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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Bicuculline, Cells, Cultured, Disease Models, Animal, Electric Stimulation, Epilepsy, Excitatory Postsynaptic Potentials, GABA Antagonists, Hippocampus, Humans, In Vitro Techniques, Interneurons, Long-Term Potentiation, Memory Disorders, Pyramidal Cells, Rats, Receptors, N-Methyl-D-Aspartate, Synaptic Transmission.
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Does a brief period of epileptiform activity strengthen excitatory synapses in the rat hippocampus in vitro? Context: We examined here whether a very short period of epileptiform activity could produce lasting modifications of synaptic strength and network properties in the rat hippocampus in vitro. Synaptic transmission at CA3-CA1 and at CA3-CA3 pyramidal cell synapses was monitored in hippocampal slice cultures before and after a very brief episode of epileptiform activity (20-180 s) induced with bicuculline methochloride. We show here that a brief period of epileptiform activity induces long-lasting potentiation of glutamatergic transmission at CA3-CA1 and at CA3-CA3 pyramidal cell synapses. This potentiation also was observed at synapses formed by pairs of monosynaptically connected neurons. It was dependent on N-methyl-d-aspartate (NMDA) receptors, occluded classic long-term potentiation, and could be depotentiated by low-frequency stimulation at 3 Hz. Recruitment of polysynaptic pathways within area CA3 was facilitated after epileptiform activity indicating that the induced potentiation enhanced overall hippocampal network excitability.
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These changes in synaptic transmission may contribute to the genesis of epilepsy and to seizure-associated memory deficits. Final Decision: yes