Temporal changes in neuronal dropout following inductions of lithium/pilocarpine seizures in the rat.
Estimates of neuronal dropout for approximately 100 structures as defined by Paxinos-Watson were completed for brains of male Wistar albino rats between 1 and 50 days after status epilepticus was evoked by a single systemic injection of lithium and pilocarpine. Sample estimates of neuronal loss were strongly correlated with direct measures of cell density. The most extensive immediate damage occurred within the substantia nigra reticulata, CA1 field of the hippocampus, the piriform cortex and the reuniens and paratenial nuclei of the thalamus. Neuronal dropout continued in many other structures over a 50-day period. Structures that showed the greatest 2-deoxyglucose (2-DG) uptake during discrete seizures and waxing and waning seizures within the early stages of status epilepticus but the least 2-DG uptake at the time of late continuous spiking and fast spiking with pauses [Neuroscience 64 (1995) 1057, 1075] exhibited the most neuronal dropout. Relationships between the delay of injection of acepromazine (which facilitated survival) and the amount of damage suggested that the source of the process that results in permanent brain damage may originate within the region of the piriform cortices and its subcortices.
Peredery
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Neuroscience Laboratory, Departments of Psychology and Biology, Laurentian University, Ontario, P3E 2C6, Sudbury, Canada.
Persinger
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MA
Parker
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G
Mastrosov
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L
D000818:Animals; D001921:Brain / Q000473:pathology*; D002470:Cell Survival / Q000502:physiology; D008094:Lithium; D008297:Male; D018721:Muscarinic Agonists; D009474:Neurons / Q000473:pathology*; D010862:Pilocarpine; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000139:chemically induced / Q000473:pathology*; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology*
D018721:Muscarinic Agonists; D010862:Pilocarpine; D008094:Lithium