Abstract
Sensory processing in the cortex adapts to the history of stimulation but the mechanisms are not understood. Imaging the primary visual cortex of mice we find here that an increase in stimulus contrast is not followed by a simple decrease in gain of pyramidal cells; as many cells increase gain to improve detection of a subsequent decrease in contrast. Depressing and sensitizing forms of adaptation also occur in different types of interneurons (PV, SST and VIP) and the net effect within individual pyramidal cells reflects the balance of PV inputs, driving depression, and a subset of SST interneurons driving sensitization. Changes in internal state associated with locomotion increase gain across the population of pyramidal cells while maintaining the balance between these opposite forms of plasticity, consistent with activation of both VIP->SST and SST->PV disinhibitory pathways. These results reveal how different inhibitory microcircuits adjust the gain of pyramidal cells signalling changes in stimulus strength.
Highlights
Sensory processing in the cortex adapts to the history of stimulation but the mechanisms are not understood
Experiments in anaesthetized animals have reported that depressing adaptation is dominant in V128,29 but these results demonstrate that in awake mice there are two opposite forms of plasticity, depression and sensitization, that are roughly balanced to maintain stable levels of activity aross the population of pyramidal cells (PCs)
This investigation demonstrates that pyramidal cells in layer 2/3 of V1 adapt to a high-contrast stimulus to varying degrees and with opposite forms of plasticity
Summary
Opposite forms of adaptation across the population of pyramidal cells. To investigate contrast adaptation in V1 we used awake mice in which inhibitory activity was intact[16]. PV interneurons are relatively isolated within inhibitory networks of the cortex, establishing strong and direct connections with PCs but not transmitting significantly to SST or VIP interneurons[37], thereby making it easier to interpret their role in adaptation We expressed both ChrimsonR41 and GCaMP6f in PV cells to assess how increased excitation altered the dynamics of their response to the high-contrast stimulus. An illumination power that reduced the initial response of PCs by an average factor of 61% caused a simultaneous shift in AI towards depression (Fig. 6F; n = 535 cells; significant at p = 10−7, WSR test) This result appears paradoxical at first; over-activating or inhibiting VIP interneurons both push the population of PCs towards depression.
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