Event Title

Delay and Trace Conditioning in Middle and Older Age

Mentor 1

Ira Driscoll

Location

Union Wisconsin Room

Start Date

29-4-2016 1:30 PM

End Date

29-4-2016 3:30 PM

Description

Fear conditioning, a type of associative learning, is a behavioral paradigm where a conditioned stimulus (CS) becomes paired with an aversive stimulus (UCS), such that presentation of the CS alone elicits a conditioned response (CR). Previous research has shown that delay conditioning, a procedure in which the UCS co-terminates with the CS, is dependent on the amygdala. Trace conditioning, a procedure that uses a temporal gap (trace interval) between the CS and the UCS presentation, is hippocampus-dependent. Given that the hippocampus is vulnerable while the amygdala seems to be resilient to the deleterious effects of aging, the current study investigated delay and trace conditioning in a group of healthy, community-dwelling middle-aged and older adults. Montreal Cognitive Assessment was used to screen participants who would be considered “at risk” for mild cognitive impairments. The fear conditioning paradigm consisted of three colored shape presentations, where two of the shapes were paired with a shock for 500ms. The conditioned stimuli consisted of the CS-, in which no shock was applied, the CS+, which co-terminated with the shock and the CStrace consisted of a 10s interval prior to the shock. On each trial, the participants were asked to rate their shock expectancy level, from 0 to 100, while the shape was presented on the screen. There were no significant differences in SCR between middle-aged (CS+ and CS-, t(10)=.417, p=.681; CS+ and CStrace, t(10)=.463, p=.649; CS- and CStrace, t(10)=.540, p=.978), older (CS+ and CS-, t(9)=.131, p=.897; CS+ and CStrace, t(9)= -.401, p=.693; CS- and CStrace, t(9)=.511, p=.616), and “at risk” (CS+ and CS-, t(10)=.891, p=.829; CS+ and CStrace, t(10)=.963, p=.757; CS- and CStrace, t(10)=.865, p=.917) groups. There were no group differences in SCR between conditions (CS+, F(2,29)=.993, p=.383; CS-, F(2,29)=1.174, p=.323; CStrace, F(2,29)=.739, p=.486). All groups showed significant learning of the associations between the stimuli based on shock expectancy ratings (middle-aged: CS- vs. CS+, t(10)=17.467, p< .05; CS- vs. CStrace, t(10)=-15.878, p< .05) (older: CS- vs. CS+, t(9)=5.724, p< .05; CS- vs. CStrace, t(9)=5.049, p < .05) (“at risk”: CS- vs. CS+, t(10)=9.012, p< .05; CS- vs CStrace, t(10)=8.140, p< .05). Our results suggest that neither the delay nor trace conditioning are compromised by both normal aging or in those “at risk “ for cognitive impairment.

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Apr 29th, 1:30 PM Apr 29th, 3:30 PM

Delay and Trace Conditioning in Middle and Older Age

Union Wisconsin Room

Fear conditioning, a type of associative learning, is a behavioral paradigm where a conditioned stimulus (CS) becomes paired with an aversive stimulus (UCS), such that presentation of the CS alone elicits a conditioned response (CR). Previous research has shown that delay conditioning, a procedure in which the UCS co-terminates with the CS, is dependent on the amygdala. Trace conditioning, a procedure that uses a temporal gap (trace interval) between the CS and the UCS presentation, is hippocampus-dependent. Given that the hippocampus is vulnerable while the amygdala seems to be resilient to the deleterious effects of aging, the current study investigated delay and trace conditioning in a group of healthy, community-dwelling middle-aged and older adults. Montreal Cognitive Assessment was used to screen participants who would be considered “at risk” for mild cognitive impairments. The fear conditioning paradigm consisted of three colored shape presentations, where two of the shapes were paired with a shock for 500ms. The conditioned stimuli consisted of the CS-, in which no shock was applied, the CS+, which co-terminated with the shock and the CStrace consisted of a 10s interval prior to the shock. On each trial, the participants were asked to rate their shock expectancy level, from 0 to 100, while the shape was presented on the screen. There were no significant differences in SCR between middle-aged (CS+ and CS-, t(10)=.417, p=.681; CS+ and CStrace, t(10)=.463, p=.649; CS- and CStrace, t(10)=.540, p=.978), older (CS+ and CS-, t(9)=.131, p=.897; CS+ and CStrace, t(9)= -.401, p=.693; CS- and CStrace, t(9)=.511, p=.616), and “at risk” (CS+ and CS-, t(10)=.891, p=.829; CS+ and CStrace, t(10)=.963, p=.757; CS- and CStrace, t(10)=.865, p=.917) groups. There were no group differences in SCR between conditions (CS+, F(2,29)=.993, p=.383; CS-, F(2,29)=1.174, p=.323; CStrace, F(2,29)=.739, p=.486). All groups showed significant learning of the associations between the stimuli based on shock expectancy ratings (middle-aged: CS- vs. CS+, t(10)=17.467, p< .05; CS- vs. CStrace, t(10)=-15.878, p< .05) (older: CS- vs. CS+, t(9)=5.724, p< .05; CS- vs. CStrace, t(9)=5.049, p < .05) (“at risk”: CS- vs. CS+, t(10)=9.012, p< .05; CS- vs CStrace, t(10)=8.140, p< .05). Our results suggest that neither the delay nor trace conditioning are compromised by both normal aging or in those “at risk “ for cognitive impairment.