from 0.175 to 1.6 nM and Bmax from 16 to 482 fmol/mg protein) and the D2-subtype by labelled spiroperidol (Kd ranging from 0.087 to 1.35 nM and Bmax from 12 to 1500 fmol/mg protein) and more selectively by iodosulpiride (Kd 0.6 nM and Bmax 82 fmol/mg protein) or methylspiperone (Kd 0.14 nM and Bmax 223 fmol/mg protein). 3. Retinal dopamine receptors have been also shown to be positively coupled with adenylate cyclase activity in most species, arguing for the existence of D1-subtype, whereas in some others (lower vertebrates and rats), a negative coupling (D2-subtype) has been also detected in peculiar pharmacological conditions implying various combinations of dopamine or a D2-agonist with a D1-antagonist or a D2-antagonist in the absence or presence of forskolin. 4. A subpopulation of autoreceptors of D2-subtype (probably not coupled to adenylate cyclase) also seems to be involved in the modulation of retinal dopamine synthesis and/or release. 5. Light/darkness conditions can affect the sensitivity of retinal dopamine D1 and/or D2-receptors, as studied in binding or pharmacological experiments (cAMP levels, dopamine synthesis, metabolism and release). 6. Visual function(s) of retinal dopamine receptors were connected with the regulation of electrical activity and communication (through gap junctions) between horizontal cells mediated by D1 and D2 receptor stimulation. Movements of photoreceptor cells and migration of melanin granules in retinal pigment epithelial cells as well as synthesis of melatonin in photoreceptors were on the other hand mediated by the stimulation of D2-receptors. 7. Other physiological functions of dopamine D1-receptors respectively in rabbit and in embryonic avian retina would imply the modulation of acetylcholine release and the inhibition of neuronal growth cones.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Bidirectional regulation of cAMP generating system by dopamine-D1 and D2-receptors in the rat retina.

Accumulation or inhibition of cAMP formation in response to dopamine or dopamine related drugs in the absence or in the presence of forskolin and/or IBMX was investigated in isolated rat retina. While the existence of D1-receptors (positively coupled with adenylate cyclase) was confirmed, D2-receptors (negatively coupled to adenylate cyclase) were also revealed by using a selective D1-antagonist (SCH 23390), a D2-agonist (LY 171555) or two D2-antagonists (S-sulpiride, spiroperidol). These results indicate that rat retina may be used for the study of both types of dopamine-receptors.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Accumulation of cyclic AMP elicited by vasoactive intestinal peptide is potentiated by noradrenaline, histamine, adenosine, baclofen, phorbol esters, and ouabain in mouse cerebral cortical slices: studies on the role of arachidonic acid metabolites and protein kinase C.

In mouse cerebral cortical slices, noradrenaline (NA) potentiates cyclic AMP (cAMP) accumulation elicited by vasoactive intestinal peptide (VIP) through alpha 1-adrenergic receptors. This synergism is inhibited by indomethacin, and the prostaglandins E2 and F2 alpha mimic the effect of NA. In the present study, we observed that the synergism between VIP and NA is not inhibited by the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) or the diacylglycerol-lipase inhibitor RHC 80267, thus further stressing the role of phospholipase A2 activation. Various neuroactive agents that potentiate the stimulatory effect of VIP on cAMP formation were also examined. As with NA, the potentiation by histamine and adenosine is inhibited by indomethacin. In contrast to NA, histamine, and adenosine, the synergistic interaction between phorbol esters and VIP on cAMP formation is abolished by H-7 but not by indomethacin. The potentiation by baclofen, a gamma-aminobutyric acidB receptor agonist, is partially inhibited by the 5-lipoxygenase inhibitor nafazatrom. The synergism between ouabain and VIP is reduced by H-7 but not by indomethacin and nafazatrom. These data indicate that the stimulation of cAMP formation elicited by VIP is under the modulation of various neuroactive agents that trigger diverse intracellular mechanisms to potentiate the effect of the peptide.

Adenosine↗
PubMed1987

Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on dopamine synthesis and release in the rabbit retina in vitro.

The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on the synthesis and release of dopamine (DA) was investigated in the retina of the rabbit in vitro. The results indicated that MPTP did not affect the synthesis of DA, but increased its release. Blockade of the activity of monoamine oxidase (MAO) with pargyline (100 microM) did not abolish the capacity of MPTP to release DA. Similarly, these pharmacological effects of MPTP were not dependent on the presence or absence of melanin.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Investigation of dopamine content, synthesis, and release in the rabbit retina in vitro: I. Effects of dopamine precursors, reserpine, amphetamine, and L-DOPA decarboxylase and monoamine oxidase inhibitors.

The basal catecholamine content of rabbit retina was determined by liquid chromatography with electrochemical detection (LC-EC) and 3,4-dihydroxyphenylethylamine (dopamine, DA) found to be the major catecholamine. The immediate DA precursor, 3,4-dihydroxyphenylalanine (L-DOPA), and the metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), were also detected at about 2.8% and 17% of DA levels, respectively. When added exogenously, L-tyrosine did not increase the rate of DA synthesis over the basal level. In contrast, exogenous L-DOPA led to a 3.5-fold increase in DA, and to a 20-fold increase in DOPAC content. The monoamine oxidase inhibitors pargyline and (-)-deprenyl differentially affected the degradation of DA, since 100 microM pargyline was apparently more effective than 100 microM (-)-deprenyl. Reserpine and (+/-)-amphetamine each induced a Ca2+-independent decrease of DA stores. The separate actions of reserpine and (+/-)-amphetamine in lowering tissue DA levels were additive, suggesting two separate pools of DA available for release from presynaptic stores. The present study demonstrates that the LC-EC technique may be used to investigate the modulation of the synthesis and release of retinal DA in vitro, without the prior uptake of radiolabelled transmitter.

3,4-Dihydroxyphenylacetic Acid↗