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See detail11-Deoxycortisol impedes GABAergic neurotransmission and induces drug-resistant status epilepticus in mice
Kaminski, R. M.; Venkatesan, Kumar ULg; Mazzuferi, Manuela ULg et al

in Neuropharmacology (2011), 60(7-8), 1098-1108

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See detailbeta-carbolines induce apoptosis in cultured cerebellar granule neurons via the mitochondrial pathway
Hans, Grégory ULg; Malgrange, Brigitte ULg; Lallemend, François et al

in Neuropharmacology (2005), 48(1), 105-117

N-Butyl-beta-carboline-3-carboxylate (betaCCB) is, together with 2-methyl-norharmanium and 2,9-dimethylnorharmanium ions, an endogenously occurring beta-carboline. Due to their structural similarities ... [more ▼]

N-Butyl-beta-carboline-3-carboxylate (betaCCB) is, together with 2-methyl-norharmanium and 2,9-dimethylnorharmanium ions, an endogenously occurring beta-carboline. Due to their structural similarities with the synthetic neurotoxin 1-methy14-phenyl-1,2,3,6-tetrahydropyridine (MPTP), harman and norharman compounds have been proposed to be involved in the pathogenesis of Parkinson's disease. While also structurally related, betaCCB has received much less interest in that respect although we had previously demonstrated that it induces the apoptotic cell death of cultured cerebellar granule neurons (CGNs). Herein, we have investigated the molecular events leading to CGN apoptosis upon betaCCB treatment. We first demonstrated that betaCCB-induced apoptosis occurs in neurons only, most likely as a consequence of a specific neuronal uptake as shown using binding/uptake experiments. Then we observed that, in betaCCB-treated CGNs, caspases 9, 3 and 8 were successively activated, suegesing an activation of the mitochondrial pathway. Consistently, betaCCB also induced the release from the mitochondrial intermembrane space of two pro-apoptotic factors. i.e. cytochrome c and apotptosis inducing factor (AIF). Interestingly, no mitochondrial membrane depolarisation was associated with this release. suggesting a mitochondrial permeability transition pore-independent mechanism. The absence of any neuroprotective effect provided by two mPTP inhibitors. i.e. cyclosporine A and bongkrekic acid. further supported this hypothesis. Together. these results show that betaCCB is specifically taken up by neuronal cells where it triggers a specific permeabilization of the outer mitochondrial membrane and a subsequent apoptotic cell death. (C) 2004 Elsevier Ltd. All rights reserved. [less ▲]

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See detailEvidence for a Non-Gabaergic Action of Quaternary Salts of Bicuculline on Dopaminergic Neurones
Seutin, Vincent ULg; Scuvée-Moreau, Jacqueline ULg; Dresse, Albert ULg

in Neuropharmacology (1997), 36(11-12, Nov-Dec), 1653-7

Intracellular recordings were made from neurones, presumed to be dopaminergic, in the rat midbrain slice preparation. Bicuculline methiodide (BMI) and methochloride (BMC) reversibly blocked the slow ... [more ▼]

Intracellular recordings were made from neurones, presumed to be dopaminergic, in the rat midbrain slice preparation. Bicuculline methiodide (BMI) and methochloride (BMC) reversibly blocked the slow, apamin-sensitive component of the afterhyperpolarization in these cells. The IC50 for this effect was about 26 microM. In comparison, BMC antagonized the input resistance decrease evoked by muscimol (3 microM) with an IC50 of 7 microM. The base of bicuculline was less potent in blocking the slow afterhyperpolarization. SR95531 (2-[carboxy-3'-propyl]-3-amino-6-paramethoxy-phenyl-pyridaziniu m bromide), another competitive GABA(A) antagonist, and picrotoxin, a non-competitive GABA(A) antagonist, also blocked the action of muscimol (IC50s: 2 and 12 microM respectively), but had no effect on the afterhyperpolarization at a concentration of up to 100 microM. Moreover, 100 microM SR95531 did not affect the blockade of the afterhyperpolarization by BMC. This blockade persisted in the presence of tetrodotoxin and was apparently not due to a reduction of calcium entry, suggesting that it involved a direct action on the channels which mediate this afterhyperpolarization. These results strongly suggest that quaternary salts of bicuculline act on more than one target in the central nervous system. Thus, the involvement of GABA(A) receptors in a given effect cannot be proven solely on the basis of its blockade by these agents. [less ▲]

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See detailAcetaldehyde-induced changes in the monoamine and amino acid extracellular microdialysate content of the nucleus accumbens
Ward, Roberta J.; Colantuoni, Carlo; Dahchour, Abdelkhader et al

in Neuropharmacology (1997), 36(2), 225-232

The effect of an acute intraperitoneal (i.p.) injection of acetaldehyde, 20 mglkg or 100mg/kg, on the microdialysate content of both amino acids and monoamine was studied in the nucleus accumbens (NA) by ... [more ▼]

The effect of an acute intraperitoneal (i.p.) injection of acetaldehyde, 20 mglkg or 100mg/kg, on the microdialysate content of both amino acids and monoamine was studied in the nucleus accumbens (NA) by a microdialysis technique. Acetaldehyde (ACH) which was detectable at levels of 50-130 µmol/g brain tissue 10 min after injection, evoked a significantd ecrease in the extracellular microdialysis dopamine content, which was sustained for the period of the study, i.e. 120 min. Homovanillicacid, HVA, decreased significantly when the lower dose of ACH was administered while dihydrophenylaceticacid, DOPAC, showed no significant change with either dose of ACH during the period of the study. Serotonin levels decreased significantly after both doses of acetaldehyde, with significant increases of its major metabolite, hydroxyindolacetic acid, 5-HIAA, with the higher acetaldehyde dose. Taurine increased significantly, only during the first twenty minutes, after both doses of acetaldehyde, although neither of the excitatory amino acids assayed, glutamate and aspartate, nor the inhibitoryamino acid, GABA, showed any significant changes. Acetaldehyde clearly evokes significant perturbation in the monoamine content of the NA, such changes being the converse to those reported for monoamine after ethanol administration, which might indicate a negative reinforcement effect. [less ▲]

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