Mercury causes degradation of spatial cognition in a model songbird species.

Mercury is a widespread pollutant of increasing global concern that exhibits a broad range of deleterious effects on organisms, including birds. Because the developing brain is well-known to be particularly vulnerable to the neurotoxic insults of mercury, many studies have focused on developmental effects such as on the embryonic brain and resulting behavioral impairment in adults. It is not well understood how the timing of exposure, for example exclusively in ovo versus throughout life, influences the impact of mercury. Using dietary exposure to environmentally relevant methylmercury concentrations, we examined the role that timing and duration of exposure play on spatial learning and memory in a model songbird species, the domesticated zebra finch (Taeniopygia guttata castanotis). We hypothesized that developmental exposure was both necessary and sufficient to disrupt spatial memory in adult finches. We documented profound disruption of memory for locations of hidden food at two spatial scales, cage- and room-sized enclosures, but found that both developmental and ongoing adult exposure were required to exhibit this behavioral impairment. Methylmercury-exposed birds made more mistakes before mastering the spatial task, because they revisited unrewarded locations repeatedly even after discovering the rewarded location. Contrary to our prediction, hippocampal volume was not affected in birds exposed to methylmercury over their lifetimes. The disruption of spatial cognition that we detected is severe and would likely have implications for survival and reproduction in wild birds; however, it appears that individuals that disperse or migrate from a contaminated site might recover later in life if no longer exposed to the toxicant.

No Effect of Lifelong Methylmercury Exposure on Oxidative Status in Zebra Finches (Taeniopygia guttata): A Demonstration of Methylmercury-Induced Selection?

Songbirds exposed to methylmercury (MeHg) often exhibit reduced reproductive success and cognitive abilities. To better understand whether oxidative stress plays a role, we dosed zebra finches (Taeniopygia guttata) with a contaminated (1.2 ppm MeHg-cysteine) or control diet for their entire lives, including during development in the egg. Levels of antioxidant enzymes [superoxide dismutase (SOD1 and SOD2)], oxidative damage (4-hydroxynonenal; 4-HNE), and antioxidant transcription factors [nuclear factor (erythroid-derived 2)-like 2; Nrf2] were measured in the liver and pectoralis muscle of adults. MeHg treatment did not affect levels of 4-HNE or liver SOD2 or Nrf2. Birds in the MeHg treatment differed significantly from controls in pectoralis SOD1 and Nrf2, and tended to differ in liver SOD1 and pectoralis SOD2; however, we detected no overall pattern of effect of MeHg on oxidative status in dosed finches. We suspect that this is a consequence of the differential survival of MeHg-tolerant birds.