title: Flat and steep terminal negativity in the DC-potential after deprivation of oxygen and glucose in human neocortical slices.
abstract: The so-called terminal negativity (TN) of the DC-potential is a characteristic reaction of neuronal tissue to hypoxia or ischemia. In a previous study on human neocortical slices, two types of TN with flat and steep slopes of rise (< or >10 mV/min) were found with hypoxia. The aim of the present study was to further investigate causes underlying the occurrence of flat and steep TN. Experiments were performed on 23 human neocortical slices (500 micron) resected from 13 patients (epilepsy and tumour surgery). DC-potential and evoked potentials (white matter stimulation) were recorded in layer III. The extracellular potassium concentration ([K+]o) was measured by K+-sensitive microelectrodes. In an interface type chamber, ischemic episodes were induced by oxygen and glucose deprivation. They were terminated when TN had peaked. Both flat and steep TN also existed with ischemic conditions. There was a linear correlation between the slope of rise of TN and the associated slope of rise in [K+]o, respectively, but none regarding latencies of TN or recovery of evoked potentials. Peak levels in [K+]o were 13.9+/-0.9 mmol/l. Compared to control, the slope of rise and latency of TN were clearly increased by addition of dimethyl sulfoxide (DMSO, 0.4%) to the bath solution, whereas nimodipine (40 micromol/l) in 0.4% DMSO had neither an effect on slope of rise of TN nor on latency of TN. As a whole, our observations suggest, that the actual metabolic state determines the occurrence of flat or steep TN.
authors.affiliation: Institut für Physiologie, Universität Münster, Robert-Koch-Str. 27a, 48149 Münster, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Schmidinger
authors.forename: C
authors.initials: C
authors.lastname: Greiner
authors.forename: S
authors.initials: S
authors.lastname: Reinker
authors.forename: R
authors.initials: R
authors.lastname: Köhling
authors.forename: A
authors.initials: A
authors.lastname: Lücke
authors.forename: H
authors.initials: H
authors.lastname: Straub
authors.forename: E
authors.initials: E
authors.lastname: Speckmann
authors.forename: D
authors.initials: D
authors.lastname: Moskopp
authors.forename: H
authors.initials: H
authors.lastname: Wassmann
authors.forename: R
authors.initials: R
authors.lastname: Lahl
authors.forename: H
authors.initials: H
authors.lastname: Pannek
authors.forename: F
authors.initials: F
authors.lastname: Oppel
mesh_terms: D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology*; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000502:physiology; D005947:Glucose / Q000172:deficiency*; D006801:Humans; D002534:Hypoxia, Brain / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D016014:Linear Models; D019579:Neocortex / Q000098:blood supply / Q000378:metabolism / Q000502:physiology*; D018696:Neuroprotective Agents / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000502:physiology*; D011930:Reaction Time / Q000187:drug effects
chemical_list: D018696:Neuroprotective Agents; D005947:Glucose; D011188:Potassium