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Simulated predator stimuli reduce brain cell proliferation in two electric fish species, and . | LitMetric

AI Article Synopsis

  • The study investigates how exposure to predators and tail injuries impact brain cell proliferation in electric fish, expanding on previous findings that showed a correlation between predator presence and reduced cell growth.
  • Researchers simulated predator encounters through tail amputations and simulated chases to directly test effects on brain proliferation, measuring cell density and cortisol levels.
  • Results indicated that both tail amputation and simulated predator exposure reduced brain cell proliferation in the telencephalon, with varying cortisol responses, highlighting the complex relationship between stress, injury, and brain plasticity in electric fish.

Article Abstract

The brain structure of many animals is influenced by their predators, but the cellular processes underlying this brain plasticity are not well understood. Previous studies showed that electric fish () naturally exposed to high predator () density and tail injury had reduced brain cell proliferation compared with individuals facing few predators and those with intact tails. However, these field studies described only correlations between predator exposure and cell proliferation. Here, we used a congener and another electric fish to experimentally test the hypothesis that exposure to a predator stimulus and tail injury causes alterations in brain cell proliferation. To simulate predator exposure, we either amputated the tail followed by short-term (1 day) or long-term (17-18 days) recovery or repeatedly chased intact fish with a plastic rod over a 7 day period. We measured cell proliferation (PCNA+ cell density) in the telencephalon and diencephalon, and plasma cortisol, which commonly mediates stress-induced changes in brain cell proliferation. In both species, either tail amputation or simulated predator chase decreased cell proliferation in the telencephalon in a manner resembling the effect of predators in the field. In , cell proliferation decreased drastically in the short term after tail amputation and partially rebounded after long-term recovery. In , tail amputation elevated cortisol levels, but repeated chasing had no effect. In , tail amputation elevated cortisol levels in the short term but not in the long term. Thus, predator stimuli can cause reductions in brain cell proliferation, but the role of cortisol is not clear.

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Source
http://dx.doi.org/10.1242/jeb.158246DOI Listing

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