https://medweb4.unige.ch/labnic/papers/PV_Neuron2001.pdf

Effects of attention and emotion on face processing in the human brain: An event-related fMRI study

LELONG A., HEGARET H., SOUDANT P. AND BATES S.S. 2012. Pseudo-nitzschia (Bacillariophyceae) species, domoic acid and amnesic shellfish poisoning: revisiting previous paradigms. Phycologia 51: 168-216. DOI: 10.2216/11-37 Pseudo-nitzschia is a globally distributed diatom genus, some species of which produce domoic acid (DA), the neurotoxin that causes amnesic shellfish poisoning. This toxin killed at least three humans in 1987, launching numerous studies concerning the identification, distribution, ecology and physiology of Pseudo-nitzschia spp. Since previous reviews in 1998, knowledge has been gained about the fate of DA, including its accumulation by marine animals and its degradation by light and bacteria. Molecular techniques and more precise microscopy have enabled the description of new Pseudo-nitzschia species, 15 since 2002, including ones that are cryptic and pseudo-cryptic. An increasing number of the 37 identified species, including oceanic and coastal species, have been studied in laboratory culture. The sexual reproduction of 14 species has been documented. Fourteen species have now been shown to be toxigenic, although some strains are not always toxic under the testing conditions. The biotic and abiotic factors that modify DA production are reviewed, with a focus on how new discoveries have changed our original hypotheses about control mechanisms. Recent studies confirm that silicate and phosphate limitation trigger DA production. However, stress by low concentrations of iron or high concentrations of copper are newly discovered triggers, suggesting a trace-metal chelation role for DA. Organic sources of nitrogen (urea and glutamine), as well as changes in pH, CO2, salinity and bacterial concentration, also enhance DA production. Laboratory and field studies sometimes give divergent results for conditions that are conducive to toxin production. Gaps in knowledge include further information about the whole genome of Pseudo- nitzschia (including sexual stages), mechanisms of DA production and decline, presence or absence of a resting stage, heterotrophic ability, impact of viruses and fungi, and a more complete description of the ecological and physiological roles of DA.

Pseudo-nitzschia (Bacillariophyceae) species, domoic acid and amnesic shellfish poisoning: revisiting previous paradigms

Domoic acid was identified as the toxin responsible for an outbreak of human poisoning that occurred in Canada in 1987 following consumption of contaminated blue mussels [Mytilus edulis]. The poisoning was characterized by a constellation of clinical symptoms and signs. Among the most prominent features described was memory impairment which led to the name Amnesic Shellfish Poisoning [ASP]. Domoic acid is produced by certain marine organisms, such as the red alga Chondria armata and planktonic diatom of the genus Pseudo-nitzschia. Since 1987, monitoring programs have been successful in preventing other human incidents of ASP. However, there are documented cases of domoic acid intoxication in wild animals and outbreaks of coastal water contamination in many regions world-wide. Hence domoic acid continues to pose a global risk to the health and safety of humans and wildlife. Several mechanisms have been implicated as mediators for the effects of domoic acid. Of particular importance is the role played by glutamate receptors as mediators of excitatory neurotransmission and the demonstration of a wide distribution of these receptors outside the central nervous system, prompting the attention to other tissues as potential target sites. The aim of this document is to provide a comprehensive review of ASP, DOM induced pathology including ultrastructural changes associated to subchronic oral exposure, and discussion of key proposed mechanisms of cell/tissue injury involved in DOM induced brain pathology and considerations relevant to food safety and human health.

/pdf/domoic-acid-toxicologic-pathology-a-review-2wj94ep0sw.pdf

Domoic acid toxicologic pathology: a review.

Domoic acid: a fascinating marine toxin

The participation of NMDA and non-NMDA receptors in domoic acid-induced neurotoxicity was investigated in cultured rat cerebellar granule cells (CGCs). Neurons were exposed to 300 microM L-glutamate or 10 microM domoate for 2 h in physiologic buffer at 22 degrees C followed by a 22-h incubation in 37 degrees C conditioned growth media. Excitotoxic injury was monitored as a function of time by measurement of lactate dehydrogenase (LDH) activity in both the exposure buffer and the conditioned media. Glutamate and domoate evoked, respectively, 50 and 65% of the total 24-h increment in LDH efflux after 2 h. Hyperosmolar conditions prevented this early response but did not significantly alter the extent of neuronal injury observed at 24 h. The competitive NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid and the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX) reduced glutamate-induced LDH efflux totals by 73 and 27%, respectively, whereas, together, these glutamate receptor antagonists completely prevented neuronal injury. Domoate toxicity was reduced 65-77% when CGCs were treated with competitive and noncompetitive NMDA receptor antagonists. Unlike the effect on glutamate toxicity, NBQX completely prevented domoate-mediated injury. HPLC analysis of the exposure buffer revealed that domoate stimulates the release of excitatory amino acids (EAAs) and adenosine from neurons. Domoate-stimulated EAA release occurred almost exclusively through mechanisms related to cell swelling and reversal of the glutamate transporter. Thus, whereas glutamate-induced injury is mediated primarily through NMDA receptors, the full extent of neurodegeneration is produced by the coactivation of both NMDA and non-NMDA receptors. Domoate-induced neuronal injury is also mediated primarily through NMDA receptors, which are activated secondarily as a consequence of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor-mediated stimulation of EAA efflux.

Domoic Acid Neurotoxicity in Cultured Cerebellar Granule Neurons Is Mediated Predominantly by NMDA Receptors that Are Activated as a Consequence of Excitatory Amino Acid Release

M. Teresa Ferna´ndez-Sa´nchez

Papers

Domoic acid-containing toxic mussels produce neurotoxicity in neuronal cultures through a synergism between excitatory amino acids