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Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea‐pig hippocampal pyramidal cells.
Author(s) -
Bianchi R,
Wong R K
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp020908
Subject(s) - depolarization , bursting , metabotropic glutamate receptor , excitatory postsynaptic potential , neuroscience , chemistry , glutamate receptor , metabotropic receptor , biophysics , neurotransmission , quisqualic acid , biology , receptor , ampa receptor , inhibitory postsynaptic potential , biochemistry
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.