Abstract
Although electrical properties of the dendrites are going to be clarifying, little is known about the physiological roles of dendritic spike. Since spike backpropagation could depolarize the inhibitory postsynapses, it may induce transient suppression of GABAergic inhibition (DSI) through an activation of presynaptic cannabinoid receptor (CBR). In this study, we examined whether action potentials induce DSI in mouse hippocampal neurons. Whole-cell voltage-clamp or current-clamp recording was made from the soma and/or the dendrite of CA1 neurons, and changes in amplitude of IPSCs (or IPSPs) after antidromic action potentials were analyzed. We found that train of antidromic spikes could induce transient suppression of GABAergic IPSCs (or IPSPs), which have CBR-dependent and TEA-sensitive components. However, depolarization by current injection to the dendrite failed to induce CBR-dependent suppression, indicating that somatic depolarization was required. In the presence of TEA, application of phorbol ester, which facilitates spike backpropagation, enhanced DSI, and application of somatostatine, which inhibits backpropagation, reduced DSI. These results suggest that in physiological condition antidromic invasion of Na+ spikes into dendrites induce DSI in hippocampal GABAergic synapses. Supported by a grant from Japanese Ministry of Education, Science, Sports and Culture (to H.T). [J Physiol Sci. 2007;57 Suppl:S153]
