The nonrecurring-items delayed nonmatching-to-sample (DNMS) task is an integral part of
contemporary monkey models of brain-damage-produced amnesia. This thesis began the development
of a comparable rat model of brain-damage-produced amnesia. First, a DNMS task for rats was
designed by adapting key features of the monkey task. Then, the rat DNMS task was studied in three
experiments; each assessed the comparability of the rat DNMS task to the monkey DNMS task.
Experiment 1 determined the rate at which the rat DNMS task is learned and the asymptotic level at
which it is performed, Experiment 2 assessed the memory abilities that it taps, and Experiment 3
investigated the brain structures that are involved i n its performance.
In Experiment 1, rats were trained on the DNMS task and their performance was assessed at
retention delays of 4, 15, 60, 120, and 600 s. All of the rats learned the DNMS task, and their
performance was comparable to that commonly reported for monkeys in terms of both the rate at
which they acquired the nonmatching rule at a brief retention delay and their asymptotic accuracy at
delays of up to 120 s. These results establish that rats can perform a DNMS task that closely resembles
the monkey DNMS task and that they can approximate the level of performance that is achieved by
monkeys.
Experiment 2 examined the effects of distraction during the retention delay on the DNMS performance of rats. Rats were tested at retention delays of 60 s. On half of the trials, the rats
performed a distraction task during the retention delay; on the other half, they did not. Consistent with
findings from monkeys and humans, distraction during the retention delay disrupted the DNMS
performance of rats. This suggests that similar memory abilities are involved in the DNMS
performance of rats, monkeys, and humans. Experiment 3 investigated the effects of separate and combined bilateral lesions of the
hippocampus and the amygdala on DNMS performance in pretrained rats. Rats were tested both
before and after surgery at retention delays of 4, 15, 60, 120, and 600 s. Each experimental rat received
bilateral lesions of the hippocampus, amygdala, or both. There were no significant differences among
the three experimental groups, and the rats in each of the three experimental groups were significantly
impaired, in comparison to no-surgery control rats, only at the 600-s delay. In contrast, rats that had
sustained inadvertent entorhinal and perirhinal cortex damage during surgery displayed profound
D N M S deficits. These results parallel the results of recent studies of the neural basis of DNMS in
monkeys. They suggest that, in contrast to one previously popular view, neither the hippocampus nor
the amygdala play a critical role in the DNMS of pretrained animals and that the entorhinal and
perirhinal cortex are critically involved.
On the basis of these findings, it appears that the rat DNMS task may prove to be a useful
component of rat models of brain-damage-produced amnesia. This conclusion is supported by the
preliminary results of several experiments that are currently employing the task. / Arts, Faculty of / Psychology, Department of / Graduate
| Identifer | oai:union.ndltd.org:UBC/oai:circle.library.ubc.ca:2429/3293 |
| Date | 05 1900 |
| Creators | Mumby, David Gerald |
| Source Sets | University of British Columbia |
| Language | English |
| Detected Language | English |
| Type | Text, Thesis/Dissertation |
| Format | 4495793 bytes, application/pdf |
| Rights | For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use. |
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