title: Thalamic gating of corticostriatal signaling by cholinergic interneurons.
abstract: Salient stimuli redirect attention and suppress ongoing motor activity. This attentional shift is thought to rely upon thalamic signals to the striatum to shift cortically driven action selection, but the network mechanisms underlying this interaction are unclear. Using a brain slice preparation that preserved cortico- and thalamostriatal connectivity, it was found that activation of thalamostriatal axons in a way that mimicked the response to salient stimuli induced a burst of spikes in striatal cholinergic interneurons that was followed by a pause lasting more than half a second. This patterned interneuron activity triggered a transient, presynaptic suppression of cortical input to both major classes of principal medium spiny neuron (MSN) that gave way to a prolonged enhancement of postsynaptic responsiveness in striatopallidal MSNs controlling motor suppression. This differential regulation of the corticostriatal circuitry provides a neural substrate for attentional shifts and cessation of ongoing motor activity with the appearance of salient environmental stimuli.
authors.affiliation: Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
authors.forename: Jun B
authors.initials: JB
authors.lastname: Ding
authors.forename: Jaime N
authors.initials: JN
authors.lastname: Guzman
authors.forename: Jayms D
authors.initials: JD
authors.lastname: Peterson
authors.forename: Joshua A
authors.initials: JA
authors.lastname: Goldberg
authors.forename: D James
authors.initials: DJ
authors.lastname: Surmeier
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000502:physiology; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D002540:Cerebral Cortex / Q000166:cytology* / Q000502:physiology*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003042:Cocaine / Q000494:pharmacology; D003342:Corpus Striatum / Q000166:cytology / Q000502:physiology*; D018492:Dopamine Antagonists / Q000494:pharmacology; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D049452:Green Fluorescent Proteins / Q000235:genetics; D066298:In Vitro Techniques; D007395:Interneurons / Q000502:physiology*; D008464:Mecamylamine / Q000494:pharmacology; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D009434:Neural Pathways / Q000502:physiology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D017447:Receptors, Dopamine D1 / Q000235:genetics; D017448:Receptors, Dopamine D2 / Q000235:genetics; D013469:Sulpiride / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects; D013788:Thalamus / Q000502:physiology*; D013997:Time Factors
chemical_list: D000596:Amino Acids; D018492:Dopamine Antagonists; D018765:Dopamine Uptake Inhibitors; D018733:Nicotinic Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; C098463:dolaisoleucine; D049452:Green Fluorescent Proteins; D008464:Mecamylamine; D013469:Sulpiride; D002795:Choline O-Acetyltransferase; D003042:Cocaine; D000109:Acetylcholine