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. Author manuscript; available in PMC: 2015 Jun 22.
Published in final edited form as: Nature. 2015 Mar 30;520(7546):180–185. doi: 10.1038/nature14251

Extended Data Figure 10. Deletion of somatostatin-expressing interneuron impairs performance improvement after motor learning.

Extended Data Figure 10

a, Rotarod performance in control and SST-deleted mice subjected to forward–forward running or forward–backward running. When forward running on the accelerated rotarod was followed by backward running, SST-deleted mice displayed a reduction in their performance (the average speed animals achieved) as compared to control mice when tested again in forward running (P < 0.05, unpaired t-test). Data are mean ± s.e.m. b, A model showing the importance of BSDCS for inducing synaptic changes that affect L5 neuronal output duringmotor skill learning. Dendritic spines active (1, pink) at the time of spike generation (2) show enhanced Ca2+ activity and changes in synaptic strength (red) following the Ca2+ spike. Ca2+ spike-induced potentiation of synapses contributes to persistent synaptic changes, potentiated Ca2+ activity at the apical trunk and L5 soma, as well as improvements in performance over training sessions. In control mice, different motor tasks (that is, forward, backward running) induce Ca2+ spikes on different tuft branches of L5 neurons (not shown). Inactivation of SST interneurons results in individual dendritic branches generating Ca2+ spikes in response to both tasks (3). Loss of spatial segregation of Ca2+ spikes results in the depotentiation of synaptic changes-induced by previous learning in tuft dendritic branches and reduced Ca2+ activity in the apical trunk nexus and L5 soma when a different task is learned. SST interneuron inactivation induces a state of interference that impairs motor performance when several tasks are learned.