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Volume 16, Number 19, Issue of October 1, 1996 pp. 6079-6088
Copyright ©1996 Society for Neuroscience

Activation of a Metabotropic Excitatory Amino Acid Receptor Potentiates Spike-Driven Calcium Increases in Neurons of the Dorsolateral Septum

Received Jan. 23, 1996; revised July 2, 1996; accepted July 9, 1996.

Fang Zheng^{1, 3}, Joel P. Gallagher², and John A. Connor^{1, 4}

¹ Roche Institute of Molecular Biology, Nutley, New Jersey 07110-1199, ² Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555-1031, ³ Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia 30322, and ⁴ The Lovelace Institute, Albuquerque, New Mexico 87105

(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), an agonist for metabotropic glutamate receptors (mGluRs), causes depolarization and burst firing in rat dorsolateral septal nucleus (DLSN) neurons and results in long-term potentiation (LTP) at DLSN synapses. In the present study, we investigated whether these actions of 1S,3R-ACPD are attributable to the release of calcium from an inositol triphosphate-sensitive store after activation of mGluRs coupled to phospholipase C. Our data demonstrated that the ACPD-induced depolarization was associated with a small but significant decrease, not an increase, in [Ca²⁺]_i; however, changes of [Ca²⁺]_i during ACPD-induced bursting were up to seven times larger than those produced by regular firing. Depletion of internal calcium stores by thapsigargin or ryanodine had a small to insignificant effect on the maximum changes of [Ca²⁺]_i associated with ACPD-induced bursting. Thus, elevation of [Ca²⁺]_i during firing by 1S,3R-ACPD is likely attributable to enhancement of calcium influx through voltage-gated channels and not to calcium release from internal stores. ACPD-induced burst firing elevated somatic and dendritic calcium levels up to 3 and 6 µM, respectively. Such an increase may be the underlying mechanism for ACPD-induced LTP as well as ACPD-induced acute cell death in rat DLSN.

Key words: metabotropic glutamate receptors; intracellular calcium; long-term potentiation; neurotoxicity; thapsigargin; ryanodine; voltage-gated calcium channels

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