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Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

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Cell volume decrease as a link between azaspiracid-induced cytotoxicity and c-Jun-N-terminal kinase activation in

Carmen Vale¹, Kyriacos C Nicolaou, Michael O Frederick

¹Departamento de Farmacología, Facultad de Veterinaria, Universidad de Santiago de Compostela, Lugo 27002, Spain.

Toxicological Sciences : an Official Journal of the Society of Toxicology

|October 10, 2009

Summary

Marine toxins called azaspiracids (AZAs) cause neurotoxicity by disrupting ion fluxes and decreasing neuronal volume in immature neurons. Inhibiting these effects protected against AZA-1 toxicity and JNK activation.

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Area of Science:

Marine toxicology
Neuroscience
Cellular physiology

Background:

Azaspiracids (AZAs) are emerging marine toxins with increasing global distribution.
AZA-1, a predominant analog, exhibits significant neurotoxicity, particularly affecting the central nervous system.
Mussels are frequently implicated in AZA-related food poisoning, posing a growing human health concern.

Purpose of the Study:

To investigate the mechanism of AZA-1 neurotoxicity in primary cultured neurons.
To identify cellular targets and pathways involved in AZA-1-induced cytotoxicity.
To evaluate pharmacological interventions against AZA-1 neurotoxicity.

Main Methods:

Primary cultured neurons were used to assess AZA-1 effects on membrane potential and neuronal volume.
Pharmacological agents were employed to inhibit AZA-1-induced cytotoxic effects.
Levels of phosphorylated c-Jun-N-terminal kinase (JNK) were measured to assess cellular stress responses.

Main Results:

AZA-1 induced concentration-dependent hyperpolarization in immature cerebellar granule cells but not mature neurons.
AZA-1 decreased membrane depolarization evoked by high K+ in immature neurons.
Inhibition of ion fluxes using DIDS, SITS, NPPB, amiloride, or ouabain reduced AZA-1 neurotoxicity and JNK activation.
Short AZA-1 exposure decreased neuronal volume, an effect reversed by DIDS or amiloride.

Conclusions:

AZA-1 neurotoxicity involves disruption of ion fluxes in immature neurons.
The observed JNK activation is a secondary effect of AZA-1-induced decrease in cellular volume.
Pharmacological inhibition of ion transport may offer a protective strategy against AZA-1 toxicity.