Population spike was recorded from the medial and central nucleus of the amygdala (AMG) in an in vitro slice preparation following stimulation of the stria terminalis (ST). The population spike was completely suppressed by 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM), a non-NMDA receptor antagonist, but not affected by 3-[(+)-2-carboxypiperazine-4-yl-]-propyl-1-phosphonic acid (CPP) (20 μM), a competitive NMDA receptor antagonist. Tetanic stimulation to the ST induced long-term potentiation (LTP) in both the medial and central AMG. Tetanic stimulation of 20 s in duration and 50 Hz in frequency most effectively potentiated the population spike. All the NMDA antagonists tested, such as CPP (20 μM), (+)-5-methyl-10,1 1-dihydro-5H-dibenzo-[a,d]-cyclohepten-5,10-imine-hydrogen maleate (30 gmM) and 7-chlorokynurenic acid (30 gmM), significantly depressed the formation of LTP in the medial AMG. 2-Amino-3-phosphonopropionate ( 1 mM), a metabotropic glutamate receptor antagonist, and intracerebral ventricular injection of ilet activating protein had no significant effects on the formation of LTP. Furthermore, the LTP formation of EPSP was completely blocked in BAPTA [bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid]-loaded medial AMG neurons. These results indicate that Ca2+ influx mainly through NMDA receptors is crucial for the induction of LTP in the ST-medial AMG neuron synapses.
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