[Involvement of protein kinase C in NMDAR-dependent long-term potentiation in rat amygdala.]

The mechanism of long-term potentiation (LTP) in basolateral amygdala (BLA) was explored using field potential recording in rat brain slice preparation. Field potentials (field excitatory post-synaptic potentials, fEPSPs) in BLA were evoked with sharpened steel bipolar stimulating electrodes placed in the external capsule (EC). Two theta burst stimulations (TBS, interval=10 min) induced LTP in BLA. TBS-induced synaptic potentiation lasted for more than 30 min after the second TBS. LTP in BLA was input-specific and was blocked by N-methyl-D-aspartate receptor (NMDAR) antagonist 2-amino-5-phosphonovaleric acid (APV). The effect of protein kinase C (PKC) on LTP was then determined using PKC inhibitor chelerythrine chloride. Bath application of chelerythringe chloride had no effect on basic field potentials and paired-pulse ratio (PPR). However, in the presence of chelerythrine chloride, two TBS failed to induce LTP. In contrast, bath application of chelerythrine chloride 10 min after the second TBS did not affect the maintenance of LTP in BLA. These results indicate that LTP is NMDAR-dependent and PKC is involved in the induction and early maintenance of LTP in BLA.