Acute combined pressure and temperature exposures on a shallow-water crustacean: novel insights into the stress response and high pressure neurological syndrome.

Little is known about the ecological and physiological processes governing depth distribution limits in species. Temperature and hydrostatic pressure are considered to be two dominant factors. Research has shown that some marine ectotherms are shifting their bathymetric distributions in response to rapid anthropogenic ocean surface warming. Shallow-water species unable to undergo latitudinal range shifts may depend on bathymetric range shifts to seek refuge from warming surface waters. As a first step in constraining the molecular basis of pressure tolerance in shallow water crustaceans, we examined differential gene expression in response to acute pressure and temperature exposures in juveniles of the shallow-water shrimp Palaemonetes varians. Significant increases in the transcription of genes coding for an NMDA receptor-regulated protein, an ADP ribosylation factor, β-actin, two heat shock protein 70 kDa isoforms (HSP70), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were found in response to elevated pressure. NMDA receptors have been implicated in pathways of excitotoxic damage to neurons and the onset of high pressure neurological syndrome (HPNS) in mammals. These data indicate that the sub-lethal effects of acute barotrauma are associated with transcriptional disturbances within the nervous tissue of crustaceans, and cellular macromolecular damage. Such transcriptional changes lead to the onset of symptoms similar to that described as HPNS in mammals, and may act as a limit to shallow water organisms' prolonged survival at depth.