title: Removal of Ca(2+) following depolarization-evoked cytoplasmic Ca(2+) transients in freshly dissociated pyramidal neurones of the rat dorsal cochlear nucleus.
abstract: Cytoplasmic [Ca(2+)] ([Ca(2+)](i)) was measured using Fura-2 in pyramidal neurones isolated from the rat dorsal cochlear nucleus (DCN). The kinetic properties of Ca(2+) removal following K(+) depolarization-induced Ca(2+) transients were characterized by fitting exponential functions to the decay phase. The removal after small transients (<82 nM peak [Ca(2+)](i)) had monophasic time course (time constant of 6.43 +/- 0.48 s). In the cases of higher Ca(2+) transients biphasic decay was found. The early time constant decreased (from 3.09 +/- 0.26 to 1.46 +/- 0.11 s) as the peak intracellular [Ca(2+)] increased. The value of the late time constant was 18.15 +/- 1.60 s at the smallest transients, and showed less dependence on [Ca(2+)](i). Blockers of Ca(2+) uptake into intracellular stores (thapsigargin and cyclopiazonic acid) decreased the amplitude of the Ca(2+) transients and slowed their decay. La(3+) (3 mM) applied extracellularly during the declining phase dramatically changed the time course of the Ca(2+) transients as a plateau developed and persisted until the La(3+) was present. When the other Ca(2+) removal mechanisms were available, reduction of the external [Na(+)] to inhibit the Na(+)/Ca(2+) exchange resulted in a moderate increase of the time constants. It is concluded that in the isolated pyramidal neurones of the DCN the removal of Ca(2+) depends mainly on the activity of Ca(2+) pump mechanisms.
authors.affiliation: Medical and Health Science Centre, Department of Physiology, University of Debrecen, P.O. Box 22, H-4012 Debrecen, Hungary.
authors.forename: Csaba
authors.initials: C
authors.lastname: Harasztosi
authors.forename: Agnes
authors.initials: A
authors.lastname: Pór
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Rusznák
authors.forename: Géza
authors.initials: G
authors.lastname: Szûcs
mesh_terms: D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D020013:Calcium Signaling / Q000187:drug effects*; D000252:Calcium-Transporting ATPases / Q000187:drug effects / Q000378:metabolism; D027682:Cation Transport Proteins; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002469:Cell Separation; D017626:Cochlear Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007700:Kinetics; D018408:Patch-Clamp Techniques; D053499:Plasma Membrane Calcium-Transporting ATPases; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D027682:Cation Transport Proteins; D004791:Enzyme Inhibitors; D019284:Thapsigargin; D053499:Plasma Membrane Calcium-Transporting ATPases; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D000252:Calcium-Transporting ATPases