1. Competitive Place Task
Multiple memory systems: Medial caudate and higher-order habit formation
361.17
Jessica Piscopello & Bryan Devan
Laboratory of Comparative Neuropsychology, Psychology Department, Towson University, Towson, MD 21252
Summary
Competitive Place Task
Discussion
Acquisition
Retraining
Competition
The caudate nucleus together with related areas of the prefrontal cortex has been shown to contribute to various cognitive functions (e.g., see Divac & Öberg, 1992 for review). Previously, we have reported dissociations between the effects of dorsolateral and dorsomedial striatal lesions on cue-place versions of the water maze task (Devan et al, 1999; Devan & White, 1999). Unlike the place learning and/or cognitive-spatial memory impairments commonly reported for hippocampal lesions, the dorsolateral striatum may mediates a form of simple stimulus-response habit formation. The present findings suggest that while the hippocampus is directly involved in cognitive-spatial information processing, the dorsomedial striatum may contribute to the cognitive control of performance incrementally over time by strengthening responses based on higher-order habit formation (see Devan et al, 2011 for review).
A variation of the water maze competitive place task (McDonald et al., 2005; Fig 1) was used to study the role of the hippocampus (HPC) and medial caudate-putamen (mCPu) (see Fig 2) in spatial navigation and higher-order [(S-S)-R] habit formation. Rats received distributed place training for 18 days (4 trials/day) with the hidden platform located in the center of the NE quadrant (location 1) followed by mass place re-training (8 trials) to a second location in the center of the SW quadrant on day 19. A probe test was given on day 20 to measure competitive place responding. Preliminary lesion findings show that HPC damage impaired spatial learning overall (Fig 3), although non-cognitive procedural strategies such as circumnavigation spared early performance during original training, consistent with Devan et al. (1996; Fig 4). Despite the extended training to the original location, controls showed a slight bias in searching at the new location on the probe test (Fig 5) suggesting that spatial working memory had a relatively strong influence over navigational behavior. In contrast, control latencies to enter the old and new locations were approximately equal, thus optimizing potential detection of behavioral changes in either direction with this performance measure (Fig 6). HPC damage also elevated latencies to enter the new location more than the old location on the competition test. Dorsomedial striatal (mCPu) damage produced a less-severe disruption of spatial performance overall and increased the latency to enter the original/old location relative to the new location on the competition test. 1 2 3 4 3 2 4 2 4 3 1
FIG 2. electrolytic mCPu lesions were conducted using the coordinates AP: +0.7 mm; ML: ± 2.4 mm; DV: 5.7 mm, relative to skull surface and bregma. The coordinates for hippocampal KA lesions were AP: mm; ML: ±2.5 mm; DV: -3.7 mm
FIG 1. Acquisition – hidden platform at location 1, 4 trials/day (18 days); Retraining – hidden platform moved to location 3, 2 blocks of 4 trials (day 19); Competition – platform removed, 60 sec probe test (day 20).
Results
Escape Latency +/- SEM
References
Fig 3- Escape latencies during first 2 phases of the study, acquisition and retraining.
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Fig 4- Paths illustrating some of the strategies used by lesioned rats during acquisition phase.
% Quad Time (sec +/- SEM)
Fig 5- Probe test results during phase 3 competition test.
Fig 6- Probe test results during phase 3 competition test.