MUSCARINIC MODULATION OF SPIKE BACKPROPAGATION IN THE APICAL DENDRITES OF HIPPOCAMPAL CA1 PYRAMIDAL NEURONS

In pyramidal neurons from the CA1 region of the rat hippocampus, Na+-d ependent action potentials backpropagate over the dendrites in an acti vity-dependent manner. Consequently, later spikes in a train have smal ler amplitudes when recorded in the apical arbors, We studied the effe ct of the cholinergic agonist carbachol (CCh) on this pattern of activ ity when spikes were evoked synaptically or antidromically in the tran sverse slice preparation. Concentrations as low as 1 mu M were effecti ve in reversing the modulation, making the amplitude of all spikes in a train equal and independent of the frequency of spike firing, CCh di d not change the propagation of the first spike in a train. These effe cts of CCh were blocked by 1 mu M atropine, showing that only muscarin ic receptors were involved, The effects of CCh an the pattern of spike propagation were observed in the proximal and middle dendrites, but r ecordings in the distal dendrites (>300 mu m from the soma) showed tha t CCh did not boost the amplitude in this region. intracellular BAPTA (10 mM) or EGTA (10 mM) had no effect on activity-dependent backpropag ation but blocked the effect of CCh. Backpropagating spikes caused inc reases in [Ca2+](i) at all dendritic locations, in the middle and dist al dendrites these increases normally peaked at the time of the first few large action potentials. In association with the enhancement of sp ike backpropagation, CCh increased the amplitude and duration of the t rain-evoked [Ca2+](i) changes. These effects of CCh on dendritic spike potentials and associated [Ca2+](i) changes may be important in modul ating synaptic integration and plasticity in these neurons.