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The single-channel current amplitude is related to the GABA concentration resulting in a single-channel GABA affinity (EC50) in intact CA1 neurons of 17 pM with the maximal current amplitude reached with 1 nM GABA.
As Imax = i×N×P(O max, where i is unitary current, N is the number of channels, and P(O max is the maximum open probability that can be achieved, a change in any of these parameters will cause maximal current amplitude to change.
The time course of recovery of IK from inactivation was fitted with a mono-exponential function: I/Imax = A*{1 exp[−Δt/τ]}, where Imax is the maximal current amplitude; I is the current after a recovery period of Δt; τ is the time constant; A is the amplitude coefficient.
The maximal current amplitude was increased several fold due to stabilization of the activated-open state.
It is stated that "The maximal current amplitude was increased several fold due to stabilization of the activated-open state".
The relative maximal current amplitude (R max) of dopamine compared to 5-HT also differed at 5-HT3A (0.08) and 5-HT3AB receptors (0.19).
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To exclude voltage-clamp errors, oocytes with maximal current amplitudes >3 μA were discarded.
With THIP as agonist, flupirtine increased maximal current amplitudes by a factor of 8.
In α1β2 receptors, GABA EC50 values were reduced in the presence of flupirtine as were maximal current amplitudes.
In addition, in two of these receptors (α1β2γ2S and α5β3γ2S), maximal current amplitudes were significantly reduced by flupirtine.
In contrast to A749G, mutation G407R reduced maximal current amplitudes and caused no change in activation voltage dependence.
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