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Concanavalin A enhances quisqualate-induced calcium influx in cerebellar granule cells in culture

100%

Danysz W., Raulli R., Wroblewski J. T.

Acta Neurobiologiae Experimentalis

1996

vol. 56

issue 3

649-656

In primary cultures of cerebellar granule cells kainate produced marked influx of 45Ca2+, partially sensitive to the N-methyl-D-aspartate (NMDA) antagonist, 3-(?)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), indicating involvement of an NMDA receptor-sensitive component that may be secondary to kinate-induced glutamate release.Sodium removal partially inhibited kainate's effect.Quisqualate also produced influx of 45Ca2+, but with lower efficiacy and higher potency than kainate.This action of quiqualate was uneffected by CPP and by sodium removal.Preincubation of cells with the plant lectin concavalin A(Con A), but not with irs succinyl derivative, enhanced quisqualate -induced calcium influx, and to a lesser extend kainate' effect.Inclusion of quisqualate in preincubation medium antagonized Con A potention of quisqualate response.Also Con A was ineffective when included in the incubation medium only, without preincubation.Preincubation of rat brain cortical membranes with Con A but not with succinyl Con A increased the binding of the AMPA receptor agonist. The results suggest that Con A enhancement of quisqualate response possibly involves the modification of an AMPA recogintion site requires preincubation in the absence of an agonist (here quisqualate).

Nicotinamide and 1-methylnicotinamide reduce homocysteine neurotoxicity in primary cultures of rat cerebellar granule cells

86%

Slomka M., Zieminska E., Lazarewicz J. W.

Acta Neurobiologiae Experimentalis

2008

vol. 68

issue 1

1-9

Nicotinamide is an important cofactor in many metabolic pathways and a known neuroprotective substance, while its methylated product, 1-methylnicotinamide, is a suspected neurotoxin. Homocysteine is a risk factor in Alzheimer's disease and neurodegeneration, causing inhibition of methylation processes and inducing excitotoxicity. In this study, using primary cultures of rat cerebellar granule cells and propidium iodide staining, we investigated the neurotoxicity of nicotinamide and 1-methylnicotinamide, and their neuroprotective potential in acute and sub-acute homocysteine neurotoxicity. Our results demonstrated that nicotinamide and 1-methylnicotinamide applied for 24 h to cultures at concentrations of up to 25 mM had no effect on neuronal viability. Moreover, nicotinamide at concentrations of 5?20 mM and 1-methylnicotinamide at 1?10 mM applied to cells 24 h before, and for 24 h after an acute 30 min application of 25 mM D,L homocysteine, reduced neuronal damage. 1-Methylnicotinamide at concentrations of 250 and 500 ?M showed neuroprotective activity during a sub-acute 24-h exposure to 2.5 mM D,L-homocysteine, while 5 and 25 mM nicotinamide also evoked neuroprotection. These findings do not support suggestions that 1-methylnicotinamide may act as an endogenous neurotoxic agent; rather, they indicate the neuroprotective ability of nicotinamide and 1-methylnicotinamide in homocysteine neurotoxicity. The exact mechanisms of this neuroprotection are unclear and require further investigation.

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2 Acta Neurobiologiae Experimentalis

1 2008

1 1996

1 Danysz W.

1 Lazarewicz J. W.

1 Raulli R.

1 Slomka M.

1 Wroblewski J. T.

1 Zieminska E.

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Concanavalin A enhances quisqualate-induced calcium influx in cerebellar granule cells in culture

Nicotinamide and 1-methylnicotinamide reduce homocysteine neurotoxicity in primary cultures of rat cerebellar granule cells