title: Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia.
abstract: Increased potassium conductance during hypoxia causes membrane hyperpolarization and a resultant increase in extracellular potassium concentration ([K(+)](o)). In addition, glial buffering of [K(+)](o) is the key mechanism for clearing excess K(+) and is important for neuronal function and survival. Here, we studied the effect of glial buffering of [K(+)](o) on neural impulse conduction during hypoxia using a potassium-selective electrode and evoked potential recording in rat hippocampal slices. The increase in [K(+)](o) during hypoxia was modest and there were no significant differences between the layers. The [K(+)](o) during hypoxia was significantly elevated by addition of barium (1 mM), especially in the stratum pyramidale and stratum oriens. Although synaptic transmission was depressed during hypoxia, the presynaptic volley and antidromic population spike mostly remained unchanged. With the addition of barium, antidromic conduction was more profoundly affected than the presynaptic volley. When presynaptic inhibition was precluded by including a selective A1 adenosine receptor blocker to restore synaptic transmission, blockade of the antidromic conduction became more evident compared with the blockade of other recorded field potentials. These findings are compatible with regional differences in the increase of [K(+)](o) and suggest that glial buffering of high [K(+)](o) is important in antidromic conduction during hypoxia.
authors.affiliation: Brain Injury Laboratory, Korea University Guro Hospital, Seoul, Republic of Korea. ykapa76@yahoo.co.kr
authors.forename: Youn-Kwan
authors.initials: YK
authors.lastname: Park
authors.forename: Seok-Joon
authors.initials: SJ
authors.lastname: Kim
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D058916:Adenosine A1 Receptor Antagonists; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D015687:Cell Hypoxia / Q000187:drug effects / Q000502:physiology; D002491:Central Nervous System Agents / Q000494:pharmacology; D005071:Evoked Potentials; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D014970:Xanthines / Q000494:pharmacology
chemical_list: D058916:Adenosine A1 Receptor Antagonists; D017609:Barium Compounds; D002491:Central Nervous System Agents; D014970:Xanthines; C051360:1,3-dipropyl-8-cyclopentylxanthine; D011188:Potassium