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Titolo:
Extracellular calcium modulates persistent sodium current-dependent burst-firing in hippocampal pyramidal neurons
Autore:
Su, HL; Alroy, G; Kirson, ED; Yaari, Y;
Indirizzi:
Hebrew Univ Jerusalem, Hadassah Fac Med, Inst Med Sci, Dept Physiol, IL-91120 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91120 -91120 Jerusalem, Israel
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 12, volume: 21, anno: 2001,
pagine: 4173 - 4182
SICI:
0270-6474(20010615)21:12<4173:ECMPSC>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPIKE AFTER-DEPOLARIZATION; SYNAPTIC TRANSMISSION; EPILEPTIFORM ACTIVITY; NEOCORTICAL NEURONS; CELLS; GENERATION; POTASSIUM; INVITRO; PHENYTOIN; MECHANISMS;
Keywords:
intrinsic bursting; calcium; persistent sodium current; pyramidal cell; hippocampus; phenytoin; gap junction; PKC; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Yaari, Y Hebrew Univ Jerusalem, Sch Med, Dept Physiol, POB 12272, IL-91121Jerusalem, Israel Hebrew Univ Jerusalem POB 12272 Jerusalem Israel IL-91121 Israel
Citazione:
H.L. Su et al., "Extracellular calcium modulates persistent sodium current-dependent burst-firing in hippocampal pyramidal neurons", J NEUROSC, 21(12), 2001, pp. 4173-4182

Abstract

The generation of high-frequency spike bursts ("complex spikes"), either spontaneously or in response to depolarizing stimuli applied to the soma, isa notable feature in intracellular recordings from hippocampal CA1 pyramidal cells (PCs) in vivo. There is compelling evidence that the bursts are intrinsically generated by summation of large spike afterdepolarizations (ADPs). Using intracellular recordings in adult rat hippocampal slices, we showthat intrinsic burst-firing in CA1 PCs is strongly dependent on the extracellular concentration of Ca2+ ([Ca2+](o)). Thus, lowering [Ca2+](o) (by equimolar substitution with Mn2+ or Mg2+) induced intrinsic bursting in nonbursters, whereas raising [Ca2+](o) suppressed intrinsic bursting in native bursters. The induction of intrinsic bursting by low [Ca2+](o) was associatedwith enlargement of the spike ADP. Low [Ca2+](o)-induced intrinsic bursts and their underlying ADPs were suppressed by drugs that reduce the persistent Na+ current (I-NaP), indicating that this current mediates the slow burst depolarization. Blocking Ca2+- activated K+ currents with extracellular Ni2+ or intracellular chelation of Ca2+ did not induce intrinsic bursting. This and other evidence suggest that lowering [Ca2+](o) may induce intrinsicbursting by augmenting I-NaP. Because repetitive neuronal activity in the hippocampus is associated with marked decreases in [Ca2+](o), the regulation of intrinsic bursting by extracellular Ca2+ may provide a mechanism for preferential recruitment of this firing mode during certain forms of hippocampal activation.

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Documento generato il 31/03/20 alle ore 04:37:05