Symposium: Calcium signaling in the nervous system, Bogensee/Germany, 24.-27.06.1998.

Intradendritic Ca2+transients of hippocampal CA1 neurons and analysis of their tetanic and post-tetanic components

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

Synaptic plasticity is widely believed to be a cellular model for mechanisms involved in learning and memory processes. For the induction of synaptic plasticity in hippocampal Schaffer-collateral-CA1 synapses a rise in the intracellular Ca2+concentration during high frequency stimulation is essential. To investigate the dependency of tetanization-evoked Ca2+-transients from the strength of presynaptic activity during and immediately after tetanization, we combined confocal laser microscopy and intracellular recordings. Using the Ca2+-sensitive dye Calcium Green-1 we analysed intradendritic Ca2+ rises, evoked by different 100 Hz tetanization paradigms. We found that the normalized total area of fluorescence intensity changes were correlated both to the strength and duration of tetanization with correlation coefficients of 0.68 and 0.81, respectively (n = 8, p < 0.05). Further, the normalized area of fluorescence intensity changes during the time of tetanization (tetanic component) was dependent in a linear manner on the duration of tetanization (r = 0.96, p < 0.05). Moreover, the tetanic component strongly determined the area of the post-tetanic Ca2+ signal (r = 0.99, p < 0.05). Interestingly, the normalized relationship of the post-tetanic Ca2+ signal to the total Ca2+ change and to its tetanic component decreased exponentially when the durations of the tetanizations were increased (r = 0.68 and r = 0.69, respectively, p < 0.05). In contrast, with an increased stimulation strength, a positive correlation of the relationship of the post-tetanic component to the total amount of Ca2+ could be obtained (r = 0.41, p < 0.05). Our investigations demonstrate, that augmenting the strength of stimulation results in a respective increase of the post-tetanic Ca2+ portion within the total Ca2+ signal, whereas an increase of the tetanization duration does not. Thus, no further significant prolongation of the Ca2+ signal by intracellular mechanisms happens during prolongation of tetanization.

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