Abstract
IntroductionTrace conditioning is impaired by lesions to dorsal hippocampus, as well as by treatment with the muscarinic acetylcholine antagonist scopolamine. However, the role of muscarinic receptors within hippocampus has received little attention.MethodsThe present study examined the effects of intra‐hippocampal infusion of scopolamine (30 µg/side) in an appetitive (2 vs. 10 s) trace conditioning procedure using sucrose pellets as the unconditioned stimulus (US). Locomotor activity (LMA) was examined in a different apparatus.ResultsIntra‐hippocampal scopolamine reduced responding to the 2 s trace conditioned stimulus (CS). Intra‐hippocampal scopolamine similarly depressed responding within the inter‐stimulus interval (ISI) at both 2 and 10 s trace intervals, but there was no such effect in the inter‐trial interval. There was also some overall reduction in responding when the US was delivered; significant at the 10 s but not at the 2 s trace interval. A similar pattern of results to that seen in response to the CS during acquisition was shown drug‐free (in the 5 s post‐CS) in the extinction tests of conditioned responding. LMA was increased under scopolamine.ConclusionsThe results suggest that nonspecific changes in activity or motivation to respond for the US cannot explain the reduction in trace conditioning as measured by reduced CS responding and in the ISI. Rather, the findings of the present study point to the importance of associative aspects of the task in determining its sensitivity to the effects of scopolamine, suggesting that muscarinic receptors in the hippocampus are important modulators of short‐term working memory.
Highlights
Trace conditioning is impaired by lesions to dorsal hippocampus, as well as by treatment with the muscarinic acetylcholine antagonist scopolamine
The hippocampus has been identified as a key neural substrate of the ability to bridge temporal discontiguity, which is essential to the acquisition of trace condition‐ ing (Bangasser, Waxler, Santollo, & Shors, 2006; Weible, O’Reilly, Weiss, & Disterhoft, 2006)
D1 to D4 refer to the 4 days of trace conditioning, on each of which tone was followed by food at the 2 s or 10 s trace interval, for a 30 trials per day and in the presence of the experimental background stimulus
Summary
Trace conditioning procedures test the cognitive capacity to associ‐ ate events separated by an intervening time or “trace” interval. The majority of studies conducted to examine the neural sub‐ strates of trace conditioning have used aversive eyeblink (Chen et al, 2014; Thomas & Tran, 2012; Weible et al, 2006; Weible, McEchron, & Disterhoft, 2000; Weible, Weiss, & Disterhoft, 2003) or fear con‐ ditioning (Bang & Brown, 2009; Bangasser et al, 2006; Baysinger, Kent, & Brown, 2012; Pang et al, 2010; Quinn et al, 2002) proce‐ dures These studies have included examination of the effects of scopolamine administered directly by microinfusion, for example, in perirhinal cortex (Bang & Brown, 2009) and amygdala (Baysinger et al, 2012), in both cases using rats tested with a 16 s trace interval in a conditioned freezing procedure. Delay conditioning groups were not included because appetitive delay conditioning is not impaired by hippocampal lesions (Thibaudeau et al, 2007, 2009), and the available evidence shows no effect of scopolamine on (in this case, aversive) delay conditioning (Pang et al, 2010; Pezze et al, 2017)
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