title: Anoxic terminal negative DC-shift in human neocortical slices in vitro.
abstract: In animal models, the hallmark of a hypoxic condition is a strong negative shift of the DC potential (anoxic terminal negativity, ATN). This DC-shift is interpreted to be primarily due to a breakdown of the membrane potential of neurons. Such massive neuronal depolarizations have not been reported for all human neocortical neurons in vitro even during prolonged hypoxic periods. This poses the question whether ATN develop also in human neocortical slices made hypoxic. ATN could be observed when human brain slice preparations (n = 15, 13 patients) were subjected to periods of hypoxia (10 to 120 min). These ATN were usually monophasic and appeared with a latency of 16 +/- 4 min (mean +/- S.E.M.). Separating the ATN according to their slopes of rise, steep (> 10 mV/min) and flat (< 10 mV/min) ATN could be distinguished. Steep and flat ATN may be regarded as two different entities of reactions since steep ATN had also greater amplitudes and slopes of decay as compared a flat ATN. With repetitive hypoxias, the latency of both the steep and flat ATN was reduced for the following hypoxic episodes. During hypoxic DC-shifts, evoked potentials were suppressed. With the 1st through 4th hypoxia, they recovered fully within 30 min after reoxygenation when hypoxia was terminated at the plateau of ATN; with extension of hypoxia, recovery was only partial. From the 5th hypoxia onwards, recovery usually did not take place or was not complete.
authors.affiliation: Institut für Physiologie, Universität Münster, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Köhling
authors.forename: A
authors.initials: A
authors.lastname: Schmidinger
authors.forename: S
authors.initials: S
authors.lastname: Hülsmann
authors.forename: S
authors.initials: S
authors.lastname: Vanhatalo
authors.forename: A
authors.initials: A
authors.lastname: Lücke
authors.forename: H
authors.initials: H
authors.lastname: Straub
authors.forename: E J
authors.initials: EJ
authors.lastname: Speckmann
authors.forename: I
authors.initials: I
authors.lastname: Tuxhorn
authors.forename: P
authors.initials: P
authors.lastname: Wolf
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
authors.forename: C
authors.initials: C
authors.lastname: Greiner
authors.forename: D
authors.initials: D
authors.lastname: Moskopp
authors.forename: H
authors.initials: H
authors.lastname: Wassmann
mesh_terms: D000293:Adolescent; D000328:Adult; D002540:Cerebral Cortex / Q000503:physiopathology*; D002648:Child; D002675:Child, Preschool; D004827:Epilepsy / Q000503:physiopathology / Q000601:surgery; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D006801:Humans; D002534:Hypoxia, Brain / Q000503:physiopathology*; D066298:In Vitro Techniques; D007223:Infant; D008297:Male; D017729:Presynaptic Terminals / Q000502:physiology*