Halothane alters electrical activity and calcium dynamics in cultured mouse cortical, spinal cord, and dorsal root ganglion neurons

Artur W. Wamil, John J. Franks, Piotr Janicki, Jean Louis Horn, William T. Franks

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Halothane inhibits neural plasma membrane Ca2+-ATPase, a pump that ejects Ca2+ from the cell after influx through voltage- or ligand-activated channels. Intracellular microelectrode recordings in mouse embryonic cortical and spinal cord neurons showed that halothane and eosin, a pump inhibitor, prolonged repolarization associated with spontaneous bursts of depolarization. These agents also prolonged the repolarization phases of electrically induced action potentials and of capsaicin-mediated Ca2+-dependent depolarization in mouse adult dorsal root ganglion neurons. In keeping with these findings, confocal microfluorimetry showed that halothane delayed clearance of intracellular Ca2+ accumulated by N-methyl-D-aspartate stimulation of single neurons.

Original languageEnglish (US)
Pages (from-to)93-96
Number of pages4
JournalNeuroscience Letters
Volume216
Issue number2
DOIs
StatePublished - Sep 27 1996

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Spinal Nerve Roots
Spinal Ganglia
Halothane
Spinal Cord
Calcium
Neurons
Cytophotometry
Calcium-Transporting ATPases
Capsaicin
Microelectrodes
N-Methylaspartate
Eosine Yellowish-(YS)
Action Potentials
Cell Membrane
Ligands

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Wamil, Artur W. ; Franks, John J. ; Janicki, Piotr ; Horn, Jean Louis ; Franks, William T. / Halothane alters electrical activity and calcium dynamics in cultured mouse cortical, spinal cord, and dorsal root ganglion neurons. In: Neuroscience Letters. 1996 ; Vol. 216, No. 2. pp. 93-96.
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Halothane alters electrical activity and calcium dynamics in cultured mouse cortical, spinal cord, and dorsal root ganglion neurons. / Wamil, Artur W.; Franks, John J.; Janicki, Piotr; Horn, Jean Louis; Franks, William T.

In: Neuroscience Letters, Vol. 216, No. 2, 27.09.1996, p. 93-96.

Research output: Contribution to journalArticle

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