The Noise of Membrane Capacitance Measurements in the Whole-Cell Recording Configuration

Chen, Peng; Gillis, Kevin D.

doi:10.1016/s0006-3495(00)76464-2

Cited by 46 publications

(38 citation statements)

References 19 publications

(34 reference statements)

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“…It complements the electrophysiological methods for study of exocytosis (Chen & Gillis 2000, Xue et al 2009a. It has been revealed by TIRFM that secretory vesicles, such as large dense core secretory vesicles (LDCVs) in neuroendocrine cells and synaptic vesicles (SVs) in neurons, undergo constant trafficking in the subplasmalemmal region (Holz & Axelrod 2008).…”

Section: Compartmentalization Of Leptin and Resistinmentioning

confidence: 99%

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Ye¹,

Than²,

Zhao³

et al. 2010

Journal of Endocrinology

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Adipose tissue is a highly active endocrine organ secreting a variety of signaling molecules called adipokines. Leptin and resistin are two adipokines critically involved in metabolic homeostasis. Nevertheless, the secretory pathways of these adipokines and their interplays are poorly elucidated. In this work, we have comparatively studied several key aspects of leptin and resistin secretion from 3T3-L1 adipocytes. It was found that leptin and resistin molecules are compartmentalized into different secretory vesicles. The trafficking of leptin and resistin vesicles, and the secretion of leptin and resistin are oppositely regulated by insulin/glycolytic substrates and cAMP/protein kinase A. Interestingly, these two adipokines adversely influence each other on secretion and vesicle trafficking. Finally, we demonstrated that both leptin and resistin secretion are Ca 2C dependent.

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Section: Compartmentalization Of Leptin and Resistinmentioning

confidence: 99%

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Ye¹,

Than²,

Zhao³

et al. 2010

Journal of Endocrinology

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“…Briefly, during kiss-and-run exocytosis, the ⍀-form fusion intermediate adds an element to the normally simple equivalent circuit of a voltage-clamped chromaffin cell. In frequencydomain capacitance recordings, the additional circuit element includes the fusion pore conductance, which contributes to the Johnson noise of the circuit and increases the variance of the capacitance signal (Chen and Gillis, 2000). Thus, accumulation of ⍀-figures during kiss-and-run exocytosis increases capacitance variance by an amount proportional to the total number of fusion events.…”

Section: Variance Analysis Indicates Actin and Myosin II Regulate Fusmentioning

confidence: 99%

Myosin II Activation and Actin Reorganization Regulate the Mode of Quantal Exocytosis in Mouse Adrenal Chromaffin Cells

Doreian¹,

Fulop²,

Smith³

2008

J. Neurosci.

108

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Chromaffin cells of the adrenal medulla are innervated by the sympathetic nervous system. Stimulation causes chromaffin cells to fire action potentials, leading to the exocytosis of various classes of transmitters into the circulation. Low-frequency electrical stimulation (action potentials delivered at 0.5 Hz) causes adrenal chromaffin cells to selectively release catecholamines through a kiss-and-run fusion event. Elevated electrical stimulation (action potentials at 15 Hz) evokes fusion pore dilation, full granule collapse, and additional release of the neuropeptide-containing proteinaceous granule core. Here we apply single-cell electrophysiological, electrochemical, and fluorescence measurements to investigate the cellular mechanism for this shift in exocytic behavior. We show that at low-frequency stimulation, a filamentous-actin cell cortex plays a key role in stabilizing the kiss-and-run fusion event. Increased stimulation disrupts the actin cortex, driving full granule collapse. We show that pharmacological perturbation of the actin cortex supersedes stimulus frequency in controlling exocytic mode. Finally, we show that nonmuscle myosin II activation contributes to the cytoskeleton-dependent control of the fusion event. Inhibition of myosin II or myosin light chain kinase under elevated stimulation frequencies inhibits fusion pore dilation and maintains the granule in a kiss-and-run mode of exocytosis. These results demonstrate an essential role for activity-evoked cytoskeletal rearrangement and the action of myosin II in the regulation of catecholamine and neuropeptide exocytosis and represent an essential element of the sympathetic stress response.

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“…We utilized capacitance variance analysis to assay for accumulation of Ω-figures at the cell surface. Briefly, the variance analysis approach [5] takes advantage of the fact that the major source of variance in frequency-domain capacitance signals is introduced as a resistance-dependent thermal noise from the cell equivalent circuit [29]. Ω-figures introduce additional resistive elements in the form of fusion pores (Fig.…”

Section: ω-Figures Persist Under 05 Hz Ape Stimulationmentioning

confidence: 99%

Dynamin I plays dual roles in the activity-dependent shift in exocytic mode in mouse adrenal chromaffin cells

Fulop

Doreian

Smith

2008

Archives of Biochemistry and Biophysics

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Under low stimulation, adrenal chromaffin cells release freely-soluble catecholamines through a restricted granule fusion pore while retaining the large neuropeptide-containing proteinacious granule core. Elevated activity causes dilation of the pore and release of all granule contents. Thus, physiological differential transmitter release is achieved through regulation of fusion pore dilation. We examined the mechanism for pore dilation utilizing a combined approach of peptide transfection, electrophysiology, electrochemistry and quantitative imaging techniques. We report that disruption of dynamin I function alters both fusion modes. Under low stimulation, interference with dynamin I does not affect granule fusion but blocks its re-internalization. In full collapse mode, disruption of dynamin I limits fusion pore dilation, but does not block membrane re-internalization. These data suggest that dynamin I is involved in both modes of exocytosis by regulating contraction or dilation of the fusion pore and thus contributes to activity-dependent differential transmitter release from the adrenal medulla.

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The Noise of Membrane Capacitance Measurements in the Whole-Cell Recording Configuration

Cited by 46 publications

References 19 publications

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Myosin II Activation and Actin Reorganization Regulate the Mode of Quantal Exocytosis in Mouse Adrenal Chromaffin Cells

Dynamin I plays dual roles in the activity-dependent shift in exocytic mode in mouse adrenal chromaffin cells

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