(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) induces burst firing via an inositol-1,4,5-triphosphate-independent pathway at rat dorsolateral septal nucleus.

We have previously reported that a L-2-amino-3-phosphonopropionate (L-AP3)-sensitive metabotropic glutamate receptor was required for the induction of long-term potentiation (LTP) in rat dorsolateral septal nucleus neurons. (1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), a selective agonist for metabotropic glutamate receptors, also causes burst firing of dorsolateral septal nucleus (DLSN) neurons. In this study, we investigated whether this response was mediated by a phospholipase C-(PLC) coupled metabotropic glutamate receptor. The threshold concentration of 1S,3R-ACPD for the induction of burst firing was about 5 microM, while 10 microM 1S,3R-ACPD produced a maximal effect. L-AP3 (50 microM) reduced the burst firing induced by 1S,3R-ACPD (5 microM). Although 1S,3R-ACPD stimulated the formation of inositol-1,4,5-triphosphate [Ins(1,4,5)P3] suggesting the presence of PLC-coupled metabotropic glutamate receptors, it was only effective in a higher (30-100 microM) concentration range. In addition, the 1S,3R-ACPD-stimulated formation of Ins(1,4,5)P3 level was not affected by L-AP3. These observations suggest that the 1S,3R-ACPD induced burst firing is not mediated by PLC-coupled metabotropic glutamate receptors.