Abstract
In this work, we highlight an electrophysiological feature often observed in recordings from mouse CA1 pyramidal cells that has so far been ignored by experimentalists and modelers. It consists of a large and dynamic increase in the depolarization baseline (i.e., the minimum value of the membrane potential between successive action potentials during a sustained input) in response to strong somatic current injections. Such an increase can directly affect neurotransmitter release properties and, more generally, the efficacy of synaptic transmission. However, it cannot be explained by any currently available conductance-based computational model. Here we present a model addressing this issue, demonstrating that experimental recordings can be reproduced by assuming that an input current modifies, in a time-dependent manner, the electrical and permeability properties of the neuron membrane by shifting the ionic reversal potentials and channel kinetics. For this reason, we propose that any detailed model of ion channel kinetics for neurons exhibiting this characteristic should be adapted to correctly represent the response and the synaptic integration process during strong and sustained inputs.
Highlights
The standard experimental current-clamp protocols, used routinely and almost exclusively to establish the electrophysiological properties and the excitability profile of neurons, are to inject different currents into the soma and record its membrane voltage for a few hundreds of milliseconds
The peak amplitude of the action potentials (APs) was not changed significantly (Mann-Whitney test, p 1⁄4 0.244, calculated from the first AP of traces for 0.15- and 0.4-nA current injection). This is surprising, given that the increase of the depolarization baseline (DBL) should result in incomplete Naþ current recovery from inactivation. These results suggest that pyramidal neurons of mice, at least in the CA1 region of the hippocampus, may harbor an intrinsic electrophysiological mechanism responsible for limiting membrane repolarization after an AP, during a sustained input, without affecting the peak AP amplitude
We investigated what would happen in a CA1 pyramidal cell during a bursting excitatory synaptic activity eliciting up and down states similar to those observed during spatial exploration [26] or expected from a theta-burst long term potentiation (LTP) induction protocol [27–30]
Summary
The standard experimental current-clamp protocols, used routinely and almost exclusively to establish the electrophysiological properties and the excitability profile of neurons, are to inject different currents into the soma and record its membrane voltage for a few hundreds of milliseconds. Different variations on this common theme are applied to study specific characteristics or properties. We introduce and investigate a new electrophysiological feature often observed experimentally in mice It consists of a large and transient increase in the average depolarization baseline (DBL), defined as the minimum value of the membrane potential between action potentials during a sustained input, as a function of current injection. We present a model that addresses this and suggest that it can be caused by a previously unnoticed and uncharacterized large dynamic change in the local cell’s ionic permeability
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