TY - JOUR
T1 - Changes of neuronal activity in areas CA1 and CA3 during anoxia and normoxic or hyperoxic reoxygenation in juvenile rat organotypic hippocampal slice cultures
AU - Hoffmann, Ulrike
AU - Pomper, Jörn
AU - Graulich, Johannes
AU - Zeller, Melanie
AU - Schuchmann, Sebastian
AU - Gabriel, Siegrun
AU - Maier, Rolf F.
AU - Heinemann, Uwe
N1 - Funding Information:
This research was supported by grants from the Sanderstiftung, from the Deutsche Forschungs Gemeinschaft to the SFB 507 and to the Graduate School 238. We are grateful for critical comments, technical and secretarial assistance to Dr. L. de Hoz, Dr. H.J. Gabriel, Dr. H. Siegmund and S. Frosinski.
PY - 2006/1/19
Y1 - 2006/1/19
N2 - In neonates, asphyxia is usually followed by hyperoxic treatment. In order to study whether hyperoxic reoxygenation might cause additional impairment of neuronal function, we subjected organotypic hippocampal slice cultures of juvenile rats (7 DIV, P6-8) to 30 min anoxia followed by 60 min hyperoxic or normoxic reoxygenation (95% or 19% O2, respectively). Spontaneous and evoked field potentials as well as [Ca2+]o were recorded in the pyramidal layer of area CA1 or area CA3. In area CA1, 30 min of anoxia led to decline of evoked field potential amplitudes by on average 67% and to profound changes in field potential characteristics and Ca2+ homeostasis which were not related to outcome after reoxygenation. Hyperoxic reoxygenation resulted first in a fast recovery of the field potential amplitude to 82% of the control value and then, in 75% of slice cultures, in a large negative field potential shift accompanied by a prolonged decrease of [Ca 2+]o and loss of excitability outlasting the experiment. Recovery of field potential amplitude under normoxic conditions stayed poor, with a first increase to 51% and a second decrease to 22%. In contrast, field potential amplitude in area CA3 recovered to 80% of the initial amplitude, irrespective of the reoxygenation mode. The selective loss of function during hyperoxic reoxygenation in area CA1 might be a first sign of neuronal injury that we observed 1 h after end of hyperoxic reoxygenation in a previous study. Whether the poor outcome after normoxic reoxygenation would favour long-term recovery remains to be determined.
AB - In neonates, asphyxia is usually followed by hyperoxic treatment. In order to study whether hyperoxic reoxygenation might cause additional impairment of neuronal function, we subjected organotypic hippocampal slice cultures of juvenile rats (7 DIV, P6-8) to 30 min anoxia followed by 60 min hyperoxic or normoxic reoxygenation (95% or 19% O2, respectively). Spontaneous and evoked field potentials as well as [Ca2+]o were recorded in the pyramidal layer of area CA1 or area CA3. In area CA1, 30 min of anoxia led to decline of evoked field potential amplitudes by on average 67% and to profound changes in field potential characteristics and Ca2+ homeostasis which were not related to outcome after reoxygenation. Hyperoxic reoxygenation resulted first in a fast recovery of the field potential amplitude to 82% of the control value and then, in 75% of slice cultures, in a large negative field potential shift accompanied by a prolonged decrease of [Ca 2+]o and loss of excitability outlasting the experiment. Recovery of field potential amplitude under normoxic conditions stayed poor, with a first increase to 51% and a second decrease to 22%. In contrast, field potential amplitude in area CA3 recovered to 80% of the initial amplitude, irrespective of the reoxygenation mode. The selective loss of function during hyperoxic reoxygenation in area CA1 might be a first sign of neuronal injury that we observed 1 h after end of hyperoxic reoxygenation in a previous study. Whether the poor outcome after normoxic reoxygenation would favour long-term recovery remains to be determined.
KW - Hypoxia
KW - Organotypic hippocampal slice culture
KW - Reoxygenation
UR - http://www.scopus.com/inward/record.url?scp=31344450182&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=31344450182&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2005.11.025
DO - 10.1016/j.brainres.2005.11.025
M3 - Article
C2 - 16380097
AN - SCOPUS:31344450182
SN - 0006-8993
VL - 1069
SP - 207
EP - 215
JO - Brain Research
JF - Brain Research
IS - 1
ER -