1. Augmentation and ionic mechanism of effect of beta-N-methylamino-L-alanine in presence of bicarbonate on membrane potential of Retzius nerve cells of the leech Haemopis sanguisuga
- Author
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Dusan Cemerikic, Vladimir Nedeljkov, and Srdjan Lopicic
- Subjects
Physiology ,Bicarbonate ,Neurotoxins ,Excitotoxicity ,medicine.disease_cause ,Biochemistry ,Membrane Potentials ,chemistry.chemical_compound ,Leeches ,medicine ,Animals ,Haemopis sanguisuga ,Molecular Biology ,Alanine ,Membrane potential ,Neurons ,biology ,Cyanobacteria Toxins ,Glutamate receptor ,Amino Acids, Diamino ,biology.organism_classification ,Bicarbonates ,chemistry ,Receptors, Glutamate ,CNQX ,Biophysics ,Ionotropic effect - Abstract
The role of neurotoxic non-protein amino acid beta-N-methylamino- l -alanine (L-BMAA) as a putative causative agent of Western pacific amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC) has recently been reinvigorated. In view of this data we have investigated the strength and mechanism of effect of L-BMAA in presence of 20 mmol/L bicarbonate (a cofactor for BMAA) on membrane potential of the Leech Haemopis sanguisuga . Our results show that L-BMAA has excitatory effect in bicarbonate containing solution, which is more potent than in nominally bicarbonate free solution. This potentiation by bicarbonate is L-BMAA specific, as it was not exhibited by beta-N-oxalylamino- l -alanine. The effect of L-BMAA was partially blocked by non-NMDA receptor antagonist CNQX. Application of L-BMAA caused a decrease in input membrane resistance, an increase of intracellular sodium activity, and a decrease of intracellular potassium activity. Present findings indicate that BMAA could initiate excitotoxicity through activation of non-NMDA ionotropic glutamate receptors.
- Published
- 2008