Society for Neuroscience 28th Annual Meeting, 07.11-12.11.1998, Los Angeles / USA.

Synaptically driven intradendritic Ca2+ waves in rat hippocampal CA1 neurons signals

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

LTP has for a long time been believed to be input-specific. However, Engert & Bonhoeffer have recently shown (Nature 388, 279-284) that input specificity of LTP is not detectable within 70 µm from the stimulated synapse and that synapses in close proximity to a site of potentiation are also potentiated. We postulate, that the propagation of the second messenger Ca2+, which we were able to observe in the form of Ca2+ waves, represents a special kind of intracellular signaling in neurons during LTP induction, possibly being responsible for the lack of input-specifity.
We show, using confocal microscopy, that local LTP-relevant electrical stimulation of the Schaffer collaterals of CA1 neurons can elicit an increase in intradendritic Ca2+ concentration which propagates as a wave within the dendrite. In 7 of 10 cells (Na+ spikes blocked by QX-314; 30 mM) the fluorescence signal could be described as biphasic: consisting of a fast initial component due to Ca2+-influx, primarily through NMDA receptor channels; and a second component, which propagates as a wave with the speed of up to 100 µm/s. The characteristics of the first component of the transients remained comparable in several dendritic regions, whereas the second component showed obvious differences in the time after which its maximal value was reached. Furthermore, we found the existence of a threshold for the appearance of the late component of the Ca2+ transients. The relatively high speed of waves, points to the involvement of mechanisms other than Ca2+ diffusion, e.g. InsP3- and/or Ca2+-induced Ca2+ release from internal stores.
We conclude that synaptically-driven slow-spreading Ca2+ waves might function in support of mechanisms essential for the induction and maintenance of synaptic plasticity, by potentiating neighboring synaptic inputs that have not been synaptically activated.
This work was supported by the DFG (SFB 426).

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