کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4342795 | 1295892 | 2006 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A role for glutamate and glia in the fast network oscillations preceding spreading depression
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
fEPSP(RS)-α-cyclopropyl-4-phosphonophenylglycineCPPGMCPGTHADNQXCPPN-methyl-d-aspartateNMDAFACPSDACFaCSF(RS)-α-Methyl-4-carboxyphenylglycine - (RS) -α-Methyl-4-carboxyphenylglycine6,7-dinitroquinoxaline-2,3-dione - 6،7-dinitroquinoxaline-2،3-dioneStratum - استراتومPopulation spike - افزایش جمعیتEpilepsy - بیماری صرعSt. - خیابانIschemic penumbra - ستون ایسکمیکStroke - سکته مغزیAutocorrelation function - عملکرد ارتباط خودکارFluoroacetate - فلوئوراستاتFluorocitrate - فلوروکراتراتartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیaction potential - پتانسیل عمل Field excitatory postsynaptic potential - پتانسیل پستنیپتیک مزمن تحریک پذیرSpreading depression - گسترش افسردگیGlu - گلوglutamate - گلوتامات
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The mechanism of the propagation of spreading depression is unclear. Classical theories proposed a self-maintained cycle fed by elevated potassium and/or glutamate in the extracellular space. Earlier we found in vivo a characteristic oscillatory field activity that is synchronous in a strip of tissue ahead of the oncoming wave of neuron depolarization and that occurs before the extracellular potassium level begins to rise [Herreras O, Largo C, Ibarz JM, Somjen GG, MarrÃn del RÃo R (1994) Role of neuronal synchronizing mechanisms in the propagation of spreading depression in the in vivo hippocampus. J Neurosci 14:7087-7098]. We investigated here the possible participation of glutamate and the role of glia in the prodromal field oscillations using extra and intracellular recordings and pharmacological manipulations in rat hippocampal slices. As earlier shown in vivo, field oscillations propagated ahead of the negative potential shift covering distances of up to 1 mm. The oscillatory prodromals were initially subthreshold but then each wave became crowned by a population spike. The frequency of the oscillatory prodromals was variable among slices (80-115 Hz), but constant in individual slices. The blockade of ionotropic glutamate receptors decreased the frequency of prodromal oscillations, retarded spreading depression propagation, and shortened the duration of depolarization. Blocking the glutamate membrane transport increased the oscillatory frequency. The selective metabolic poisoning of astrocytes led to gradual disorganization of prodromal oscillations whose frequency first increased and then decreased. Also, the amplitude of the population spikes within the burst diminished as individual cells fired fewer action potentials, although still phase-locked with population spikes. The effects of glial metabolic impairment were observed within the period when neuron electrical properties were still normal, and were blocked by glutamate receptor antagonists. These data suggest that glutamate released from glial cells and possibly also from neurons has a role in the generation of oscillations and neuron firing synchronization that precede the spreading depression-related depolarization, but additional mechanisms are required to fully explain the onset and propagation of spreading depression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 141, Issue 2, 2006, Pages 1057-1068
Journal: Neuroscience - Volume 141, Issue 2, 2006, Pages 1057-1068
نویسندگان
B. Larrosa, J. Pastor, L. López-Aguado, O. Herreras,