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See detailCharacterization of the neurotoxicity induced by the extract of Magnistipula butayei (Chrysobalanaceae) in rat: Effects of a new natural convulsive agent
Karangwa, Charles; Esters, Virginie ULg; Tits, Monique ULg et al

in Toxicon (2007), 49(8), 1109-1119

This study was designed to document convulsant and neurotoxic properties of extracts of a tropical tree, Magnistipula butayei subsp. Montana, and to investigate the involvement of the glutamatergic system ... [more ▼]

This study was designed to document convulsant and neurotoxic properties of extracts of a tropical tree, Magnistipula butayei subsp. Montana, and to investigate the involvement of the glutamatergic system in these effects. Continuous behavioral observations and electroencephalographic (EEG) records were obtained after per os administration of an aqueous extract of Magnistipula (MBMAE) in rats. MBMAE (800 mg/kg) induced behavioral changes resembling motor limbic seizures: staring and head tremor, automatisms, forelimb clonic movements and violent tonic-clonic seizures leading to death in all animals. Concomitantly, important seizure activity that gradually evolved to epileptiform activity was recorded on the EEG. Moreover, c-Fos immunohistochemistry has revealed an increased c-Fos expression in the dentate gyrus and in piriform, peri- and entorhinal cortices 2 and 4h after treatment. This expression pattern suggested that the mechanism of action for the MBMAE is similar to that observed in glutamate-induced models of epilepsy. The MBMAE increased cell death also in hippocampal cell cultures. Furthermore, the build-up of convulsive activity and epileptic discharges induced by MBMAE in rat were abolished by MK-801, an NMDA receptor antagonist. Our study suggests that MBMAE contains a potent toxin, with a powerful neurotoxic activity in rat, and corresponding to a new natural component(s) that act as an NMDA-mediated convulsant molecule. [less ▲]

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See detailLe coenzyme Q10: biochimie, physiopathologie de sa carence et interet potentiel d'une augmentation de ses apports.
Malchair, P.; Van Overmeire, Lionel ULg; Boland, André ULg et al

in Revue Médicale de Liège (2005), 60(1), 45-51

After a brief reminding of the synthesis and function of coenzyme Q10, this article tries to summarise the current state of knowledge about the consequences of its deficiency and about the potential ... [more ▼]

After a brief reminding of the synthesis and function of coenzyme Q10, this article tries to summarise the current state of knowledge about the consequences of its deficiency and about the potential benefits of an increased intake of this coenzyme. We then describe the arguments in favour of such an increase in cardiac diseases and in Parkinson's disease. [less ▲]

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See detailElectrophysiological characterization of the SK channel blockers methyl-laudanosine and methyl-noscapine in cell lines and rat brain slices
Scuvée-Moreau, Jacqueline ULg; Boland, André ULg; Graulich, Amaury ULg et al

in British Journal of Pharmacology (2004), 143(6), 753-764

We have recently shown that the alkaloid methyl-laudanosine blocks SK channel-mediated afterhyperpolarizations (AHPs) in midbrain dopaminergic neurones. However, the relative potency of the compound on ... [more ▼]

