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Pretest exposure to novelty or injections of beta-endorphin can enhance passive avoidance (PA) retention (e.g., IzquierdoMcGaugh, 1985). Enhanced retention may result from a "state-dependent" match between the CNS state during test and the novelty-induced beta-endorphin state that is obtained during training in a novel apparatus. Our Experiment 1 suggests that, unlike PA, Pavlovian fear conditioning in a conditioned lick suppression (CLS) paradigm may be beta-endorphin "state-independent." Rats were given one tone-shock pairing in a novel environment. Baseline lick rates and CLS tested 48 h later in a familiar environment were not affected by pretest exposure to novelty and/or injections of 3.33 mg/kg naloxone HCl. In Experiment 2, the same rats were PA trained/tested in a new apparatus. Saline or naloxone injections and various exposure (novel, familiar, none) conditions preceded (1h) the 24-h retention test. Pretest exposure to novelty reduced retention and naloxone eliminated that deficit. In Experiment 3, naive rats given pretest exposure to novelty also showed a PA retention deficit. The results of Experiments 2 and 3 may complement rather than contradict previous findings. Pretest induction of a beta-endorphin state by novelty may either enhance state-dependent retrieval of a "weak" memory trace or make a "strong/well consolidated" training memory more vulnerable to retroactive interference from "new learning" during the pretest exposure period.

Objective. To determine if neurologic impairment is related to progressive autoimmune disease in 3 murine models of systemic lupus erythematosus (SLE): MRL/lpr, NZB, and NZB/WF1 Methods. Sensorimotor function, learning, and memory were tested within strains at specific ages, before and after the appearance of SLE. These parameters were also compared between strains for young and older lupus mice and their congenic controls with reduced autoimmune disease (MRL/lpr versus MRL/+; NZB versus NZB/xid). Results. Abnormal neurologic features were present at a much higher frequency in MRL/lpr mice than in age-matched MRL/+ control mice, and sensorimotor function deficits were also seen in NZB/WF1 mice. Strains that develop lupus showed deficits on a water-escape, distal cue discrimination task and on a food-rewarded, proximal cue discrimination task, but the cognitive impairments were not global. Conclusion. MRL/lpr, NZB, and NZB/WF1 mice differed in terms of which behaviors were impaired as well as when those impairments appeared.

Rats were trained to lick and were tested for lick suppression to a tone in one apparatus/context. They were conditioned (tone-shock) in a different apparatus/context. Prior to conditioning, they received unreinforced preexposure to the tone (PCE) in the lick test box (Group A), in the conditioning box (Group X), or in a box different from both the test and conditioning boxes (Group B), or they received no PCE (Group N). In both Experiments 1 and 2, Group A was the only group to show latent inhibition (i.e., to show less conditioned lick suppression than did Group N). Context-dependent retrieval of “this CS signals nothing” information acquired during PCE reduces lick suppression when PCE and test contexts match, but not when PCE and conditioning contexts match.

Recently, Wright, Skala, and Peuser (1986) reported a failure to find latent inhibition in rats given unreinforced preconditioning exposure to a tone (PCE) when PCE and conditioning (tone-shock) occurred in the same apparatus/context and testing for lick suppression occurred in a different context. The no-PCE control group used for comparison had not been exposed to the tone or the conditioning context prior to conditioning. In the present experiment, the no-PCE control/comparison group received preexposure to the conditioning context, but not to the tone. Although the three groups given 12, 28, or 60 PCEs in the conditioning context did not differ from each other, they all showed less lick suppression in the test context than the no-PCE control group.