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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.

The experiment was designed to test effects of experimentally induced hyperlysinemia on maze learning ability in the mouse. Six% L-lysine was placed in the drinking water during gestation, and/or during nursing and/or during postweaning in a factorial combination. The young were tested at 40 days of age in a water-escape T maze. A week later all animals were retested for retention. Findings revealed that overloads of lysine resulted in temporary impairment, but permanent impairment occurred only if excess lysine was administered during gestation. Biochemical analysis revealed a sharp decrease in urea nitrogen in the urine, and a blood ammonia and lysine increase.

A parametric estimation was conducted on the concentrations of certain substances in CSF as a function of time after electroconvulsive shock treatment that produced retrograde amnesia in rat. The substances of particular interest were hexoses, and the electrolytes sodium, potassium, calcium and magnesium. The concentrations of each substance were expressed as percent change after treatment from an initial concentration taken from each animal before treatment. Considerable increases in hexose and calcium concentrations were observed at 5 min after electroshock treatment, while concentrations for sodium, potassium and magnesium demonstrated little change at the 5 min observation. Values for all five biochemical variables comparable to their control values were observed at subsequent time intervals. Concentrations for these five biochemical variables were established for both CSF and blood in rat, and compared to those values reported for rabbit. The argument is advanced that protein synthesis inhibition following ECS is secondary to the disruption of membrane surface glycoproteins and that the disruption of these glycoproteins plays a major role in the production of retrograde amnesia.

The state dependent learning paradigm was used with a one-trial, passive avoidance task. Forty male rats were equally distributed among four groups: One group received intrathoracic injections of sodium pentobarbital immediately after the acquisition trial and immediately before the retention test trial; a second group received equivalent injections of 0.9% saline; a third group was drugged after acquisition and given saline prior to retention testing and the fourth group was given saline after acquisition and drug prior to retention testing. All groups showed increased latencies on the retention trial but marked group differences in retention test latencies indicate that there was significantly more retention of training when drug states were the same during the memory storage interval and the memory retrieval interval. Intrathoracic injection proved to be a practical substitute for intravenous injection in assuring rapid onset of drug effect.

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.