Spike timing and synaptic plasticity in the premotor pathway of birdsong

Abstract

The neural circuits of birdsong appear to utilize specific time delays in their operation. In particular, the anterior forebrain pathway (AFP) is implicated in an approximately 40- to 50- ms time delay, ΔT, playing a role in the relative timing of premotor signals from the nucleus HVc to the nucleus robust nucleus of the archistratium (RA) and control/learning signals from the nucleus lateral magnocellular nucleus of the anterior neostratium (lMAN) to RA. Using a biophysical model of synaptic plasticity based on experiments on mammalian hippocampal and neocortical pyramidal neurons, we propose an understanding of this ≈ 40- to 50- ms delay. The biophysical model describes the influence of Ca2+ influx into the postsynaptic RA cells through NMDA and AMPA receptors and the induction of LTP and LTD through complex metabolic pathways. The delay, ΔT, between HVc → RA premotor signals and lMAN → RA control/learning signals plays an essential role in determining if synaptic plasticity is induced by signaling from each pathway into RA. If ΔT is substantially larger than 40 ms, no plasticity is induced. If ΔT is much less than 40 ms, only potentiation is expected. If ΔT≈ 40 ms, the sign of synaptic plasticity is sensitive to ΔT. Our results suggest that changes in ΔT may influence learning and maintenance of birdsong. We investigate the robustness of this result to noise and to the removal of the Ca2+ contribution from lMAN → RA NMDA receptors.