Two multiple-schedule experiments with pigeons examined the effect of adding food reinforcement from an alternative source on the resistance of the reinforced response (target response) to the decremental effects of satiation and extinction. In Experiment 1, key pecks were reinforced by food in two components according to variable-interval schedules and, in some conditions, food was delivered according to variable-time schedules in one of the components. The rate of key pecking in a component was negatively related to the proportion of reinforcers from the alternative (variable-time) source. Resistance to satiation and extinction, in contrast, was positively related to the overall rate of reinforcement in the component. Experiment 2 was conceptually similar except that the alternative reinforcers were contingent on a specific concurrent response. Again, the rate of the target response varied as a function of its relative reinforcement, but its resistance to satiation and extinction varied directly with the overall rate of reinforcement in the component stimulus regardless of its relative reinforcement. Together the results of the two experiments suggest that the relative reinforcement of a response (the operant contingency) determines its rate, whereas the stimulus-reinforcement contingency (a Pavlovian contingency) determines its resistance to change.Key words: alternative reinforcement, response rate, resistance to change, concurrent schedules, multiple schedules, satiation, extinction, key peck, pigeon Experimental analysis has distinguished two aspects of operant behavior: the rate of a response and the resistance of that rate to reduction by procedures such as satiation and extinction. These two aspects of behavior are of interest because they vary in orderly ways as functions of rate of reinforcement (Catania & Reynolds, 1968;Nevin, 1974Nevin, , 1979Skinner, 1938Skinner, , 1950 and because of their relation to the theoretical concept of response strength. Although response rate has been taken as equivalent to response strength (Skinner, 1938(Skinner, , 1950 to be (Nevin, 1974(Nevin, , 1979Smith, 1974). Consequently, it is of some importance to examine the variables that influence resistance to change (Fath, Fields, Malott, & Grossett, 1983;Nevin, 1974Nevin, , 1979Nevin, , 1984Nevin, Mandell, & Yarensky, 1981;Nevin, Smith, & Roberts, 1987).The rate of a target response maintained by a given rate of reinforcement decreases when reinforcers are added concurrently from an alternative source. This decrease occurs both when reinforcers are added noncontingently (Rachlin & Baum, 1972) and when they are contingent on a different, concurrent response (Catania, 1963). Adding reinforcers from an alternative source may be viewed as degrading the operant contingency, in that the correlation between the occurrence of the target response and the reinforcer is thereby weakened. Thus, alternative reinforcement might reduce response rate by degrading the operant contingency.If a target response's rate and resistance to chan...

The aggregation of neurocognitive impairments in the parents of COS probands provides further evidence of etiologic continuity between COS and AOS. A substantial subgroup of parents of COS probands had a worse neurocognitive performance than that of any of the parents of ADHD and CC probands. Receiver operating characteristic curves showed that when rigorous cutoffs define neurocognitive impairments, the combination of scores on certain neurocognitive tasks produced a level of diagnostic accuracy in the parents of COS probands that is sufficient for use in genetic linkage studies.

ne prominent emphasis in attempts to understand the pathogen-0 esis of schizophrenia involves the search for factors in genetic proneness or vulnerability to schizophrenia. Although the evidence for genetic factors in schizophrenia is overwhelming, the nature of heritable components to schizophrenia has remained elusive (Gottesman & Shields, 1982;Kendler & Diehl, 1993). Part of the problem may be that it is not schizophrenia itself that is heritable but that several underlying factors associated with vulnerability or liability to schizophrenia may be genetically transmitted. These vulnerability components may contribute to the varying forms of the clinical illness that we call schizophrenia but would also be expected to be present in other individuals This research was supported by National Institute of Mental Health Grants MH37705, MH49716, MH45112, and MH30911. We thank our colleagues George Bartzokis.

Minnesota Multiphasic Personality Inventory (MMPI) scores were examined for 50 parents of children with an onset of schizophrenia prior to 14 years of age, 153 parents of children with attention deficit hyperactivity disorder (ADHD), and 168 parents of community comparison children. The parents were participants in the UCLA Family Study. The mean scores on all standard MMPI scales were within normal limits for all three groups of participants. Parents of schizophrenia probands were significantly higher on scale Sc than parents of community comparison children. Previous research has shown that scale Sc may be associated with a genetic liability to developing schizophrenia. Thus, scale Sc shows promise as an indicator of a heightened risk for the development of schizophrenia. The parents of the ADHD probands were significantly higher on standard clinical scale Pd than community comparison parents. Mothers of both schizophrenia and ADHD probands shared some personality indicators of stress reactivity. Although this study, like all non-adoptee family studies, cannot disentangle genetic effects on the development of these personality characteristics from environmental effects, we speculate that the emotional distress resulting in higher levels of the MMPI characteristics seen in the patients' mothers reflects the impact of raising a psychiatrically ill offspring.