Footshock In Context Research Articles

Neonatal alcohol exposure and the hippocampus in developing male rats: effects on behaviorally induced CA1 c-Fos expression, CA1 pyramidal cell number, and contextual fear conditioning

Rats exposed to a high binge-like dose of alcohol over postnatal days (PD) 4–9 show reductions in CA1 pyramidal cells and impairments on behavioral tasks that depend on the hippocampus. We first examined hippocampal c-Fos expression as a marker of neuronal activity in normally developing rats following different phases of the context preexposure facilitation effect (CPFE) paradigm (Experiment 1). During the CPFE, preexposure to the training context facilitates contextual conditioning to an immediate shock given on a subsequent occasion. We then examined the relationship between CPFE impairment, hippocampal cell loss, and c-Fos expression in rats exposed to alcohol over PD 4–9 (Experiment 2). Normally developing (Experiment 1), sham-intubated control (SI), and PD 4–9 alcohol-exposed (4.00 g and 5.25 g/kg/d; Experiment 2) juvenile male rats were trained on the CPFE. The CPFE occurs over three phases separated by 24 h. Starting on PD 31, rats were preexposed to Context A or Context B for 5 min. After 24 h, all rats received an immediate 1.5-mA foot shock in Context A. Finally, rats were tested for contextual conditioning in Context A on PD 33. Normally developing and SI rats preexposed to Context A showed enhanced contextual fear compared with those preexposed to Context B (Experiment 1) or alcohol-exposed rats preexposed to Context A (Experiment 2). Rats were sacrificed 2 h following different phases of the CPFE and processed for c-Fos immunohistochemistry (Experiments 1 and 2) and CA1 pyramidal cell quantification (Experiment 2). In Experiment 1, c-Fos positive (c-Fos+) cells in the dentate gyrus (DG) were consistently high among rats preexposed to Context A (Pre), Context B (No Pre), or sacrificed directly from their home cage (Home) and did not differ across CPFE phases. CA3 and CA1 c-Fos+ cells were highest during preexposure and decreased across training phases, with Group No Pre showing greater numbers of c-Fos+ cells during training than Group Pre and Controls. In Experiment 2, SI rats had greater numbers of CA1 c-Fos+ cells compared with alcohol-exposed rats, differing significantly from rats exposed to the high alcohol dose (5.25 g) over PD 4-9. Experiment 2 also revealed a linear decline in CA1 pyramidal cells across treatment groups, again with rats from the high-alcohol dose group showing significantly fewer CA1 pyramidal cells compared with SI. Our results reveal that context novelty may be a significant contributor to differential hippocampal c-Fos expression following different phases of the CPFE. In addition, lower levels of c-Fos+ cells in alcohol-exposed rats following preexposure may be related to general reductions in the number of CA1 pyramidal cells in these rats. The significant CPFE impairments in rats exposed to the lower alcohol dose (4.00 g), who show a 15% reduction in CA1 pyramidal cells compared with SI rats, highlight the sensitivity of the CPFE to hippocampal insult.

Postacquisition unexpected footshock disrupts appetitively motivated instrumental performance based on short-term retention

Water-deprived rats were trained to run for water in an E-maze on a delayed-alternation task with a 5-min retention interval. Each day, long before encountering and again long after having encountered the delayed-alternation task, all subjects consistently experienced weak footshock in Context A and no footshock in Context B. Contexts A and B were highly dissimilar to each other and to the E-maze. On delayed-alternation probe trials, subjects were exposed to Context A or Context B for the middle 30 sec of the delayed-alternation retention interval. Performance on these trials was unaffected when weak footshock occurred in Context A or no footshock occurred in Context B. However, when weak footshock occurred in Context B, retention was impaired. An absence of footshocks in Context A produced a nonsignificant tendency towards impairment. Thus, the disruptive effects of unexpected events that occur during the retention interval do not appear to depend upon the target and unexpected events’ having similar reinforcers or even having reinforcers of the same valence. The results are interpreted in terms of unexpected events’ recruiting more of the limited information-processing capacity of the subject than do otherwise similar expected events. Moreover, the tendency of unexpected shock to interfere with performance more than does unexpected nonshock suggests that the degree to which an unexpected event recruits processing capacity depends on the affective value of the event as well as on its unexpectedness.