Synaptic plasticity of the CA3 commissural projection in epileptic rats: an in vivo electrophysiological study.
The hippocampal commissural system has recently been found to participate in the generation of mirror foci after kainate-induced epileptiform discharges. In the present study we have evaluated the electrophysiological alterations in the ventral commissural hippocampal system that originates in the pyramidal CA3 cells and connects to the contralateral CA3 pyramidal cells. The recordings were performed in epileptic rats 24 h after an early behavioural spontaneous seizure between 5 and 21 days after pilocarpine-induced status epilepticus. Epileptic animals presented a marked increase in neuronal excitability after contralateral CA3 stimulation, characterized by a shift to the left in the input-output curve and the clear appearance of a population spike. Input-output curves showed that maximum population excitatory postsynaptic potential (pEPSP) amplitude was decreased by 30%, which could be related to cell death in these regions. Using paired-pulse protocols to evaluate a fast form of synaptic plasticity (i.e. paired-pulse facilitation) we observed that, despite the similar pEPSP amplitude between control and experimental groups, only epileptic animals showed strong paired-pulse population spike facilitation up to 500 ms interstimulus intervals. Despite increased excitability and pyramidal cell death, epileptic animals presented a more robust potentiation after high-frequency stimulation than controls, a protocol used to evaluate a slow form of synaptic plasticity (i.e. long-term potentiation). The increased excitability in CA3 pyramidal neurons enhanced the probability of burst activity in these neurons; this could lead to greater CA1 synchronization. The present results might have relevance for the understanding of epileptogenesis and of learning and memory deficits seen in temporal lobe epilepsy.
Queiroz
Claudio M T
CM
Department of Physiology, UNIFESP-EPM, Rua Botucatu, 862-04023-062, São Paulo, SP, Brazil.
Mello
Luiz Eugênio
LE
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D016923:Cell Death / Q000502:physiology; D003292:Convulsants; D003344:Cortical Synchronization; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004833:Epilepsy, Temporal Lobe / Q000503:physiopathology*; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000166:cytology / Q000503:physiopathology*; D008297:Male; D008569:Memory Disorders / Q000209:etiology / Q000503:physiopathology; D019599:Mossy Fibers, Hippocampal / Q000502:physiology / Q000648:ultrastructure; D009410:Nerve Degeneration / Q000209:etiology / Q000503:physiopathology; D009434:Neural Pathways / Q000166:cytology / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology*; D010862:Pilocarpine; D017966:Pyramidal Cells / Q000166:cytology / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013226:Status Epilepticus / Q000139:chemically induced / Q000503:physiopathology
D003292:Convulsants; D010862:Pilocarpine