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Differential Cholinergic Modulation of Ca²⁺ Transients Evoked by Backpropagating Action Potentials in Apical and Basal Dendrites of Cortical Pyramidal Neurons

¹Department of Physiology, College of Medicine, and ²Catholic Neuroscience Center, The Catholic University of Korea, Seoul, South Korea

Submitted 18 January 2008; accepted in final form 14 April 2008

The effect of the cholinergic agonist carbachol (CCh) on backpropagating action potential (bAP)–evoked Ca²⁺ transients in distal apical and basal dendrites of layer 2/3 pyramidal neurons in the primary visual cortex of rats was studied using whole cell recordings and confocal Ca²⁺ imaging. In the presence of CCh (20 µM), initial bAP-evoked Ca²⁺ transients were followed by large propagating secondary Ca²⁺ transients that were restricted to proximal apical dendrites 40 µm from the soma. In middle apical dendrites (41–100 µm from the soma), Ca²⁺ transients evoked by AP bursts at 20 Hz, but not by single APs, were increased by CCh without secondary transients. CCh failed to increase the bAP-evoked Ca²⁺ transients in distal apical dendrites (101–270 µm from the soma). In contrast, in basal dendrites, CCh increased Ca²⁺ transients evoked by AP bursts, but not by single APs, and these transients were relatively constant over the entire length of the dendrites. CCh further increased the enhanced bAP-evoked Ca²⁺ transients in the presence of 4-aminopyridine (200 µM), an A-type K⁺ channel blocker, in basal and apical dendrites, except in distal apical dendrites. CCh increased large Ca²⁺ transients evoked by high-frequency AP bursts in basal dendrites, but not in distal apical dendrites. CCh-induced increase in Ca²⁺ transients was mediated by InsP₃-dependent Ca²⁺-induced Ca²⁺-release. These results suggest that cholinergic stimulation differentially increases the bAP-evoked increase in [Ca²⁺]_i in apical and basal dendrites, which may modulate synaptic activities in a location-dependent manner.