Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.18.102913v1?rss=1 Authors: Murphy, C. A., Banks, M. I. Abstract: While their behavioral effects are well-characterized, the mechanisms by which anesthetics induce loss of consciousness are largely unknown. Anesthetics may disrupt integration and propagation of information in corticothalamic networks. Recent studies have shown that isoflurane diminishes synaptic responses of thalamocortical (TC) and corticocortical (CC) afferents in a pathway-specific manner. However, whether the synaptic effects of isoflurane observed in extracellular recordings persist at the cellular level has yet to be explored. Here, we activate TC and CC layer 1 inputs in non-primary mouse neocortex in ex vivo brain slices and explore the degree to which isoflurane modulates synaptic responses in pyramidal cells and in two inhibitory cell populations, somatostatin-positive (SOM+) and parvalbumin-positive (PV+) interneurons. We show that the effects of isoflurane on synaptic responses and intrinsic properties of these cells varies among cell type and by cortical layer. Layer 1 inputs to L4 pyramidal cells were suppressed by isoflurane at both TC and CC synapses, while those to L2/3 pyramidal cells and PV+ interneurons were not. TC inputs to SOM+ cells were rarely observed at all, while CC inputs to SOM+ interneurons were robustly suppressed by isoflurane. These results suggest a mechanism by which isoflurane disrupts integration and propagation of incoming cortical signals. Copy rights belong to original authors. Visit the link for more info