Differential cholinergic modulation of Ca2+ transients evoked by backpropagating action potentials in apical and basal dendrites of cortical pyramidal neurons.
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 microM), initial bAP-evoked Ca2+ transients were followed by large propagating secondary Ca2+ transients that were restricted to proximal apical dendrites < or =40 microm from the soma. In middle apical dendrites (41-100 microm 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 microm 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 microM), 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.
Cho
Kwang-Hyun
KH
Department of Physiology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul 137-701, South Korea.
Jang
Hyun-Jong
HJ
Lee
Eun-Hui
EH
Yoon
Shin Hee
SH
Hahn
Sang June
SJ
Jo
Yang-Hyeok
YH
Kim
Myung-Suk
MS
Rhie
Duck-Joo
DJ
D015761:4-Aminopyridine / Q000494:pharmacology; D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D000818:Animals; D000925:Anticoagulants / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D004396:Coloring Agents / Q000494:pharmacology; D003712:Dendrites / Q000187:drug effects / Q000502:physiology*; D004307:Dose-Response Relationship, Radiation; D005246:Feedback / Q000187:drug effects / Q000502:physiology*; D006493:Heparin / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D017966:Pyramidal Cells / Q000166:cytology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012430:Ruthenium Red / Q000494:pharmacology; D014793:Visual Cortex / Q000166:cytology*
D000925:Anticoagulants; D018679:Cholinergic Agonists; D004396:Coloring Agents; D026902:Potassium Channel Blockers; D012430:Ruthenium Red; D002217:Carbachol; D006493:Heparin; D015761:4-Aminopyridine; D000109:Acetylcholine; D002118:Calcium