Mating avoidance in female olive baboons (Papio anubis) infected by Treponema pallidum.

Sexually transmitted infections (STIs) are ubiquitous within wild animal populations, yet it remains largely unknown whether animals evolved behavioral avoidance mechanisms in response to STI acquisition. We investigated the mating behavior of a wild population of olive baboons (Papio anubis) infected by the bacterium Treponema pallidum. This pathogen causes highly conspicuous genital ulcerations in males and females, which signal infectious individuals. We analyzed data on 876 mating attempts and associated acceptance or rejection responses in a group of about 170 baboons. Our findings indicate that females are more likely to avoid copulation if either the mating partner or females themselves have ulcerated genitals. We suggest that this outcome is linked to the overall higher choosiness and infection-risk susceptibility typically exhibited by females. Our results show that selection pressures imposed by pathogens induce individual behavioral modifications, leading to altered mate choice and could reduce promiscuity in a wild nonhuman primate population.

Electrophysiological properties of rat hippocampal principal cells are unaltered by prenatal protein malnutrition.

There is growing evidence that prenatal protein malnutrition alters the development of the hippocampal formation in rats (Morgane et al., 1993; Galler et al., 1996; Almeida et al., 1996, for reviews). Little is known, however, of the possible functional consequences of prenatal malnutrition on the physiology of principal cells in the hippocampus. We have addressed this issue by comparing the electrophysiological properties of hippocampal neurons (dentate granule cells and CA1 pyramidal cells) in slices prepared from control and from prenatally protein malnourished adult male and female Sprague-Dawley rats. We found no significant effect of the prenatal protein malnutrition insult upon a number of intrinsic membrane properties measured with whole-cell current clamp recordings, including: resting membrane potential, input resistance, and membrane time constant, or on action potential characteristics such as threshold, amplitude, and/or firing frequency. Additionally, we saw no effect of prenatal malnutrition upon extracellular measures of glutamatergic synaptic transmission such as the presynaptic fiber volley, excitatory postsynaptic potential or population spike amplitude at the perforant path to dentate granule cell synapse or at the Schaffer collateral to CA1 pyramidal cell synapse. In conclusion, we have demonstrated that prenatal protein malnutrition does not result in significant alterations of the cellular physiological properties of these two types of principal neurons in the adult rat hippocampus.