2nd International Symposium on Synaptic Transmission,
08.-09.05.1998, Barcelona / Spain.
Characteristics of intradendritic Ca2+ signals
in hippocampal CA1 neurons induced by a variety of LTP-paradigms
T. Jäger, T. Behnisch and K.G. Reymann
Changes in the intracellular Ca2+ concentration evoked by intense synaptic stimulation result in the modulation of second messenger cascades which are responsible for the induction of long-term potentiation (LTP) of Schaffer-collateral-CA1 synapses. We investigated Ca2+ rises, evoked by different 100 Hz tetanization paradigms, which are commonly used to induce LTP. The data was obtained with the combined use of confocal laser scanning microscopy of Ca2+ dependent fluorescence changes and intracellular electrophysiological recordings.
Our results reveal, that the normalized total area of fluorescence-intensity changes is correlated both to the strength and the duration of tetanization. Subdividing the overall fluorescence signal into a tetanic and a post-tetanic component demonstrate that: (i) The normalized area of fluorescence-intensity changes during the time of tetanization is correlated linearly to the tetanization duration. (ii) The tetanic component strongly determines the area of the post-tetanic Ca2+ signal. (iii) The normalized relationship of the post-tetanic Ca2+ signal to the total Ca2+ change decreases when the tetanization duration was prolonged. (iv) With an increased stimulation strength, a positive correlation of the relationship of the post-tetanic component to the total amount Ca2+ could be observed. Furthermore, a strong dependence between the time constants of the decay phase of the Ca2+ transients and the duration of tetanization was found, indicating that the time constant is not uniform but dependent upon the employed tetanization paradigm.
Blocking action potential-mediated activation of voltage-dependent Ca2+ channels, thus minimizing the Ca2+-entry into neurons, allows a subtle investigation of the different local Ca2+ sources involved in the tetanization-induced Ca2+ rise in dendrites. Our pharmacological investigation of the fluorescence-intensity changes induced by two different tetanizations have shown that the Ca2+ signal in dendrites can be reduced by (i) metabotropic glutamate receptor (mGluR) class I agonists, (ii) mGluR class I antagonists and (iii) depletors of the intracellular Ca2+ stores.
Detailed investigation of the tetanic and post-tetanic Ca2+ components reveals a shift in the ratio of the post-tetanic/tetanic area: the mGluR agonist increases the part of the tetanic area, whereas the depletors of the intracellular Ca2+ stores raise the part of the post-tetanic area in relation to the overall Ca2+ signal. These data show the impact of Ca2+ release from intracellular Ca2+ stores within the total Ca2+ signal upon LTP-relevant tetanizations.
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