Schreckstoff
In 1938, the Austrian ethologist Karl von Frisch made his first report on the existence of the chemical alarm signal known as Schreckstoff (fright substance) in minnows.
[1] This chemical alarm signal is released only when the sender incurs mechanical damage, such as when it has been caught by a predator, and is detected by the olfactory system.
Chemical alarm systems have been identified in a number of different taxa, including gastropods,[2] echinoderms,[3] amphibians[4] and fishes.
[5] The production of schreckstoff has been shown to be metabolically expensive and is therefore part of a conditional strategy that can only be employed by individuals with access to sufficient resources.
For example, young brook sticklebacks (Culaea inconstans) are more likely to be caught in minnow traps that have been baited with conspecific skin extracts than adults.
[10] This result indicates young brook sticklebacks do not make the association between schreckstoff and the potential presence of a predator as readily as adults.
It would be detrimental to a male to produce schreckstoff while building a nest, as it would inadvertently repel females, thereby decreasing the likelihood of obtaining a mate.
Direct evidence that schreckstoff inhibits the growth of aquatic pathogens and parasites would provide additional support for the immunity hypothesis.
Some evidence exists in support of the first assumption that the release of schreckstoff confers quantifiable advantages to the receivers of this chemical signal.
A laboratory experiment[16] revealed that fathead minnows exposed to conspecific schreckstoff survived 39.5% longer than controls when placed in a tank with a predatory northern pike (Esox lucius).
This finding suggests schreckstoff increases vigilance in receivers, resulting in a quicker reaction time following detection of the predator.
The second assumption, that individuals in the order Ostariophysi associate with close family members, does not appear to be supported by empirical evidence.
Fathead minnows have also been found to produce fewer epidermal alarm substance cells (and therefore less schreckstoff) when in the presence of familiar shoalmates.
In conclusion, evidence does not support the hypothesis that schreckstoff evolved because it bolstered the inclusive fitness of the sender through increased survival of kin.
This experiment revealed that schreckstoff extracted from the skin of fathead minnows attracted both northern pike (Esox lucius) and predatory diving beetles (Colymbetes sculptilis).
Support for this condition comes from the observation that many small fishes in natural populations exhibit scars, presumably from failed predator attempts.
A recent comprehensive study[27] revealed that exposure to parasites and pathogens that penetrate the skin of ostariophysans stimulated the production of alarm cells.
The role of schreckstoff in immune response was further strengthened by the finding that skin extracts from fathead minnows inhibited the growth of Saprolegnia ferax (a water mould) in culture.
In contrast, skin extracts from swordtails (Xiphophorus helleri), which are not believed to produce schreckstoff, increased S. ferax growth compared to controls.
[29] Furthermore, a follow-up study[30] treated fathead minnows with cortisol, a well-known immunosuppressant, which significantly reduced alarm cell investment in conjunction with leukocyte activity.
The results of these extensive studies strongly suggest schreckstoff's main function is to provide immunity against a number of environmental threats aimed at the fish's epidermis.
[31] Additionally, this finding indicates males are at a greater risk from UVB radiation, as well as parasite and pathogen infection, during the breeding season.