We have recently shown that the alkaloid methyl-laudanosine blocks SK channel-mediated afterhyperpolarizations (AHPs) in midbrain dopaminergic neurones. However, the relative potency of the compound on the SK channel subtypes and its ability to block AHPs of other neurones were unknown. Using whole-cell patch-clamp experiments in transfected cell lines, we found that the compound blocks SK1, SK2 and SK3 currents with equal potency: its mean IC(50)s were 1.2, 0.8 and 1.8 microM, respectively. IK currents were unaffected. In rat brain slices, methyl-laudanosine blocked apamin-sensitive AHPs in serotonergic neurones of the dorsal raphe and noradrenergic neurones of the locus coeruleus with IC(50)s of 21 and 19 microM, as compared to 15 microM in dopaminergic neurones. However, at 100 microM, methyl-laudanosine elicited a constant hyperpolarization of serotonergic neurones of about 9 mV, which was inconsistently (i.e. not in a reproducible manner) antagonized by atropine and hence partly due to the activation of muscarinic receptors. While exploring the pharmacology of related compounds, we found that methyl-noscapine also blocked SK channels. In cell lines, methyl-noscapine blocked SK1, SK2 and SK3 currents with mean IC(50)s of 5.9, 5.6 and 3.9 microM, respectively. It also did not block IK currents. Methyl-noscapine was slightly less potent than methyl-laudanosine in blocking AHPs in brain slices, its IC(50)s being 42, 37 and 29 microM in dopaminergic, serotonergic and noradrenergic neurones, respectively. Interestingly, no significant non-SK effects were observed with methyl-noscapine in slices. At a concentration of 300 microM, methyl-noscapine elicited the same changes in excitability in the three neuronal types than did a supramaximal concentration of apamin (300 nM). Methyl-laudanosine and methyl-noscapine produced a rapidly reversible blockade of SK channels as compared with apamin. The difference between the IC(50)s of apamin (0.45 nM) and methyl-laudanosine (1.8 microM) in SK3 cells was essentially due to a major difference in their k(-1) (0.028 s(-1) for apamin and >or=20 s(-1) for methyl-laudanosine). These experiments demonstrate that both methyl-laudanosine and methyl-noscapine are medium potency, quickly dissociating, SK channel blockers with a similar potency on the three SK subtypes. Methyl-noscapine may be superior in terms of specificity for the SK channels. [less ▲]

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See detailPre- and post-treatment with pirlindole and dehydropirlindole protects cultured brain cells against nitric oxide-induced death.
Boland, André ULg; Gérardy, Jean; Mossay, Danielle ULg et al

in European Journal of Pharmacology (2003), 466

We have previously shown that pirlindole and dehydropirlindole, two monoamine oxidase type-A inhibitors, protect cultured brain cells against iron-induced toxicity through a mechanism unrelated to ... [more ▼]

We have previously shown that pirlindole and dehydropirlindole, two monoamine oxidase type-A inhibitors, protect cultured brain cells against iron-induced toxicity through a mechanism unrelated to monoamine oxidase type-A inhibition. The current study was performed to test whether the protective effect of pirlindole and dehydropirlindole could be extended to a nitric oxide (NO)-induced insult. A comparison with other monoamine oxidase inhibitors (brofaromine, moclobemide and deprenyl) and with trolox was made. In a first series of experiments, rat hippocampal or cortical cultured cells were exposed to a drug for 3 h, then 5 muM sodium nitroprusside, a NO donor, was added and the incubation was continued for 16 h. Cell survival assessment showed that pirlindole, dehydropirlindole and trolox significantly protected cultures against NO-induced toxicity in a concentration-dependent manner with respective EC50's of 7, 3 and 17 muM. Similarly, pirlindole, dehydropirlindole or trolox, at a concentration of 50 muM, significantly decreased both intracellular peroxide production and lipoperoxidation. Other drugs were ineffective. In a post-hoc treatment protocol (3- or 6-h pre-incubation in the presence of sodium nitroprusside, then addition of one of the above mentioned compounds), only pirlindole and dehydropirlindole significantly improved cell survival in a concentration-dependent manner with respective EC50'S of 9 and 4 muM. The maximal protection in terms of cell survival was 90% and 78% after 3 and 6 h, respectively. They also reduced the production of both lipoperoxides and endoperoxides. Our results show that pirlindole and dehydropirlindole protect neurons against NO-induced toxicity at pharmacologically relevant concentrations. Moreover, their protective effect is still apparent when they are applied after the start of the insult. Therefore, our preclinical study suggests a new strategy that may be efficient to reduce NO-induced damage in the central nervous system. (C) 2003 Elsevier Science B.V. All rights reserved. [less ▲]

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See detailPirlindole and dehydropirlindole protect rat cultured neuronal cells against oxidative stress-induced cell death through a mechanism unrelated to MAO-A inhibition
Boland, André ULg; Gerardy, J.; Breeur, Danielle ULg et al

in British Journal of Pharmacology (2002), 135(3), 713-720

1 It has been shown that the MAO (monoamine oxidase)-B inhibitor deprenyl (DPR, selegiline) protects some cell types against oxidative stress. By decreasing H2O2 production, MAO-A inhibitors could also ... [more ▼]

