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 |
Externally published | Yes |
Bibliographical note
Funding Information:This study was supported by the Brain Korea 21 project in 2002 and a grant to Dr Youn-Kwan Park from the Korea University Medical Science Research Center (Grant No. HO311000). All procedures were in accordance with guidelines outlined by the Institutional Animal care and Use Committee of Korea University.
Keywords
- Depolarization
- EPSP/spike dissociation
- High K irrigation
- Hippocampus
ASJC Scopus subject areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology