Dissociation between conditioned taste aversion and radial maze learning following seizure-induced multifocal brain damage: Quantitative tests of serial vs. parallel circuit models of memory

Persinger, Michael A.; Bureau, Y; Peredery, Oksana

doi:10.1016/0031-9384(94)90188-0

Cited by 42 publications

(13 citation statements)

References 28 publications

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“…Cognitive deterioration was evident several days after generalized seizures and lasted for up to 5 months [55,58,60]. Similar results indicating long-lasting impairment of learning and memory were received using pilocarpineinduced seizures [61][62][63][64][65][66]. These observations were additionally reinforced by the data obtained from such chronic epilepsy/epileptogenesis models like electric kindling or pentylenetetrazole (PTZ)-induced kindling (PTZK), models utilizing chronic administration of chemoconvulsant agent or repetitive electrical stimulation of epileptogenic structures like amygdala or hippocampus.…”

Section: Experimental Datasupporting

confidence: 66%

Single Seizure and Cognition: Clinical and Translational Implications

2016

ARC Journal of Neuroscience

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Section: Experimental Datasupporting

confidence: 66%

Single Seizure and Cognition: Clinical and Translational Implications

2016

ARC Journal of Neuroscience

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“…The approximately 11 5 structures that exhibited neuronal loss but whose scores did not differ between the groups are not shown. The magnitude of the damage within these structures did not differ by more than 5% from those reported elsewhere (Persinger et al, 1994).…”

Section: Resultssupporting

confidence: 45%

Normal Spatial Memory Following Postseizure Treatment with Ketamine: Selective Damage Attenuates Memory Deficits in Brain-Damaged Rodents

Santi

Cook

Persinger

et al. 2001

International Journal of Neuroscience

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Within 30 min after the initiation of status epilepticus (SE) by lithium and pilocarpine, rats were injected with either acepromazine or ketamine. Compared to the rats that had received the acepromazine, the group that had received the ketamine displayed more accurate spatial memory. Their scores did not differ significantly from normal (non-seized) controls. Although the ketamine treatment did not significantly change the amount of neuronal loss within about 100 Paxinos and Watson structures, it was neuroprotective for several structures within the thalamus and portions of the temporal and parietal cortices. Ketamine-treated rats, however, displayed markedly more damage within the entorhinal cortices and amygdalohippocampal area.

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“…Structural anomalies within various regions of the hippocampus, induced by surgery or seizures, have been associated with alterations in spatial memory (Whishaw et al 1994), conditioned taste aversion (Persinger et al 1994) and contextual fear conditioning (Stewart & Persinger 2000). Other rats that had been exposed prenatally to the same complex sequence magnetic field that produced the increased quantitative anomalies in cell organization in the present study also showed alterations in spatial learning (McKay et al 2002), open field behavior (Persinger & St-Pierre 2001), taste aversion, and contextual fear conditioning (St-Pierre & Persinger 2007).…”

Section: Discussionmentioning

confidence: 99%