title: Low-magnesium medium induces epileptiform activity in mouse olfactory bulb slices.
abstract: Magnesium-free medium can be used in brain slice studies to enhance glutamate receptor function, but this manipulation causes seizure-like activity in many cortical areas. The rodent olfactory bulb (OB) slice is a popular preparation, and potentially ictogenic ionic conditions have often been used to study odor processing. We studied low Mg(2+)-induced epileptiform discharges in mouse OB slices using extracellular and whole cell electrophysiological recordings. Low-Mg(2+) medium induced two distinct types of epileptiform activity: an intraglomerular delta-frequency oscillation resembling slow sniff-induced activity and minute-long seizure-like events (SLEs) consisting of large negative-going field potentials accompanied by sustained depolarization of output neurons. SLEs were dependent on N-methyl-D-aspartate receptors and sodium currents and were facilitated by α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors. The events were initiated in the glomerular layer and propagated laterally through the external plexiform layer at a slow time scale. Our findings confirm that low-Mg(2+) medium should be used with caution in OB slices. Furthermore, the SLEs resembled the so-called slow direct current (DC) shift of clinical and experimental seizures, which has recently been recognized as being of great clinical importance. The OB slice may therefore provide a robust and unique in vitro model of acute seizures in which mechanisms of epileptiform DC shifts can be studied in isolation from fast oscillations.
authors.affiliation: Dept. of Physiology, Univ. of Otago, PO Box 913, Dunedin 9054, New Zealand. kajsa.igelstrom@otago.ac.nz
authors.forename: Kajsa M
authors.initials: KM
authors.lastname: Igelström
authors.forename: Cristina H
authors.initials: CH
authors.lastname: Shirley
authors.forename: Philip M
authors.initials: PM
authors.lastname: Heyward
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000208:Acute Disease; D000818:Animals; D021461:Animals, Outbred Strains; D000927:Anticonvulsants / Q000494:pharmacology; D003470:Culture Media / Q000494:pharmacology; D004594:Electrophysiology / Q000379:methods; D004829:Epilepsy, Generalized / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D018698:Glutamic Acid / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism* / Q000494:pharmacology; D008275:Magnesium Deficiency / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D051379:Mice; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000502:physiology; D009830:Olfactory Bulb / Q000166:cytology / Q000378:metabolism / Q000503:physiopathology*; D009924:Organ Culture Techniques; D010672:Phenytoin / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D018091:Receptors, AMPA / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D000927:Anticonvulsants; D003470:Culture Media; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D010672:Phenytoin; D012964:Sodium; D008274:Magnesium; D011188:Potassium