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Comparison of N- and P/Q-Type Voltage-Gated Calcium Channel Current Inhibition
  • K. Currie, A. Fox
  • Chemistry, Medicine
  • The Journal of Neuroscience
  • 15 June 1997
The data suggest that changes in the kinetics of the G-protein/channel interaction alone cannot explain the differences in the inhibition of the N- and P/Q-type calcium channels, and the subtle differences in inhibition may facilitate the selective regulation of neurotransmitter release. Expand
ATP Serves as a Negative Feedback Inhibitor of Voltage-Gated Ca2+ Channel Currents in Cultured Bovine Adrenal Chromaffin Cells
It is shown that stimulation of chromaffin cells results in the release of an "endogenous inhibitor" that suppresses I(Ca), and a negative feedback pathway is identified that may serve as an important regulatory mechanism for catecholamine secretion in chromaffIn cells. Expand
Regulation of Ca(V)2 calcium channels by G protein coupled receptors.
This review focuses on the inhibition of Ca(V)2 (N- and P/Q-type) Ca²⁺-channels by G protein coupled receptors (GPCRs), which exerts important autocrine/paracrine control over synaptic transmission and neuroendocrine secretion. Expand
The role of dynamic palmitoylation in Ca2+ channel inactivation.
The results suggest that native N- and P/Q-type Ca(2+) channels containing beta(2a) subunits may be regulated by dynamic palmitoylation, possibly by alterations in beta subunit palMIToylation. Expand
Differential facilitation of N‐ and P/Q‐type calcium channels during trains of action potential‐like waveforms
Inhibition of presynaptic voltage‐gated calcium channels by direct G‐protein βγ subunit binding is a widespread mechanism that regulates neurotransmitter release. Voltage‐dependent relief of thisExpand
Activation of Ca(2+)-dependent currents in cultured rat dorsal root ganglion neurones by a sperm factor and cyclic ADP-ribose.
The results indicate that both SF and cADPR release intracellular Ca2+ pools in DRG neurones and that they appear to act on subtly distinct stores or distinct intrACEllular Ca 2+ release mechanisms, possibly by modulating CICR. Expand
Aspects of calcium-activated chloride currents: a neuronal perspective.
The whole cell ICl(Ca) can be identified by sensitivity to increased Ca2+ buffering capacity of the cell, anion substitution studies and reversal potential measurements, as well as by the actions of Cl- channel blockers, and can be used as a physiological index of intracellular Ca 2+ close to the cell membrane. Expand
Calpains play a role in insulin secretion and action.
It is reported that short-term exposure to the cell-permeable calpain inhibitors calpain inhibitor II and E-64-d increases the insulin secretory response to glucose in mouse pancreatic islets and is consistent with a role for calpains in the regulation of insulin secretion and insulin action. Expand
Calcium‐activated currents in cultured neurones from rat dorsal root ganglia
The authors' data may reflect (a) different degrees of association between Ca2+‐activated channels with voltage‐gated Ca2- channels, (b) distinct relationships between channels and intracellularCa2+ stores and Ca2+. homeostatic mechanisms, (c) regulation of Ca2 +‐ activated channels by second messengers, and (d) varying channel sensitivity to Ca2+, in the cell body of DRG neurones. Expand
G-Proteins Modulate Cumulative Inactivation of N-Type (CaV2.2) Calcium Channels
The data identify and characterize a novel effect of G-proteins on ICa, and could have important implications for understanding how G-protein-coupled receptors control Ca2+ entry and Ca2-dependent events such as neurotransmitter and hormone release. Expand