Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea-pig hippocampal pyramidal cells.
1. Intracellular and extracellular recordings of CA1 and CA3 neurones were performed in guinea-pig hippocampal slices to examine synaptic activities dependent on metabotropic glutamate receptors (mGluRs). 2. Long burst activities were elicited by 4-aminopyridine in the presence of ionotropic glutamate receptor and GABAA receptor blockers (6-cyano-7-nitroquinoxaline-2,3-dione and 3-(RS-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, and picrotoxin). Long bursts were also elicited by alpha-dendrotoxin. 3. Long bursts consisted of a 5-25 s depolarization with overriding action potentials and occurred rhythmically at intervals ranging from 1 to 20 min. Long bursts were generated in a population of CA3 neurones and the synchronized output elicited long bursts in CA1 cells. Depolarizing potentials underlying long bursts in CA1 cells had a reversal potential of -14.8 +/- 5.1 mV. 4. Long burst-associated depolarizations in CA1 neurones were suppressed by local application of L-(+)-2-amino-3-phosphonopropionic acid (L-AP3) and of the phenylglycine derivatives (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), S-4-carboxyphenylglycine (S-4CPG) and S-4-carboxy-3-hydroxyphenylglycine (S-4C3HPG). (-)-MCPG or atropine application did not affect the long burst-associated depolarization. 5. Bath perfusion of (+)-MCPG (0.5 mM), S-4CPG (0.5 mM), S-4C3HPG (0.5 mM) or L-AP3 (1 mM) blocked the occurrence of long bursts. 6. The results suggest that the long burst-associated depolarizations are synaptic potentials dependent on mGluR activation. Activation of mGluRs may also be involved in the generation of synchronized long bursts in the CA3 region.
Bianchi
R
R
Department of Pharmacology, State University of New York Health Science Center, Brooklyn 11203, USA.
Wong
R K
RK
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D004594:Electrophysiology; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D018684:Glycine Agents / Q000494:pharmacology; D006168:Guinea Pigs; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology*; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists / Q000378:metabolism*; D013570:Synaptic Membranes / Q000187:drug effects / Q000502:physiology*
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D018684:Glycine Agents; D018094:Receptors, Metabotropic Glutamate; D002118:Calcium