Reinforcer Efficacy, Response Persistence, and Delay of Reinforcement

In an evaluation of the effects of delayed reinforcement on response persistence, two pigeons were exposed to a series of conditions in which reinforcement that either immediately followed or was delayed from the response that produced it alternated across blocks of sessions. Responding was maintained by a progressive-ratio schedule in which the response requirements incremented for successive reinforcers. The effects of signaled and unsignaled delay values of 1, 5, 10, and 20 s were investigated. In general, responding was more persistent, as measured as the point at which responding ceased for 300 s, with shorter delays, regardless of whether the delays were correlated with a distinct stimulus (that is signaled) or not. The results complement earlier findings showing that reinforcement delays affect reinforcer efficacy or response persistence by showing similar effects using an index of response strength that is independent of response rate. They also extend the general effects of delay of reinforcement to a schedule in which they previously have not been demonstrated.

Penicillin G-Induced Chlamydial Stress Response in a Porcine Strain ofChlamydia pecorum

Chlamydia pecorumcauses asymptomatic infection and pathology in ruminants, pigs, and koalas. We characterized the antichlamydial effect of the beta lactam penicillin G onChlamydia pecorumstrain 1710S (porcine abortion isolate). Penicillin-exposed and mock-exposed infected host cells showed equivalent inclusions numbers. Penicillin-exposed inclusions contained aberrant bacterial forms and exhibited reduced infectivity, while mock-exposed inclusions contained normal bacterial forms and exhibited robust infectivity. Infectious bacteria production increased upon discontinuation of penicillin exposure, compared to continued exposure.Chlamydia-induced cell death occurred in mock-exposed controls; cell survival was improved in penicillin-exposed infected groups. Similar results were obtained both in the presence and in the absence of the eukaryotic protein translation inhibitor cycloheximide and at different times of initiation of penicillin exposure. These data demonstrate that penicillin G induces the chlamydial stress response (persistence) and is not bactericidal, for this chlamydial species/strainin vitro, regardless of host cellde novoprotein synthesis.