Suppression of neurotoxic lesion-induced seizure activity: evidence for a permanent role for the hippocampus in contextual memory

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dc.contributor.authorSparks, Fraser T.
dc.contributor.authorLehmann, Hugo
dc.contributor.authorHernandez, Khadaryna
dc.contributor.authorSutherland, Robert J.
dc.date.accessioned2017-10-13T22:29:26Z
dc.date.available2017-10-13T22:29:26Z
dc.date.issued2011
dc.descriptionSherpa Romeo green journal; open accessen_US
dc.description.abstractDamage to the hippocampus (HPC) using the excitotoxin N-methyl-D-aspartate (NMDA) can cause retrograde amnesia for contextual fear memory. This amnesia is typically attributed to loss of cells in the HPC. However, NMDA is also known to cause intense neuronal discharge (seizure activity) during the hours that follow its injection. These seizures may have detrimental effects on retrieval of memories. Here we evaluate the possibility that retrograde amnesia is due to NMDAinduced seizure activity or cell damage per se. To assess the effects of NMDA induced activity on contextual memory, we developed a lesion technique that utilizes the neurotoxic effects of NMDA while at the same time suppressing possible associated seizure activity. NMDA and tetrodotoxin (TTX), a sodium channel blocker, are simultaneously infused into the rat HPC, resulting in extensive bilateral damage to the HPC. TTX, co-infused with NMDA, suppresses propagation of seizure activity. Rats received pairings of a novel context with foot shock, after which they received NMDA-induced, TTX+NMDAinduced, or no damage to the HPC at a recent (24 hours) or remote (5 weeks) time point. After recovery, the rats were placed into the shock context and freezing was scored as an index of fear memory. Rats with an intact HPC exhibited robust memory for the aversive context at both time points, whereas rats that received NMDA or NMDA+TTX lesions showed a significant reduction in learned fear of equal magnitude at both the recent and remote time points. Therefore, it is unlikely that observed retrograde amnesia in contextual fear conditioning are due to disruption of non-HPC networks by propagated seizure activity. Moreover, the memory deficit observed at both time points offers additional evidence supporting the proposition that the HPC has a continuing role in maintaining contextual memories.en_US
dc.description.peer-reviewYesen_US
dc.identifier.citationSparks, F. T., Lehmann, H., Hernandez, K., & Sutherland, R. J. (2011). Suppression of neurotoxic lesion-induced seizure activity: Evidence for a permanent role for the hippocampus in contextual memory. PLoS ONE, 6(11), e27426. doi:10.1371/journal.pone.0027426en_US
dc.identifier.urihttps://hdl.handle.net/10133/4932
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.publisher.departmentDepartment of Neuroscienceen_US
dc.publisher.facultyArts and Scienceen_US
dc.publisher.institutionUniversity of Lethbridgeen_US
dc.publisher.institutionTrent Universityen_US
dc.subjectContextual memoryen_US
dc.subjectRetrograde amnesiaen_US
dc.subjectMemory impairmentsen_US
dc.subjectSeizure activityen_US
dc.subjectExcitotoxin N-methyl-D-aspartateen_US
dc.subjectNMDAen_US
dc.subjectNeurotoxicen_US
dc.subjectLesionen_US
dc.subject.lcshHippocampus (Brain)--Research
dc.subject.lcshMemory--Research
dc.subject.lcshAmnesia
dc.subject.lcshMethyl aspartate
dc.subject.lcshAnimal memory
dc.subject.lcshRats as laboratory animals
dc.titleSuppression of neurotoxic lesion-induced seizure activity: evidence for a permanent role for the hippocampus in contextual memoryen_US
dc.typeArticleen_US
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