Distance-dependent Modifiable Threshold for Action Potential Back-propagation in Hippocampal Dendrites
Overview
Physiology
Authors
Affiliations
In hippocampal CA1 pyramidal neurons, action potentials generated in the axon back-propagate in a decremental fashion into the dendritic tree where they affect synaptic integration and synaptic plasticity. The amplitude of back-propagating action potentials (b-APs) is controlled by various biological factors, including membrane potential (Vm). We report that, at any dendritic location (x), the transition from weak (small-amplitude b-APs) to strong (large-amplitude b-APs) back-propagation occurs when Vm crosses a threshold potential, x. When Vm > x, back-propagation is strong (mostly active). Conversely, when Vm < x, back-propagation is weak (mostly passive). x varies linearly with the distance (x) from the soma. Close to the soma, x << resting membrane potential (RMP) and a strong hyperpolarization of the membrane is necessary to switch back-propagation from strong to weak. In the distal dendrites, x >> RMP and a strong depolarization is necessary to switch back-propagation from weak to strong. At approximately 260 micrometer from the soma, 260 approximately RMP, suggesting that in this dendritic region back-propagation starts to switch from strong to weak. x depends on the availability or state of Na+ and K+ channels. Partial blockade or phosphorylation of K+ channels decreases x and thereby increases the portion of the dendritic tree experiencing strong back-propagation. Partial blockade or inactivation of Na+ channels has the opposite effect. We conclude that x is a parameter that captures the onset of the transition from weak to strong back-propagation. Its modification may alter dendritic function under physiological and pathological conditions by changing how far large action potentials back-propagate in the dendritic tree.
Analysis of the mechanism of synaptic integration focusing on the charge held in the spine.
Tsubo T Biophys Physicobiol. 2022; 18:290-304.
PMID: 35004103 PMC: 8685514. DOI: 10.2142/biophysico.bppb-v18.036.
Edelmann E, Cepeda-Prado E, Lessmann V Front Synaptic Neurosci. 2017; 9:7.
PMID: 28352224 PMC: 5348504. DOI: 10.3389/fnsyn.2017.00007.
Transient potassium channels augment degeneracy in hippocampal active dendritic spectral tuning.
Rathour R, Malik R, Narayanan R Sci Rep. 2016; 6:24678.
PMID: 27094086 PMC: 4837398. DOI: 10.1038/srep24678.
Tamagawa H, Funatani M, Ikeda K Membranes (Basel). 2016; 6(1).
PMID: 26821050 PMC: 4812417. DOI: 10.3390/membranes6010011.
Mulholland P, Spencer K, Hu W, Kroener S, Chandler L Psychopharmacology (Berl). 2014; 232(11):1995-2006.
PMID: 25510858 PMC: 4426211. DOI: 10.1007/s00213-014-3835-4.