1 It has been shown that the MAO (monoamine oxidase)-B inhibitor deprenyl (DPR, selegiline) protects some cell types against oxidative stress. By decreasing H2O2 production, MAO-A inhibitors could also reduce oxidative stress. 2 This study reports the effect of the MAO-A inhibitors, pirlindole (PIR), dehydropirlindole (DHP), brofaromine (BRO) and moclobemide (MCL) on primary-cultured brain cells exposed to iron-mediated toxicity. A comparison with trolox (TRO), a hydrosoluble vitamin-E analogue that protects against such an induced stress, was performed. 3 Rat hippocampal or cortical cultured cells were exposed either to 2 mum FeSO4 alone or in the presence of PIR, DHP, BRO, DPR, MCL or TRO. Cell survival (lactate-dehydrogenase measurements, 16 h incubation), intracellular peroxide production (DCF-fluorescence. I h incubation), lipoperoxidation (TBARS-fluorescence, 6 h incubation) and mitochondrial function (MTT-test, 16 h incubation) were assessed. 4 PIR, DHP and TRO significantly protected cultures (P<0.05) against Fe2+-induced toxicity in a concentration-dependent manner. The EC50s of these compounds were 6, 12 and 19 muM, respectively, in hippocampal cells. For cortical cell cultures incubated in the presence of iron and PIR or DHP, EC50s were 5 and 6 muM respectively. All Hill coefficients were close to unity. BRO, MCL and DPR were not protective in any type of culture. The IC50s for the inhibition of MAO-A were 2, 2 and 0.2 muM for PIR, DHP and BRO, respectively. PIR, DHP and TRO, but not DPR, induced a significant decrease in both intracellular peroxide production and lipoperoxidation. They also improved mitochondrial function. 5 These experiments show that PIR and DHP can protect hippocampal and cortical neurons against oxidative stress at pharmacologically relevant concentrations. This protective effect seems unrelated to inhibition of MAO-A, but possibly involves free radical scavenging. [less ▲]

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See detailEffect of intermittent and continuous exposure to electromagnetic fields on cultured hippocampal cells
Boland, André ULg; Gabriel, Danielle ULg; Breeur, Danielle ULg et al

in Bioelectromagnetics (2002), 23(2), 97-105

This study was designed to assess the effect of 50 Hz electromagnetic fields (EMFs) on hippocampal cell cultures in the presence or absence of either sodium nitroprusside (SNP, a NO donor) or Fe2+ induced ... [more ▼]

This study was designed to assess the effect of 50 Hz electromagnetic fields (EMFs) on hippocampal cell cultures in the presence or absence of either sodium nitroprusside (SNP, a NO donor) or Fe2+ induced oxidative stress. One week old cultured rat hippocampal cells were exposed to either intermittent EMFs (IEMFs, 50 Hz, 0-5 mT, 1 min ON/OFF cycles, repeated 10 times every 2 h, 6 times/day during 48 h) or continuous EMFs (CEMFs, 50 Hz, 0-5 mT for 48 h). In a second set of experiments, the effect on such EMFs applied in combination with oxidative stress induced by 0.5 microM Fe2+ or SNP was estimated. At the end of both sets of experiments, cell mortality was assessed by lactate dehydrogenase measurements (LDH). Neither type of exposure to EMFs was observed to modify the basal rate of cell mortality. The exposure to CEMFs in presence of either NO or Fe2+ did not induce any significant increase in cell death. However, when cells were exposed to EMFs in the presence of NO, we observed a significant increase in cell death of 11 and 23% (P<0.001) at 2.5 and 5 mT, respectively. This effect had some specificity because IEMFs did not modify the effect of Fe2+ on cell mortality. Although the effects of IEMFs reported in this study were only observed at very high intensities, our model may prove valuable in trying to identify one cellular target of EMFs. [less ▲]

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