Theoretical models of the CA3 suggest that because of its architecture, it mediates spatial pattern completion and working memory processes. The aim of this study was to determine whether with the use of drugs to block neurotransmitter action in CA3 one can separate the operation of these two processes using a visual-spatial pattern completion task for multiple cues. Rats were trained on a cheeseboard apparatus with a black curtain containing four extramaze cues. In the study phase rats removed a black block from one of 15 food wells and then after a 10- or 30-s delay in the test phase they had to return to the food well in the absence of the black block. After reaching criterion performance cannulae were bilaterally implanted into the CA3 of the rats. Rats were then given AP5, naloxone, or phosphate buffered saline (PBS) and following the standard study phase they were given the test phase with 0, 1, 2, 3, or 4 cues removed. The mean degree of error in all drugs and all cue conditions was recorded. Overall spatial inaccuracy was recorded in rats under the AP5 30-s delay condition, whereas deficits were contingent upon the number of cues available under all naloxone conditions. Results show that the blockage of glutamate via AP5 inhibited short-term or working memory, whereas the blockage of mu-opioids via naloxone disrupted visual-spatial pattern completion.
No takes yet. Share an insight, caveat, or question.
Kesner et al. (2009) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: