title: Corticothalamic Spike Transfer via the L5B-POm Pathway in vivo.
abstract: The cortex connects to the thalamus via extensive corticothalamic (CT) pathways, but their function in vivo is not well understood. We investigated "top-down" signaling from cortex to thalamus via the cortical layer 5B (L5B) to posterior medial nucleus (POm) pathway in the whisker system of the anesthetized mouse. While L5B CT inputs to POm are extremely strong in vitro, ongoing activity of L5 neurons in vivo might tonically depress these inputs and thereby block CT spike transfer. We find robust transfer of spikes from the cortex to the thalamus, mediated by few L5B-POm synapses. However, the gain of this pathway is not constant but instead is controlled by global cortical Up and Down states. We characterized in vivo CT spike transfer by analyzing unitary PSPs and found that a minority of PSPs drove POm spikes when CT gain peaked at the beginning of Up states. CT gain declined sharply during Up states due to frequency-dependent adaptation, resulting in periodic high gain-low gain oscillations. We estimate that POm neurons receive few (2-3) active L5B inputs. Thus, the L5B-POm pathway strongly amplifies the output of a few L5B neurons and locks thalamic POm sub-and suprathreshold activity to cortical L5B spiking.
authors.affiliation: Institute for Neuroscience of the Technische Universität München, 80802 Munich, Germany Department of Neurosurgery, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Mease
authors.affiliation: Institute for Neuroscience of the Technische Universität München, 80802 Munich, Germany.
authors.forename: Anton
authors.initials: A
authors.lastname: Sumser
authors.affiliation: Institute for Neuroscience of the Technische Universität München, 80802 Munich, Germany Max Planck Institute for Neurobiology, 82152 Martinsried, Germany.
authors.forename: Bert
authors.initials: B
authors.lastname: Sakmann
authors.affiliation: Institute for Neuroscience of the Technische Universität München, 80802 Munich, Germany Department of Neurosurgery, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.
authors.forename: Alexander
authors.initials: A
authors.lastname: Groh
mesh_terms: D000200:Action Potentials; D000758:Anesthesia; D000818:Animals; D003198:Computer Simulation; D019706:Excitatory Postsynaptic Potentials; D058785:GABA-A Receptor Agonists / Q000494:pharmacology; D008822:Mice, Transgenic; D008839:Microelectrodes; D008959:Models, Neurological; D009118:Muscimol / Q000494:pharmacology; D009434:Neural Pathways / Q000166:cytology / Q000502:physiology; D056347:Neuroanatomical Tract-Tracing Techniques; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D062308:Optogenetics; D013003:Somatosensory Cortex / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D013788:Thalamus / Q000166:cytology / Q000502:physiology*; D050495:Vesicular Inhibitory Amino Acid Transport Proteins / Q000235:genetics / Q000378:metabolism; D014738:Vibrissae / Q000294:innervation / Q000502:physiology
chemical_list: D058785:GABA-A Receptor Agonists; D050495:Vesicular Inhibitory Amino Acid Transport Proteins; C492244:Viaat protein, mouse; D009118:Muscimol
keywords: POm; VGAT; adaptation; barrel cortex; corticothalamic feedback; layer 5; somatosensory system; thy-1