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This study investigates the effects of brain stimulation at varying delays on passive avoidance learning in rats. After learning a task involving crossing a line to avoid a shock, rats were subjected to brain stimulation at 50, 100, and 150 ms post-training. The results showed significant differences in latency to cross the line based on the area stimulated and the timing of stimulation. Notably, stimulation of Area 1 affected memory consolidation most significantly with shorter delays, while Area 2 demonstrated a peak disruption at 100 ms, highlighting the nuanced interplay between timing and memory processes.
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Memory-Disrupting ESB Exercise 13.5 in David Howell’s “Statistical Methods for Psychology,” 4th edition
Basic Design • Passive avoidance learning • One-trial • Cross the line, get shocked • DV = latency to cross on test trial • Brain stimulation at 50, 100, 150 msec after the training shock • Delivered to Area 0, 1, or 2
Cell and Marginal Means Table 1. Mean latency (sec) to cross the line. Note: Within each row, means with the same letter in their superscript are not significantly different from one another.
The latency data were analyzed with a 3 x 3, Area x Delay, factorial ANOVA. Each effect was tested with a MSE of 29.31. Significant (p .05) effects were found for the main effect of area, F(2, 36) = 6.07, p = .005, and the Area x Delay interaction, F(4, 36) = 3.17, p = .025, but the main effect of delay fell short of statistical significance, F(2, 36) = 3.22, p = .052. As shown in Table 1, the latencies were, as expected, higher in area 0 than in the other two areas.
More interesting than the main effect of area, however, is how the effect of delay of stimulation changed when we changed the area of the brain stimulated. The significant interaction was further investigated by testing the simple main effects of delay for each level of the brain area factor. When the area stimulated was area 0, the area thought not to be involved in learning and memory, delay of stimulation had no significant effect on mean latency, F(2, 12) = 0.02, MSE = 36.1, p = .98. Delay of stimulation did, however, have a significant effect on mean latency when area 1 was stimulated, F(2, 12) = 4.53, MSE = 28.1, p = .034, and when area 2 was stimulated, F(2, 12) = 6.42, MSE =23.7, p = .013. As shown in Table 1, the disruption of consolidation of the memory produced by the brain stimulation in area 1 was greater with short delays than with long delays.
Pairwise comparisons using Fisher’s procedure indicated that the mean latency was significantly less with 50 msec delay than with the 150 msec delay, but with the smaller differences between adjacent means falling short of statistical significance. When the stimulation was delivered to brain area 2, a different relationship between latency and delay was obtained: Stimulation most disrupted consolidation at 100 msec. Fisher’s procedure indicated that mean latency with 100 msec delay was significantly less than with 50 or 150 msec delay, with mean latency not differing significantly between the 50 and 150 msec conditions.
