Effects of osmotic swelling on voltage-gated calcium channel currents in rat anterior pituitary cells

2003 ◽  
Vol 285 (4) ◽  
pp. C840-C852 ◽  
Author(s):  
Shlomo Ben-Tabou De-Leon ◽  
Edna Blotnick ◽  
Itzhak Nussinovitch
Keyword(s):  
Calcium Channel ◽  
Calcium Influx ◽  
Membrane Surface ◽  
Hormone Secretion ◽  
Calcium Currents ◽  
Type I ◽  
Pituitary Cells ◽  
Voltage Gated ◽  
Channel Currents ◽  
Stimulation Of

Decrease in extracellular osmolarity ([Os]e) results in stimulation of hormone secretion from pituitary cells. Different mechanisms can account for this stimulation of hormone secretion. In this study we examined the possibility that hyposmolarity directly modulates voltage-gated calcium influx in pituitary cells. The effects of hyposmolarity on L-type ( IL) and T-type ( IT) calcium currents in pituitary cells were investigated by using two hyposmotic stimuli, moderate (18-22% decrease in [Os]e) and strong (31-32% decrease in [Os]e). Exposure to moderate hyposmotic stimuli resulted in three response types in IL (a decrease, a biphasic effect, and an increase in IL) and in increase in IT. Exposure to strong hyposmotic stimuli resulted only in increases in both IL and IT. Similarly, in intact pituitary cells (perforated patch method), exposure to either moderate or strong hyposmotic stimuli resulted only in increases in both IL and IT. Thus it appears that the main effect of decrease in [Os]e is increase in calcium channel currents. This increase was differential ( IL were more sensitive than IT) and voltage independent. In addition, we show that these hyposmotic effects cannot be explained by activation of an anionic conductance or by an increase in cell membrane surface area. In conclusion, this study shows that hyposmotic swelling of pituitary cells can directly modulate voltage-gated calcium influx. This hyposmotic modulation of IL and IT may contribute to the previously reported hyposmotic stimulation of hormone secretion. The mechanisms underlying these hyposmotic effects and their possible physiological relevance are discussed.

Hyperosmotic regulation of voltage-gated calcium currents in rat anterior pituitary cells

1996 ◽  
Vol 75 (5) ◽  
pp. 1894-1900 ◽  
Author(s):  
O. Matzner ◽  
S. Ben-Tabou ◽  
I. Nussinovitch
Keyword(s):  
Calcium Channel ◽  
Anterior Pituitary ◽  
Calcium Influx ◽  
Hormone Secretion ◽  
Bay K 8644 ◽  
Calcium Currents ◽  
Pituitary Cells ◽  
Activation Curve ◽  
Voltage Gated ◽  
Channel Agonist

1. The sensitivity of voltage-gated calcium currents to hyperosmotic media containing mannitol or sucrose (373-723 mOsm) and to the dihydropyridine (DHP) calcium channel agonist Bay K 8644 was examined in enriched populations of rat anterior pituitary somatotrophs by using the whole cell mode of the patch-clamp technique. 2. Hyperosmotic media reduced the amplitude of voltage-gated calcium currents. With a 61.9% increase in extracellular medium osmolarity (523 mOsm), low voltage-activated (LVA) calcium currents were reduced to 67.9 +/- 17.8% of control size and high voltage-activated (HVA) calcium currents were reduced to 57.0 +/- 5.7% (mean +/- SD) of control size. The hyperosmotic suppression of HVA calcium currents was usually accompanied with a negative shift of 6.0 +/- 2.9 mV (mean +/- SD) in the activation curve of HVA currents. 3. The DHP calcium-channel agonist Bay K 8644 (10 microM), which stimulates hormone secretion from somatotrophs, increased the amplitude of HVA calcium currents to 212.6 +/- 67.2% of their control size, prolonged their tail currents, and negatively shifted the activation curve of HVA calcium currents by 6.2 +/- 2.8 mV. 4. Hyperosmotic media reduced the amplitude of DHP-sensitive HVA calcium currents and their associated prolonged tail currents, thus providing direct evidence for hyperosmotic suppression of DHP-sensitive currents. 5. Hence, exposure of pituitary cells to hyperosmotic media reduced voltage-sensitive calcium influx through LVA and DHP-sensitive HVA calcium channels. The inhibition of calcium influx through DHP-sensitive channels, which are implicated in regulation of hormone secretion in these cells, suggests that inhibitory hyperosmotic effects on hormone secretion from pituitary cells may stem from inhibition of calcium influx, before the exocytotic process. These results may also be relevant to effects of hypertonicity on neurosecretion in the nervous system.

