title: Transient recovery of synaptic transmission is related to rapid energy depletion during hypoxia.
abstract: Transient recovery (TR) of evoked synaptic potential during the late stage of hypoxic hypoglycemia (HH) insult was investigated in rat hippocampal slices using extracellular recording methods. TR was observed in association with a rapid deterioration of antidromic population spikes (aPSs) following HH insult. TR was not elicited in normoglycemic hypoxia (NH), in which a gradual and delayed deterioration of aPSs was noted. TR was not modulated by either Ca(2+)- or PKC-dependent processes. When a glycolytic inhibitor was added, NH resulted in a rapid deterioration of aPSs and prompted appearance of TR. TR was also seen in slices using lactate to generate energy via oxidative phosphorylation, when hypoxic conditions were subsequently created. Other pharmacological interventions that aimed to cause rapid deterioration of aPSs without depleting energy stores failed to reproduce TR. The evidence thus suggests that the underlying mechanisms of TR appearance during HH insult are highly correlated with rapid energy depletion.
authors.affiliation: Department of Neurosurgery, College of Medicine, Korea University, Seoul, Korea.
authors.forename: Joo Han
authors.initials: JH
authors.lastname: Kim
authors.forename: Youn Kwan
authors.initials: YK
authors.lastname: Park
authors.forename: Jong Hyun
authors.initials: JH
authors.lastname: Kim
authors.forename: Taek Hyun
authors.initials: TH
authors.lastname: Kwon
authors.forename: Hung Seob
authors.initials: HS
authors.lastname: Chung
mesh_terms: D000818:Animals; D002614:Chelating Agents / Q000494:pharmacology; D003620:Dantrolene / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D005947:Glucose / Q000008:administration & dosage; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000503:physiopathology; D007003:Hypoglycemia / Q000150:complications*; D000860:Hypoxia / Q000209:etiology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D010703:Phorbol Esters / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors
chemical_list: D002614:Chelating Agents; D004791:Enzyme Inhibitors; D010703:Phorbol Esters; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D004533:Egtazic Acid; D011189:Potassium Chloride; D003620:Dantrolene; D005947:Glucose