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Voltage‐dependent κ‐opioid modulation of action potential waveform‐elicited calcium currents in neurohypophysial terminals
Author(s) -
VelázquezMarrero Cristina M.,
Marrero Héctor G.,
Lemos José R.
Publication year - 2010
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22247
Subject(s) - chemistry , depolarization , voltage dependent calcium channel , biophysics , calcium channel , calcium , membrane potential , second messenger system , stimulation , receptor , endocrinology , biology , biochemistry , organic chemistry
Abstract Release of neurotransmitter is activated by the influx of calcium. Inhibition of Ca 2+ channels results in less calcium influx into the terminals and presumably a reduction in transmitter release. In the neurohypophysis (NH), Ca 2+ channel kinetics, and the associated Ca 2+ influx, is primarily controlled by membrane voltage and can be modulated, in a voltage‐dependent manner, by G‐protein subunits interacting with voltage‐gated calcium channels (VGCCs). In this series of experiments we test whether the κ‐ and µ‐opioid inhibition of Ca 2+ currents in NH terminals is voltage‐dependent. Voltage‐dependent relief of G‐protein inhibition of VGCC can be achieved with either a depolarizing square pre‐pulse or by action potential waveforms. Both protocols were tested in the presence and absence of opioid agonists targeting the κ‐ and µ‐receptors in neurohypophysial terminals. The κ‐opioid VGCC inhibition is relieved by such pre‐pulses, suggesting that this receptor is involved in a voltage‐dependent membrane delimited pathway. In contrast, µ‐opioid inhibition of VGCC is not relieved by such pre‐pulses, indicating a voltage‐independent diffusible second‐messenger signaling pathway. Furthermore, relief of κ‐opioid inhibition during a physiologic action potential (AP) burst stimulation indicates the possibility of activity‐dependent modulation in vivo . Differences in the facilitation of Ca 2+ channels due to specific G‐protein modulation during a burst of APs may contribute to the fine‐tuning of Ca 2+ ‐dependent neuropeptide release in other CNS terminals, as well. J. Cell. Physiol. 225: 223–232, 2010. © 2010 Wiley‐Liss, Inc.