Multiscale assessment of patterns of avian species richness

The search for a common cause of species richness gradients has spawned more than 100 explanatory hypotheses in just the past two decades. Despite recent conceptual advances, further refinement of the most plausible models has been stifled by the difficulty of compiling high-resolution databases at continental scales. We used a database of the geographic ranges of 2,869 species of birds breeding in South America (nearly a third of the world's living avian species) to explore the influence of climate, quadrat area, ecosystem diversity, and topography on species richness gradients at 10 spatial scales (quadrat area, ≈12,300 to ≈1,225,000 km2). Topography, precipitation, topography × latitude, ecosystem diversity, and cloud cover emerged as the most important predictors of regional variability of species richness in regression models incorporating 16 independent variables, although ranking of variables depended on spatial scale. Direct measures of ambient energy such as mean and maximum temperature were of ancillary importance. Species richness values for 1° × 1° latitude-longitude quadrats in the Andes (peaking at 845 species) were ≈30–250% greater than those recorded at equivalent latitudes in the central Amazon basin. These findings reflect the extraordinary abundance of species associated with humid montane regions at equatorial latitudes and the importance of orography in avian speciation. In a broader context, our data reinforce the hypothesis that terrestrial species richness from the equator to the poles is ultimately governed by a synergism between climate and coarse-scale topographic heterogeneity.

Genetic variation in vulnerability to the behavioral effects of neonatal hippocampal damage in rats.

We explored how two independent variables, one genetic (i.e., specific rat strains) and another environmental (i.e., a developmental excitotoxic hippocampal lesion), contribute to phenotypic variation. Sprague-Dawley (SD), Fischer 344 (F344), and Lewis rats underwent two grades of neonatal excitotoxic damage: small and large ventral hippocampal (SVH and LVH) lesions. Locomotion was tested before puberty [postnatal day 35 (P35)] and after puberty (P56) following exposure to a novel environment or administration of amphetamine. The behavioral effects were strain- and lesion-specific. As shown previously, SD rats with LVH lesions displayed enhanced spontaneous and amphetamine-induced locomotion as compared with controls at P56, but not at P35. SVH lesions in SD rats had no effect at any age. In F344 rats with LVH lesions, enhanced spontaneous and amphetamine-induced locomotion appeared early (P35) and was exaggerated at P56. SVH lesions in F344 rats resulted in a pattern of effects analogous to LVH lesions in SD rats--i.e., postpubertal onset of hyperlocomotion (P56). In Lewis rats, LVH lesions had no significant effect on novelty- or amphetamine-induced locomotion at any age. These data show that the degree of genetic predisposition and the extent of early induced hippocampal defect contribute to the particular pattern of behavioral outcome. These results may have implications for modeling interactions of genetic and environmental factors involved in schizophrenia, a disorder characterized by phenotypic heterogeneity, genetic predisposition, a developmental hippocampal abnormality, and vulnerability to environmental stress.