| Abstrakt: |
ONE of the most intriguing electrophysiological phenomena observed in the central nervous system is the persistent enhancement of an evoked synaptic response following brief trains of electrical stimuli. Within the hippocampus, evoked synaptic potentials can be doubled or tripled by tetanising stimulation, and such changes persist for hours to weeks1–6. Interest in the phenomenon of long term potentiation (LTP) stems from the generally held belief that synaptic plasticity of this sort may well be a physiological basis of information storage in the CNS. It is notable that this striking synaptic plasticity is observed in a structure which extensive clinical and experimental evidence suggests has a central role in information storage and/or retrieval7–11. Included in this evidence are numerous demonstrations that disrupting hippocampal activity by electrically induced epileptiform seizures also disrupts memory formation and/or retrieval12–15. In addition, the effectiveness of a variety of other treatments in disrupting behavioural plasticity seems closely related to their ability to elicit convulsive activity in the hippocampus16,17. We report here a series of experiments indicating that LTP established in the hippocampus can also be reversibly disrupted by the same kind of convulsive activity which disrupts memory functions. Specifically, we have produced LTP in the CA1 pyramidal cell synaptic field, disrupted it with electrically induced hippocampal seizures, and subsequently reinstated it with low frequency tetanic stimulation. |
