Long-term potentiation in the behaving rat
| dc.contributor.author | Jones, Sandra Joanne | en_US |
| dc.date.accessioned | 2024-08-14T17:55:48Z | |
| dc.date.available | 2024-08-14T17:55:48Z | |
| dc.date.copyright | 1993 | en_US |
| dc.date.issued | 1993 | |
| dc.degree.department | Department of Psychology | |
| dc.degree.level | Master of Science M.Sc. | en |
| dc.description.abstract | Long-term potentiation (LTP) has been postulated to be a mechanism of learning and long-term memory. A popular experimental procedure is to examine LTP in the hippocampus with stimulation of the perforant path (PP) fibers with simultaneous recording in the dentate granule cells of the hippocampus. In vitro studies of LTP using hippocampal slices are numerous. Fewer investigations of LTP have been done in awake rats with chronic electrodes. Noradrenaline is a neuromodulator that has been implicated in numerous cognitive processes including attention, learning, and memory. Although noradrenergic modulation of LTP has been studied in vitro, its effects on LTP induction in the awake rat are unknown. I intended to use implantation of a chronic chemitrode to study the effects of a β-adrenergic antagonist, timolol, on induction of L TP. The chemitrode allows for direct infusion of the drug into the dentate gyrus. However, pilot data suggested the chemitrode itself upset the normal rate of induction of LTP. In Experiment I LTP was induced in 3 groups of rats: one group with chronic chemitrodes and an infusion of artificial cerebral spinal fluid , one with chronic chemitrodes, and one with chronic electrodes. The electrode rats exhibited. more LTP than the chemitrode groups, suggesting that the presence of the chemitrode might have disrupted LTP. Experiment 2 investigated effects of the β-antagonist propranolol on induction of LTP in rats with chronic electrodes. A saline control group and 3 drug groups (10, 20, and 40 mg/kg l-propranolol) received intraperitoneal injections and then tetanic stimulation of the PP. No group differences were observed and very little LTP was observed in all groups. I speculated that the ip injection procedure may have disrupted LTP. Experiment 3 tested the hypothesis that behavioural state may effect the variability of evoked potentials. In one. group of rats data were collected only when the rat was immobile. These data were compared to the saline group from Experiment 2, which was run in the freely behaving condition. No groups differences were found in either the amount of LTP induced or the amount of variability of evoked potentials. These results more clearly define the experimental conditions under which LTP may be induced consistently. The results of Experiment 1 suggested that LTP is more reliable when induced in rats with chronic electrodes than in those with chronic chemitrodes. This obviates the use of this preparation in studies of drug effects on LTP in awake rats, with one tetanic stimulation. The results of Experiment 2 suggested that LTP may n0t be induced reliably when drug injections are given pre-tetanization. The results of Experiment 3 agree with this conclusion. They also suggest that behavioural state is not a factor in either the amount of LTP induced or in the variability of the evoked potentials. These data together suggest that using one tetanic stimulation to induce LTP may not be an appropriate method with which lo study drug effects. Future studies will have to be done to test the hypothesis that LTP can be induced more reliably in freely behaving rats when multiple tetanizations are applied over many sessions. | en |
| dc.format.extent | 76 pages | |
| dc.identifier.uri | https://hdl.handle.net/1828/18338 | |
| dc.rights | Available to the World Wide Web | en_US |
| dc.subject | UN SDG 3: Good Health and Well-Being | en |
| dc.title | Long-term potentiation in the behaving rat | en_US |
| dc.type | Thesis | en_US |
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