Grassland songbirds often nest in the same grassland-wetland complexes as waterfowl, particularly in a certain part of those complexes, namely, upland habitats surrounding wetlands. Although some wildlife management procedures directed at waterfowl, such as habitat enhancement or restoration, may also benefit songbirds , the impact of others, especially the control of waterfowl predators, remains difficult to predict. For example, most predators of waterfowl nests prey opportunistic ally on songbird nests, and removing these predators could directly increase songbird nesting success. Alternatively, small mammals such as mice and ground squirrels are important in the diet of many waterfowl-nest predators and can themselves be important predators of songbird nets. Thus. Removing waterfowl-nest predators could affect songbird nesting success through subsequent increases in small-mammal populations.

    In 1995 and 1996, researchers trapped and removed certain waterfowl-nest predators. primary raccoons and striped skunks, then observed subsequent survival rates for songbird nests. Surprisingly. They observed no significant effect on songbird nesting success. This may be due to several factors. Neither raccoons nor striped skunks consume ground squirrels, which are important predators of songbird nests. Thus, their removal may not have led to significant increases in populations of smaller predators. Additionally, both raccoons and striped skunks prefer wetlands and spend little time in upland habitats; removing these species may not have increased the nesting success of songbirds in the uplands enough to allow detection.

It was once believed that the brain was independent of metabolic processes occurring elsewhere in the body. In recent studies, however, we have discovered that the production and release in brain neurons of the neurotransmitter serotonin (neurotransmitters are compounds that neurons use to transmit signals to other cells) depend directly on the food that the body processes.

Our first studies sought to determine whether the increase in serotonin observed in rats given a large injection of the amino acid tryptophan might also occur after rats ate meals that change tryptophan levels in the blood. We found that, immediately after the rats began to eat, parallel elevations occurred in blood tryptophan, brain tryptophan, and brain serotonin levels. These findings suggested that the production and release of serotonin in brain neurons were normally coupled with blood-tryptophan increases. In later studies we found that injecting insulin into a rat’s bloodstream also caused parallel elevations in blood and brain tryptophan levels and in serotonin levels. We then decided to see whether the secretion of the animal’s own insulin similarly affected serotonin production. We gave the rats a carbohydrate-containing meal that we knew would elicit insulin secretion. As we had hypothesized, the blood tryptophan level and the concentrations of tryptophan and of serotonin in the brain increased after the meal.

Surprisingly, however, when we added a large amount of protein to the meal, brain tryptophan and serotonin levels fell. Since protein contains tryptophan, why should it depress brain tryptophan levels? The answer lies in the mechanism that provides blood tryptophan to the brain cells. This same mechanism also provides the brain cells with other amino acids found in protein, such as tyrosine and leucine. The consumption of protein increases blood concentration of the other amino acids much more, proportionately, than it does that of tryptophan. The more protein is in a meal, the lower is the ratio of the resulting blood-tryptophan concentration to the concentration of competing amino acids, and the more slowly is tryptophan provided to the brain. Thus the more protein in a meal, the less serotonin subsequently produced and released.