Abstract Hamburg

Joint Congress of the German Physiological Society (77th Meeting) and the Scandinavian Physiological Society (56th Meeting) March 8-12, 1998, Hamburg, Germany

Pflugers Archive European Journal of Physiology Suppl. to Vol. 435, No. 6, P17-7 (1998)
Metabotropic glutamate receptors are involved in intradendritic Ca²⁺ rises by local high frequency stimulation of hippocampal Schaffer-collateral CA1 synapses

T. Jäger, K.G. Reymann and T. Behnisch

Long-term synaptic efficacy enhancement is achieved by an increase in the intracellular Ca²⁺ concentration ([Ca²⁺]_i), besides the activation of a variety of signal cascades. Whereas the role of internal Ca²⁺ stores (ICSs) and their activation, e.g. by metabotropic glutamate receptors (mGluRs), in tetanization-mediated Ca²⁺ increases is still a matter of discussion, the Ca²⁺ entry via N-methyl-D-aspartate (NMDA) receptors is undoubtedly associated with hippocampal long-term potentiation (LTP) induction in rats. We used a high-speed confocal imaging system (Noran Odyssey XL) for acquisition of [Ca²⁺]_i changes, induced by 100 Hz tetanizations - commonly used for the induction of LTP. CA1-neurones were filled with both the Ca²⁺ fluorescent indicator Calcium Green-1 (2 mM) and the lidocaine derivate QX-314 (30 mM) to inhibit the sodium spike mediated activation of voltage dependent calcium channels. The tetanization-induced Ca²⁺ transients were reduced both by the mGluR class I agonist 3,5-dihydroxyphenylglycine (DHPG; 15 µM; n=3) and the mGluR class I antagonist (S)-4-carboxy-phenylglycine (4-CPG; 50 µM; n=6) by one third. After drugs were washed out, the Ca2+ rise upon tetanization recovered to the Ca²⁺ amount before drug applications. In addition, we show that the DHPG (n=3) induces a temporal increase of [Ca²⁺]_i in dendrites, probably due to the release of Ca²⁺ from ICSs. Cyclopiazonic acid (CPA; 10 µM; n=3), an compound that depletes all ICSs by blocking ATP-dependent Ca²⁺ uptake into intracellular compartments, reduced the release of Ca²⁺ in response to tetanizations by one third. No recovery of the Ca²⁺ rise was observed after CPA wash-out, in contrast to the other used drugs. We propose, that the effect of 4-CPG on the tetanization dependent Ca²⁺ rise is due to an inhibition of class I mGluRs, thus not allowing Ca²⁺ to be released from ICSs.
We conclude, that the tetanization induced increases in local intradendritic [Ca²⁺]_i is dependent upon the activation of metabotropic glutamate receptor mGluR-linked Ca²⁺ rises besides the necessary Ca²⁺ influx via NMDA receptors.
This work was supported by the DFG (SFB 426).

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