Astroglial membrane potential dynamics induced by stimulation

23), we measured astroglial membrane potential depolarization and found that it reached ~ 1.3 mV

After validating the responses of the tri-compartment model to basal stimulation, we investigated the impact of trains of stimulations on the dynamics of astroglial membrane potential .

We quantified K+ neuroglial interactions during basal and high activity, and found that Kir4.1 channels play a crucial role in K+ clearance and astroglial and neuronal membrane potential dynamics, especially during repetitive stimulations, and prominently regulate neuronal excitability for 3 to 10 Hz rhythmic activity.

The associated neuronal membrane potential is coupled with the dynamics of intracellular and extracellular Na+ and K+ levels via the dependence of the neuronal currents to the Nernst equation.

This current is the initial input of a classical Hodg-kin-Huxley model, which describes the neuronal membrane potential dynamics (entry of Na+ and exit of K+).

We obtain that K+ fluxes through Kir4.1 channels vanish around astrocytic resting membrane potential (~-80 mV) and are outward during astrocytic depolarization for a fixed [KJF]O (2.5 mM, Fig.

Where the dynamics of the membrane potential V depend on the capacitance C, leak conductance gL, resting potential EL, an adaptation variable w, DC current input IO, and fluctuating synaptic currents Isyn(t).

This causes the PSC amplitude to vary as a function of the membrane potential .

Using the same presynaptic spike times and weights delivered to the observed neurons, we then optimize the parameters of these models to match both the observed membrane potential and spike timing (Fig.

We adjusted the gain of the injected fluctuating current to produce membrane potential fluctuations with ~ 15—20 mV peak to peak amplitude and DC current to achieve postsynaptic spiking ~ 5Hz.

The average input had an amplitude of 0.15 0 (corresponding to ~ 15pA, depending on o), and membrane potential responses to injection of this current again mimicked the statistics of membrane potential fluctuations in vivo with amplitudes of 15—20mV [8,38,39].

Injected currents induced membrane potential fluctuations typical for in vivo activity [8,48,49].

However, several statistical models have been developed that explicitly aim to describe the underlying membrane potential dynamics [60,61] and tend to yield more accurate spike prediction.

However, the injected fluctuating current reproduces well the membrane potential fluctuations recorded in the soma of neocortical neurons in vivo [8,48,49].

Although the model used here does not explicitly describe the underlying fluctuations in membrane potential that result from the current injection, the contribution of the cumulative coupling terms of all inputs (N = 1024, red trace in Fig.

These results suggest that, although single trial spike prediction with the GLM is quite accurate, more precise models, with additional nonlinearities [41,42] or explicit estimates of the underlying membrane potential [43], might be necessary to provide a full account of the transformations that occur as fluctuating current input leads to spiking output.

As with other integrate-and-fire models, spikes occur when the membrane potential crosses a threshold VT, after which the potential is immediately reset to Vreset.

The change to Ih conductance accounted for the differences between dendritic sag, dendritic resting membrane potential relative to the soma, and dendritic input resistance in our experiments compared to those in rat L5 somatosensory corteX (See 82 Fig.

To estimate the width of dendritic plateau potentials in the apical dendrite with long dendritic current injection, we determine the longest depolarization sustained at 20% or more above the baseline level (defined as the most hyperpolarized membrane potential during the dendritic current injection).

(b) The difference in resting membrane potential of dendrite and soma, sag, and input resistance as a function of distance from the soma in experiments (black) and the model (blue).

(top) The somatic membrane potential with (black) and without (red) NMDA conductance, in response to increasing synaptic conductance.

(bottom) The membrane potential at the location of the synapse.