Abstract
Simultaneous recordings of orthodromic PS, fEPSP and antidromic PS revealed EPSP/spike (E-S) dissociation, indicating a conversion of input/output relations from early and brief excitability to a late and prolonged depression during the recovery from depolarization induced by high levels of potassium. E-S potentiation was partially attenuated by pre-treating the slices with BAPTA-AM and lidocaine and totally eliminated by a submaximal concentration of muscimol. The time lag for recovery was decreased by the GABAA antagonist and completely eliminated by the A1 antagonist. From these observations, we conclude that Ca2+ dependent inhibitory suppression is the main cause of a brief period of E-S potentiation, and accumulation of adenosine is the mechanism responsible for prolonged depression of synaptic transmission.
Original language | English |
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Pages (from-to) | 237-243 |
Number of pages | 7 |
Journal | Brain Research |
Volume | 975 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 2003 Jun 13 |
Keywords
- Depolarization
- EPSP/spike dissociation
- High K irrigation
- Hippocampus
ASJC Scopus subject areas
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology