Open AccessUnmyelinated axons in the rat hippocampus hyperpolarize and activate an H current when spike frequency exceeds 1 Hz
Author(s) -
A. F. Soleng,
Kenneth Chiu,
Morten Raastad
Publication year - 2003
Publication title -
journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.048058
Subject(s) - neuroscience , hyperpolarization (physics) , chemistry , stimulation , soma , bicuculline , axon , bursting , tetanic stimulation , biophysics , gabaa receptor , biology , inhibitory postsynaptic potential , excitatory postsynaptic potential , receptor , biochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
The mammalian cortex is densely populated by extensively branching, thin, unmyelinated axons that form en passant synapses. Some thin axons in the peripheral nervous system hyperpolarize if action potential frequency exceeds 1-5 Hz. To test the hypothesis that cortical axons also show activity-induced hyperpolarization, we recorded extracellularly from individual CA3 pyramidal neurons while activating their axon with trains consisting of 30 electrical stimuli. Synaptic excitation was blocked by kynurenic acid. We observed a positive correlation between stimulation strength and the number of consecutive axonal stimuli that resulted in soma spikes, suggesting that the threshold increased as a function of the number of spikes. During trains without response failures there was always a cumulative increase in the soma response latency. Intermittent failures, however, decreased the latency of the subsequent response. At frequencies of > 1 Hz, the threshold and latency increases were enhanced by blocking the hyperpolarization-activated H current (Ih)by applying the specific Ih blocker ZD7288 (25 microM) or 2 mM Cs+. Under these conditions, response failures occurred after 15-25 stimuli, independent of the stimulation strength. Adding GABA receptor blockers (saclofen and bicuculline) and a blocker of metabotropic glutamate receptors did not change the activity-induced latency increase in recordings of the compound action potential. We interpret these results as an activity-induced hyperpolarization that is partly counteracted by Ih. Such a hyperpolarization may influence transmitter release and the conduction reliability of these axons.