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Research comment
Neurological deficits in stranded California sea lions
  1. Vanessa F. Hoard and
  2. Michael G. Janech
  1. Six Flags Discovery Kingdom, Vallejo, California, USA
  2. Hollings Marine Laboratory, Department of Biology, College of Charleston, Charleston, South Carolina, USA
  1. email: janechmg{at}cofc.edu

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California sea lions (Zalophus californianus) represent a population of marine mammals that has continued to grow since the enactment of the US Marine Mammal Protection Act in 1972. The US population is now estimated to consist of approximately 250,000 individuals,1 which is around carrying capacity.

As the sea lion population grew throughout the 1980s and 1990s, mass strandings were more commonly observed. One of the agents responsible for such strandings is domoic acid – an algal toxin.2 Domoic acid is the primary cause of neurological disease in California sea lions, acting through glutamate receptors and leading to hippocampal atrophy through chronic exposure. Hippocampal atrophy in sea lions is readily detectable by MRI (Fig 1) and appears to be a good, yet not always convenient, measure for classification of domoic acid toxicosis.3,4

Fig 1: MRI of a brain section from a California sea lion with domoic acid toxicosis. The red arrow indicates the hippocampus and the white arrow indicates the temporal horn of the left ventricle. The apparent thinning of the parahippocampal gyrus and hippocampal atrophy are characteristic of domoic acid toxicosis (Photo: Sophie Dennison)

The major challenges in diagnosing domoic acid toxicosis are that historical exposure cannot be accurately determined in wild animals and the environmental prevalence of the toxin does not always follow predictable patterns. Even if ingested, the amount of toxin may not be enough to elicit overt physiological signs that permit suspicion of exposure. In addition, estimating historical dosage or prevalence of exposure in wild sea lions is unrealistic, due to high clearance rates of the toxin from the body and lack of …

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