Effect of moclobemide on rat brain monoamine oxidase A and B: Comparison with Harmaline and Clorgtline

Gerardy, J

doi:10.1016/0278-5846(94)90085-x

Cited by 9 publications

(5 citation statements)

References 12 publications

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“…This negative result is not dependent on a selective blockade of MAO A (Gerardy, 1994;Keller et al, 1987) in the presence of still-functioning MAO B. In fact, when MAO B were also inhibited by a pretreatment of the slices with deprenyl, moclobemide did not change the dopaminergic responses on the neurones.…”

Section: Moclobemidementioning

confidence: 59%

Tranylcypromine, but not moclobemide, prolongs the inhibitory action of dopamine on midbrain dopaminergic neurons: An in vitro electrophysiological study

Mercuri

Federici

Marinelli

et al. 2000

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Section: Moclobemidementioning

confidence: 59%

Tranylcypromine, but not moclobemide, prolongs the inhibitory action of dopamine on midbrain dopaminergic neurons: An in vitro electrophysiological study

Mercuri

Federici

Marinelli

et al. 2000

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“…Previous studies suggest that extracts of B. caapi may possess antiparkinsonian activity based on limited clinical experience in humans (Sanchez‐Ramos, ; Serrano‐Duenas et al, , ). This activity may relate to the monoamine oxidase inhibitory actions of the β‐carboline content of these extracts and to the subsequent effects that their actions have on dopamine metabolism and release in the striatum (Gerardy, ; Meneguz et al, ). However, alternative mechanisms have been proposed.…”

Section: Discussionmentioning

confidence: 99%

The effect of Banisteriopsis caapi (B. caapi) on the motor deficits in the MPTP‐treated common marmoset model of Parkinson's disease

Fisher

Lincoln

Jackson

et al. 2018

Phytotherapy Research

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Banisteriopsis caapi (B. caapi) contains harmine, harmaline, and tetrahydroharmine, has monoamine oxidase inhibitory activity, and has reported antiparkinsonian activity in humans when imbibed as a tea; however, its effects are poorly documented. For this reason, motor function was assessed in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated common marmosets following administration of B. caapi extract (28.4-113.6 mg/kg; po), harmine (0.1 and 0.3 mg/ kg; sc), and selegiline (10 mg/kg; sc), alone or with a submaximal dose of L-3,4-dihydroxyphenylalanine (L-DOPA; 4-7 mg/kg). L-DOPA reversed motor disability, increased locomotor activity, and induced moderate dyskinesia. B. caapi did not increase locomotor activity or induce dyskinesia but at 56.8 and 113.6 mg/kg improved motor disability. The L-DOPA response was unaltered by co-administration of B. caapi. Harmine (0.1 and 0.3 mg/kg) produced a mild improvement in motor disability without affecting locomotor activity or dyskinesia but had no effect on the L-DOPA-induced antiparkinsonian response. Selegiline (10 mg/kg) alone improved motor function to the same extent as L-DOPA, but with only mild dyskinesia, and did not alter the response to L-DOPA, although dyskinesia was reduced. The findings suggest that B. caapi alone has a mild antiparkinsonian effect but does not enhance the L-DOPA response or reduce dyskinesia.

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“…Enzyme activity was measured as described by Snyder & Hendley (1968) with minor modifications (Gerardy, 1994). In addition, minor changes were made in order to adapt the method to cell cultures: (1) After 3 h of incubation in Locke's solution in the presence of MAO‐A inhibitors (50 mm dishes), cortical cells (four pooled dishes per condition) were washed twice with 2 ml 0.25 M sucrose iced solution then scraped in the same solution (60 μl per dish).…”

Section: Methodsmentioning

confidence: 99%

Pirlindole and dehydropirlindole protect rat cultured neuronal cells against oxidative stress‐induced cell death through a mechanism unrelated to MAO‐A inhibition

Boland

Gerardy

Mossay

et al. 2002

British J Pharmacology

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1 It has been shown that the MAO (monoamine oxidase)-B inhibitor deprenyl (DPR, selegiline) protects some cell types against oxidative stress. By decreasing H 2 O 2 production, MAO-A inhibitors could also reduce oxidative stress. 2 This study reports the eect 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 mM FeSO 4 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-¯uorescence, 1 h incubation), lipoperoxidation (TBARS-¯uorescence, 6 h incubation) and mitochondrial function (MTT-test, 16 h incubation) were assessed. 4 PIR, DHP and TRO signi®cantly protected cultures (P50.05) against Fe 2+ -induced toxicity in a concentration-dependent manner. The EC 50s of these compounds were 6, 12 and 19 mM, respectively, in hippocampal cells. For cortical cell cultures incubated in the presence of iron and PIR or DHP, EC 50s were 5 and 6 mM respectively. All Hill coecients were close to unity. BRO, MCL and DPR were not protective in any type of culture. The IC 50s for the inhibition of MAO-A were 2, 2 and 0.2 mM for PIR, DHP and BRO, respectively. PIR, DHP and TRO, but not DPR, induced a signi®cant 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 eect seems unrelated to inhibition of MAO-A, but possibly involves free radical scavenging.

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Effect of moclobemide on rat brain monoamine oxidase A and B: Comparison with Harmaline and Clorgtline

Cited by 9 publications

References 12 publications

Tranylcypromine, but not moclobemide, prolongs the inhibitory action of dopamine on midbrain dopaminergic neurons: An in vitro electrophysiological study

Tranylcypromine, but not moclobemide, prolongs the inhibitory action of dopamine on midbrain dopaminergic neurons: An in vitro electrophysiological study

The effect of Banisteriopsis caapi (B. caapi) on the motor deficits in the MPTP‐treated common marmoset model of Parkinson's disease

Pirlindole and dehydropirlindole protect rat cultured neuronal cells against oxidative stress‐induced cell death through a mechanism unrelated to MAO‐A inhibition

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