Abstract
The Hebbian type of spike timing-dependent plasticity (STDP) with long-term potentiation and depression (LTP and LTD) plays a crucial role at layer 4 (L4) to L2/3 synapses in deprivation-induced map plasticity. In addition, plasticity at the L2/3 horizontal connection is suggested to play an additional role in map plasticity, especially for "spared whisker response potentiation." Unimodal STDP with only LTP, or all-LTP STDP drives circuit formation at thalamocortical, as well as L4-L2/3 synapse before the critical period. Here, we first show that the L2/3 horizontal connections exhibit all-LTP STDP when axons are extending during synapse formation before the critical period. LTP-STDP induced by pre-post timing was mediated by NMDA-R because APV blocked the induction. In addition, PKA signaling was involved because PKI 6-22 blocked the induction. However, LTP-STDP induced by post-pre timing was not mediated by NMDA-R, because APV could not block its induction. Nevertheless, PKA signaling was also involved in its induction because PKI 6-22 blocked the induction. Our finding indicates that PKA signaling plays an important role in all-LTP STDP during synaptic formation at the L2/3-L2/3 connection between neighboring columns with a distinct source of Ca(2+) influx in the developing mouse barrel cortex.