Abstract
The polarity of excitability changes associated with induction of Long-Term synaptic Depression (LTD) in CA1 pyramidal neurons is a contentious issue. Postsynaptic neuronal excitability after LTD induction is found to be reduced in certain cases (i.e. synergistic changes) but enhanced in others (i.e. compensatory or homeostatic). We examined here whether these divergent findings could result from the activation of two separate mechanisms converging onto a single learning rule linking synergistic and homeostatic plasticity. We show that the magnitude of LTD induced with low frequency stimulation (LFS) of the Schaffer collaterals determines the polarity of intrinsic changes in CA1 pyramidal neurons. Apparent input resistance (Rin) is reduced following induction of moderate LTD (<20–30%). In contrast, Rin is increased after induction of large LTD (>40%) induced by repetitive episodes of LFS. The up-regulation of Ih observed after moderate LTD results from the activation of NMDA receptors whereas the down-regulation of Ih is due to activation of mGluR1 receptors. These changes in Rin were associated with changes in intrinsic excitability. In conclusion, our study indicates that changes in excitability after LTD induction follow a learning rule describing a continuum linking synergistic and compensatory changes in excitability.
Highlights
In central neurons, changes in intrinsic neuronal excitability have been shown to occur in parallel with synaptic modifications, affecting synergistically synaptic strength and dendritic integration in the post-synaptic neuron[1,2]
Excitatory Post-Synaptic Potentials (EPSPs) were evoked in CA1 pyramidal neurons recorded in whole-cell configuration by stimulating the Schaffer collaterals at 0.1 Hz
We show here that in CA1 pyramidal neurons, Long-Term synaptic Depression (LTD) magnitude determines the changes in input resistance (Rin) and the direction of Ih regulation
Summary
Changes in intrinsic neuronal excitability have been shown to occur in parallel with synaptic modifications, affecting synergistically synaptic strength and dendritic integration in the post-synaptic neuron[1,2]. As previously reported for LTP17, modulation of Rin was not associated with significant change in Vm following induction of LTD (−62.3 ± 0.9 mV in control and −61.8 ± 0.6 mV after the 3rd episode of 3 Hz stimulation, p > 0.1; Supplementary Figure 1).
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