(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

F. Zheng, G. Lonart, K. M. Johnson, J. P. Gallagher

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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 μM, while 10 μM 1S,3R-ACPD produced a maximal effect. L-AP3 (50 μM) reduced the burst firing induced by 1S,3R-ACPD (5 μM). 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 μM) 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.

Original languageEnglish (US)
Pages (from-to)97-102
Number of pages6
JournalNeuropharmacology
Volume33
Issue number1
DOIs
StatePublished - 1994

Fingerprint

Septal Nuclei
Inositol 1,4,5-Trisphosphate
Metabotropic Glutamate Receptors
Neurons
Long-Term Potentiation
Type C Phospholipases
1-amino-1,3-dicarboxycyclopentane
2-amino-3-phosphonopropionic acid

Keywords

  • 1S
  • 3R-ACPD
  • burst firing
  • Metabotropic glutamate receptors
  • phospholipase C
  • septum

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Drug Discovery
  • Pharmacology

Cite this

(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. / Zheng, F.; Lonart, G.; Johnson, K. M.; Gallagher, J. P.

In: Neuropharmacology, Vol. 33, No. 1, 1994, p. 97-102.

Research output: Contribution to journalArticle

@article{cabee125bbfe4309a85509984ed9b9d2,
title = "(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",
abstract = "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 μM, while 10 μM 1S,3R-ACPD produced a maximal effect. L-AP3 (50 μM) reduced the burst firing induced by 1S,3R-ACPD (5 μM). 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 μM) 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.",
keywords = "1S, 3R-ACPD, burst firing, Metabotropic glutamate receptors, phospholipase C, septum",
author = "F. Zheng and G. Lonart and Johnson, {K. M.} and Gallagher, {J. P.}",
year = "1994",
doi = "10.1016/0028-3908(94)90102-3",
language = "English (US)",
volume = "33",
pages = "97--102",
journal = "Neuropharmacology",
issn = "0028-3908",
publisher = "Elsevier Limited",
number = "1",

}

TY - JOUR

T1 - (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

AU - Zheng, F.

AU - Lonart, G.

AU - Johnson, K. M.

AU - Gallagher, J. P.

PY - 1994

Y1 - 1994

N2 - 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 μM, while 10 μM 1S,3R-ACPD produced a maximal effect. L-AP3 (50 μM) reduced the burst firing induced by 1S,3R-ACPD (5 μM). 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 μM) 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.

AB - 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 μM, while 10 μM 1S,3R-ACPD produced a maximal effect. L-AP3 (50 μM) reduced the burst firing induced by 1S,3R-ACPD (5 μM). 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 μM) 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.

KW - 1S

KW - 3R-ACPD

KW - burst firing

KW - Metabotropic glutamate receptors

KW - phospholipase C

KW - septum

UR - http://www.scopus.com/inward/record.url?scp=0028179287&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028179287&partnerID=8YFLogxK

U2 - 10.1016/0028-3908(94)90102-3

DO - 10.1016/0028-3908(94)90102-3

M3 - Article

VL - 33

SP - 97

EP - 102

JO - Neuropharmacology

JF - Neuropharmacology

SN - 0028-3908

IS - 1

ER -