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 ac tivities dependent on metabotropic glutamate receptors (mGluRs). 2. Lo ng burst activities were elicited by 4-aminopyridine in the presence o f ionotropic glutamate receptor and GABA(A) receptor blockers (6-cyano -7-nitroquinoxaline-2,3-dione and 3-(RS2-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 depolarizatio n with over riding action potentials and occurred rhythmically at inte rvals ranging from 1 to 20 min. Long bursts were generated in a popula tion of CA3 neurones and the synchronized output elicited long bursts in CA1 cells. Depolarizing potentials underlying long bursts in CA1 ce lls had a reversal potential of -14.8 +/- 5.1 mV. Long burst-associate d depolarizations in CA1 neurones were suppressed by local application of L-(+)-2-amino-3-phosphonopropionic acid (L-AP3) and of the phenylg lycine derivatives (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), S-4-carboxyphenylglycine (S-4CPG) and S4-carboxy-3-hydroxyphenylglyci ne (S-4C3HPG). (-)-MCPG or atropine application did not affect the lon g 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 oc currence of long bursts. 6. The results suggest that the long burst-as sociated depolarizations are synaptic potentials dependent on mGluR ac tivation. Activation of mGluRs may also be involved in the generation of synchronized long bursts in the CA3 region.