Spontaneous action potentials initiate rhythmic intercellular calcium waves in immortalized hypothalamic (GT1-1) neurons

Citation
Jl. Costantin et Ac. Charles, Spontaneous action potentials initiate rhythmic intercellular calcium waves in immortalized hypothalamic (GT1-1) neurons, J NEUROPHYS, 82(1), 1999, pp. 429-435
Citations number
24
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROPHYSIOLOGY
ISSN journal
00223077 → ACNP
Volume
82
Issue
1
Year of publication
1999
Pages
429 - 435
Database
ISI
SICI code
0022-3077(199907)82:1<429:SAPIRI>2.0.ZU;2-4
Abstract
GT1-1 cells exhibit spontaneous action potentials and transient increases i n intracellular calcium concentration ([Ca2+](i)) that occur in individual cells and as spatially propagated intercellular Ca2+ waves. In this study, simultaneous cell-attached patch-clamp recording of action currents (indica tive of action potentials) and fluorescence imaging of [Ca2+](i) revealed t hat Ca2+ transients in GT1-1 cells were preceded by a single action current or a burst of action currents. Action currents preceded Ca2+ transients in a similar pattern regardless of whether the: Ca2+ transients were limited to the individual cell or occurred as part of an intercellular Ca2+ wave. B oth the action currents and Ca2+ transients were abolished by 1 mu M tetrod otoxin. Removal of extracellular Ca2+ abolished all spontaneous Ca2+ transi ents without inhibiting the firing of action currents. Nimodipine. which bl ocks L-type Ca2+ currents in GT1-1 cells, also abolished all spontaneous Ca 2+ signaling. Delivery of small voltage steps to the patch pipette in the c ell-attached configuration elicited action currents the latency to firing o f which decreased with increasing amplitude of the voltage step. These resu lts indicate that spontaneous intercellular Ca2+ waves are generated by a p ropagated depolarization, the firing of action potentials in individual cel ls, and the resulting influx of Ca2+ through L-type Ca2+ channels. These pa tterns of spontaneous activity may be important in driving the pulsatile re lease of GnRH from networks of cells.