POm Thalamocortical Input Drives Layer-Specific Microcircuits in Somatosensory Cortex.
Higher-order thalamic nuclei, such as the posterior medial nucleus (POm) in the somatosensory system or the pulvinar in the visual system, densely innervate the cortex and can influence perception and plasticity. To systematically evaluate how higher-order thalamic nuclei can drive cortical circuits, we investigated cell-type selective responses to POm stimulation in mouse primary somatosensory (barrel) cortex, using genetically targeted whole-cell recordings in acute brain slices. We find that ChR2-evoked thalamic input selectively targets specific cell types in the neocortex, revealing layer-specific modules for the summation and processing of POm input. Evoked activity in pyramidal neurons from deep layers is fast and synchronized by rapid feedforward inhibition from GABAergic parvalbumin-expressing neurons, and activity in superficial layers is weaker and prolonged, facilitated by slow inhibition from GABAergic neurons expressing the 5HT3a receptor. Somatostatin-expressing GABAergic neurons do not receive direct input in either layer and their spontaneous activity is suppressed during POm stimulation. This novel pattern of weak, delayed, thalamus-evoked inhibition in layer 2 suggests a longer integration window for incoming sensory information and may facilitate stimulus detection and plasticity in superficial pyramidal neurons.
Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA 15213, USA.
Nicholas J
NJ
Audette
Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA 15213, USA.
Joanna
J
Urban-Ciecko
Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA 15213, USA.
Megumi
M
Matsushita
Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA 15213, USA.
Alison L
AL
Barth
D000818:Animals; D000075402:Channelrhodopsins / Q000235:genetics / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D053444:Inhibitory Postsynaptic Potentials / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D009415:Nerve Net / Q000502:physiology*; D009434:Neural Pathways / Q000502:physiology*; D010320:Parvalbumins / Q000235:genetics / Q000378:metabolism; D010880:Piperidines / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D017966:Pyramidal Cells / Q000502:physiology*; D011810:Quinoxalines / Q000494:pharmacology; D044406:Receptors, Serotonin, 5-HT3 / Q000235:genetics / Q000378:metabolism; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013003:Somatosensory Cortex / Q000166:cytology*; D013004:Somatostatin / Q000235:genetics / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology; D013787:Thalamic Nuclei / Q000166:cytology / Q000502:physiology*; D014660:Vasoactive Intestinal Peptide / Q000235:genetics / Q000378:metabolism
C481395:4-aminopiperidine; D000075402:Channelrhodopsins; D018691:Excitatory Amino Acid Antagonists; D010320:Parvalbumins; D010880:Piperidines; D026902:Potassium Channel Blockers; D011810:Quinoxalines; D044406:Receptors, Serotonin, 5-HT3; D026941:Sodium Channel Blockers; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D014660:Vasoactive Intestinal Peptide; D013779:Tetrodotoxin; D013004:Somatostatin