Figure 4
Learning-induced hyperpolarization of the fIPSP is not dependent on PKA or CaMKKI activation. (A) Example of the effect of the PKA blocker, H89, on the fIPSP in a neuron taken from a trained rat. Amplitude of the fIPSP was recorded at several holding potentials. IPSPs were measured at the first peak, as appeared in the most depolarized recording potential. Numbers on the left of the traces note the holding membrane potential. These measurements were then used to calculate the reversal potential of the responses. (B) The reversal potentials of the synaptic responses shown in A were determined by the linear regression line, describing the amplitude of the synaptic potential as a function of the membrane holding potential. Application of H89 had no effect on the fIPSP reversal potential. (C) The averaged reversal potential of the fIPSP in neurons from trained and control rats is not modified by H89 application. Data were taken from 7 trained rats (dark bars) and 11 control rats (light bars). Values represent mean ± SE. (D) Example of the effect of the cell-penetrating peptide inhibitor, tatCN21, on the fIPSP in a neuron taken from a trained rat. Amplitude of the fIPSP was recorded at several holding potentials. IPSPs were measured at the first peak, as appeared in the most depolarized recording potential. Numbers on the left of the traces note the holding membrane potential. These measurements were then used to calculate the reversal potential of the responses. (E) The reversal potentials of the synaptic responses shown in D were determined by the linear regression line, describing the amplitude of the synaptic potential as a function of the membrane holding potential. Application of tatCN2 had no effect on the fIPSP reversal potential. (F) The averaged reversal potential of the fIPSP is in neurons from trained and control rats is not modified by tatCN2 or KN93 application. Data was taken from 9 trained rats (dark bars) and 14 control rats (light bars). Values represent mean ± SE.
