A Caltech Library Service

Calcium-Dependent Persistent Facilitation of Spike Backpropagation in the CA1 Pyramidal Neurons

Tsubokawa, Hiroshi and Offermanns, Stefan and Simon, Melvin and Kano, Masanobu (2000) Calcium-Dependent Persistent Facilitation of Spike Backpropagation in the CA1 Pyramidal Neurons. Journal of Neuroscience, 20 (13). pp. 4878-4884. ISSN 0270-6474. PMCID PMC6772269. doi:10.1523/jneurosci.20-13-04878.2000.

[img] PDF - Published Version
Creative Commons Attribution.


Use this Persistent URL to link to this item:


Sodium-dependent action potentials initiated near the soma are known to backpropagate over the dendrites of CA1 pyramidal neurons in an activity-dependent manner. Consequently, later spikes in a train have smaller amplitude when recorded in the apical dendrites. We found that depolarization and resultant Ca²⁺ influx into dendrites caused a persistent facilitation of spike backpropagation. Dendritic patch recordings were made from CA1 pyramidal neurons in mouse hippocampal slices under blockade of fast excitatory and inhibitory synaptic inputs. Trains of 10 backpropagating action potentials induced by antidromic stimulation showed a clear decrement in the amplitude of later spikes when recorded in the middle apical dendrites. After several depolarizing current pulses, the amplitude of later spikes increased persistently, and all spikes in a train became almost equal in size. BAPTA (10 mM) contained in the pipette or low-Ca^(2+) perfusing solution abolished this depolarization-induced facilitation, indicating that Ca²⁺ influx is required. This facilitation was present in Gα_q knock-out mice that lack the previously reported muscarinic receptor-mediated enhancement of spike backpropagation. Therefore, these two forms of facilitation are clearly distinct in their intracellular mechanisms. Intracellular injection of either calmodulin binding domain (100 μM) or Ca²⁺/calmodulin-kinase II (CaMKII) inhibitor 281–301 (10 μM) blocked the depolarization-induced facilitation. Bath application of a membrane-permeable CaMKII inhibitor KN-93 (10 μM) also blocked the facilitation, but KN-92 (10 μM), an inactive isomer of KN-93, had no effect. These results suggest that increases in [Ca²⁺)]_i cause persistent facilitation of spike backpropagation in the apical dendrite of CA1 pyramidal neuron by CaMKII-dependent mechanisms.

Item Type:Article
Related URLs:
URLURL TypeDescription CentralArticle
Additional Information:© 2000 Society for Neuroscience. Received Dec. 20, 1999; revised March 6, 2000; accepted March 24, 2000. This work has been supported in part by grants from the Japanese Ministry of Education, Science, Sports, and Culture (to H.T. and M.K.), the Human Frontier Science Program (to M.K.), and by Special Coordination Funds for Promoting Science and Technology from the Science and Technology Agency (to H.T. and M.K.). We thank Dr. Joseph C. Callaway for helpful comments and discussion on this manuscript.
Funding AgencyGrant Number
Ministry of Education, Culture, Sports, Science and Technology (MEXT)UNSPECIFIED
Human Frontier Science ProgramUNSPECIFIED
Science and Technology Agency of JapanUNSPECIFIED
Subject Keywords:hippocampus; pyramidal neuron; dendrite; action potential; backpropagation; Ca21/calmodulin-dependent protein kinase II; neuronal excitability; neural plasticity; intracellular signaling
Issue or Number:13
PubMed Central ID:PMC6772269
Record Number:CaltechAUTHORS:20191022-111354019
Persistent URL:
Official Citation:Calcium-Dependent Persistent Facilitation of Spike Backpropagation in the CA1 Pyramidal Neurons. Hiroshi Tsubokawa, Stefan Offermanns, Melvin Simon, Masanobu Kano. Journal of Neuroscience 1 July 2000, 20 (13) 4878-4884; DOI: 10.1523/JNEUROSCI.20-13-04878.2000
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:99390
Deposited By: Tony Diaz
Deposited On:22 Oct 2019 22:08
Last Modified:16 Nov 2021 17:46

Repository Staff Only: item control page