Ca2+ entry through a non-selective cation channel in Aplysia bag cell neurons.

Abstract:

:Ca(2+) influx through voltage-gated Ca(2+) channels is a fundamental signaling event in neurons; however, non-traditional routes, such as non-selective cation channels, also permit Ca(2+) entry. The present study examines the Ca(2+) permeability of a cation channel that drives an afterdischarge in Aplysia bag cell neurons. The firing of these neurons induces peptide release and reproduction. Single channel-containing inside-out patches excised from cultured bag cell neurons, with the cytoplasmic face bathed in K(+)-aspartate and the extracellular face bathed in artificial seawater (11 mM Ca(2+)), had a reversal potential near +50 mV. In keeping with Ca(2+) permeability, this was right-shifted to approximately +60 mV in high Ca(2+) (substituted for Mg(2+)) and left-shifted to around +40 mV in zero Ca(2+) (replaced with Mg(2+)). The current showed inward rectification between +30 and +90 mV, and a conductance of 29 pS in normal Ca(2+), 30 pS in high Ca(2+), 32 pS in Ba(2+) (substituted for Ca(2+)), but only 21 pS in zero Ca(2+). Despite a greater conductance in Ba(2+), the channel did not display anomalous mol fraction in an equimolar Ca(2+)-Ba(2+) mix. Eliminating internal Mg(2+) lowered activity, but did not alter inward rectification, suggesting intracellular Mg(2+) is a fast, voltage-independent blocker. Imaging bag cell neurons in Mn(2+) saline (substituted for Ca(2+)) revealed enhanced fura-quench following cation channel activation, consistent with Mn(2+) permeating as a Ca(2+) surrogate. Finally, triggering the cation channel while tracking capacitance revealed a Ca(2+)-dependent increase in membrane surface area, consistent with vesicle fusion. Thus, the cation channel not only drives the afterdischarge, but also passes Ca(2+) to potentially initiate secretion. In general, this may represent an alternate means by which neurons elicit neuropeptide release.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Geiger JE,Hickey CM,Magoski NS

doi

10.1016/j.neuroscience.2009.05.006

subject

Has Abstract

pub_date

2009-09-15 00:00:00

pages

1023-38

issue

4

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(09)00780-5

journal_volume

162

pub_type

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