title: Inhibitory effect of mouse neocortex layer I on the underlying cellular network.
abstract: The mammalian cortical layer I is a convergence site for axons of sub- and intracortical origin, and the apical dendritic tufts of pyramidal neurons. A prominent feature of layer I is an extensive plexus of inhibitory axons, which originate from stellate cells in all cortical laminae. The role of this inhibitory projection in the activity of cortical networks has yet to be determined. We investigated the degree to which inhibitory inputs within layer I affect the activity of the underlying cellular network. Field potentials (FPs) were recorded in layer II/III. Focal application of the GABAA blocker picrotoxin in layer I above the recording pipette or the removal of layer I resulted in larger FP amplitudes for stimulations at control-equal intensities. When inhibition was partially blocked, the removal of layer I caused a significant reduction in the threshold stimulus intensity required for generating epileptiform events, and a rise in the propagation velocity of these events. Immunocytochemistry for chemical markers of interneurons proved that the inhibitory input to layer I is predominantly somatostatin immunoreactive (SM-ir), such that layer I contains approximately one-third of all SM-ir axons in the cortex. Calretinin-immunoreactive axons were also present in layer I at a lower density. We conclude that the impact of layer I on the cortical cellular network includes a significant inhibitory component. This inhibition confers a moderate restraining influence, and its removal increases the excitability of cortical circuits, but not sufficiently to induce epileptic phenomena.
authors.affiliation: Department of Physiology and Zlotowski Center for Neuroscience, Box 653, Faculty of Health Sciences, Ben-Gurion University, Beer-Sheva, Israel 84105.
authors.forename: Dan
authors.initials: D
authors.lastname: Shlosberg
authors.forename: Saundra L
authors.initials: SL
authors.lastname: Patrick
authors.forename: Yossi
authors.initials: Y
authors.lastname: Buskila
authors.forename: Yael
authors.initials: Y
authors.lastname: Amitai
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism; D064032:Calbindin 2; D003712:Dendrites / Q000378:metabolism; D004210:Dissection; D004307:Dose-Response Relationship, Radiation; D004553:Electric Conductivity; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology*; D018756:GABA Antagonists / Q000494:pharmacology; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007395:Interneurons / Q000166:cytology / Q000378:metabolism; D008297:Male; D051379:Mice; D019579:Neocortex / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D009415:Nerve Net / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D010320:Parvalbumins / Q000378:metabolism; D010852:Picrotoxin / Q000494:pharmacology; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D013004:Somatostatin / Q000378:metabolism
chemical_list: D064032:Calbindin 2; D018756:GABA Antagonists; D010320:Parvalbumins; D010852:Picrotoxin; D064030:S100 Calcium Binding Protein G; D013004:Somatostatin; C576511:Calb2 protein, mouse