The subiculum sensitizes retrosplenial cortex layer 2/3 pyramidal neurons

Key points Neurons in the retrosplenial cortex (RSC), a cerebral region that connects synaptically with various brain regions, are known to increase neuronal activity in accordance with hippocampal sharp wave-ripples. Pyramidal cells in granular RSC (gRSC) layer 2/3, but not layer 5, exhibit slowly ramping depolarization and considerably delayed spikes in response to a step-pulse current injection. The latencies of delayed spikes in RSC layer 2/3 pyramidal neurons were shortened by a preceding current injection. This effect was mimicked by activation of axonal afferents from the subiculum, but not of neocortical afferents. The subiculum is likely to facilitate information processing and flow in the RSC. The retrosplenial cortex (RSC), a cerebral region involved in diverse cognitive functions, is an anatomical hub that forms monosynaptic connections with various brain areas. Here, we report a unique form of short-term intrinsic plasticity in mouse granular RSC layer 2/3 pyramidal cells. These cells exhibited delayed spikes in response to somatic current injection, but the spike latencies were shortened by a preceding brief depolarization (priming). This priming-induced sensitization is distinct from desensitization, which is commonly observed in other cortical neurons. The facilitatory priming effect lasted for more than 3 s, providing a time window for increased sensitivity to RSC inputs. Based on in vitro and in vivo patch-clamp recordings following optogenetic stimulation of axonal fibres, we found that preactivation of subicular afferents replicated the facilitatory priming effect. The results suggest that subicular inputs to RSC layer 2/3 neurons may modulate subsequent information integration in the RSC layer 2/3 circuits.

Automated summary

Neurons in the retrosplenial cortex (RSC) exhibit short-term intrinsic plasticity, in which delayed spikes in response to current injection can be shortened by a preceding depolarization. This priming-induced sensitization lasts for more than 3 seconds, potentially modulating subsequent information integration in RSC circuits. Activation of subicular afferents replicates this facilitatory priming effect, suggesting a role for subicular inputs in regulating RSC neuronal activity.