CALCIUM CHANNEL CURRENTS IN CULTURED PARS INTERCEREBRALIS NEUROSECRETORY CELLS OF ADULT LOCUSTA MIGRATORIA

1994 ◽  
Vol 197 (1) ◽  
pp. 393-398
Author(s):  
U Bickmeyer ◽  
W RÖssler ◽  
H Wiegand
Keyword(s):  
Calcium Channel ◽  
Calcium Influx ◽  
Locusta Migratoria ◽  
Biological Significance ◽  
Ionic Currents ◽  
Neurosecretory Cells ◽  
Calcium Currents ◽  
Pars Intercerebralis ◽  
Channel Currents

The medial neurosecretory cells (MNSCs) of the pars intercerebralis in the brain of insects release various hormonal factors that control essential physiological and developmental functions such as moulting, reproduction and metabolism (Wigglesworth, 1940; Girardie, 1966; Goldsworthy, 1969), and these cells are therefore of considerable biological significance. A culture system for locust embryonic pars intercerebralis neurosecretory cells has recently been developed (Vanhems et al. 1993), and Rossler and Bickmeyer (1993) have established an in vitro system for growing larval and adult medial neurosecretory cells. Calcium plays an important role in neural physiology: neurosecretion depends on calcium influx into the cells and calcium currents carry the rising phase of action potentials in different types of insect neurones (Orchard, 1976; Pitman, 1979); calcium also mediates other ionic currents (Thomas, 1984). It is therefore of considerable interest to characterize the types of calcium channel currents found in locust neurosecretory neurones.

Lysophospholipids Modulate Voltage-Gated Calcium Channel Currents in Pituitary Cells; Effects of Lipid-Stress

2010 ◽  
Vol 98 (3) ◽  
pp. 15a
Author(s):  
Galia Ben-Zeev ◽  
Michael Telias ◽  
Daniel Bert ◽  
Itzhak Nussinovitch
Keyword(s):  
Calcium Channel ◽  
Pituitary Cells ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel ◽  
Channel Currents

Cortisol rapidly suppresses intracellular calcium and voltage-gated calcium channel activity in prolactin cells of the tilapia (Oreochromis mossambicus)

2004 ◽  
Vol 286 (4) ◽  
pp. E626-E633 ◽  
Author(s):  
Gregory N. Hyde ◽  
Andre P. Seale ◽  
E. Gordon Grau ◽  
Russell J. Borski
Keyword(s):  
Protein Synthesis ◽  
Calcium Channel ◽  
Time Course ◽  
Hormone Secretion ◽  
Oreochromis Mossambicus ◽  
Bay K 8644 ◽  
Free Calcium ◽  
Pituitary Cells ◽  
Channel Activity ◽  
Voltage Gated

Cortisol was previously shown to rapidly (10-20 min) reduce the release of prolactin (PRL) from pituitary glands of tilapia ( Oreochromis mossambicus). This inhibition of PRL release by cortisol is accompanied by rapid reductions in 45Ca2+ and cAMP accumulation. Cortisol's early actions occur through a protein synthesis-independent pathway and are mimicked by a membrane-impermeable analog. The signaling pathway that mediates rapid, nongenomic membrane effects of glucocorticoids is poorly understood. Using the advantageous characteristics of the teleost pituitary gland from which a nearly pure population of PRL cells can be isolated and incubated in defined medium, we examined whether cortisol rapidly reduces intracellular free calcium ([Formula: see text]) and suppresses L-type voltage-gated ion channel activity in events that lead to reduced PRL release. Microspectrofluorometry, used in combination with the Ca2+-sensitive dye fura 2 revealed that cortisol reversibly reduces basal and hyposmotically induced [Formula: see text] within seconds ( P < 0.001) in dispersed pituitary cells. Somatostatin, a peptide known to inhibit PRL release through a membrane receptor-coupled mechanism, similarly reduces [Formula: see text]. Under depolarizing [K+], the L-type calcium channel agonist BAY K 8644, a factor known to delay the closing of L-type Ca2+ channels, stimulates PRL release in a concentration-dependent fashion ( P < 0.01). Cortisol (and somatostatin) blocks BAY K 8644-induced PRL release ( P < 0.01; 30 min), well within the time course over which its actions occur, independent of protein synthesis and at the level of the plasma membrane. Results indicate that cortisol inhibits tilapia PRL release through rapid reductions in [Formula: see text] that likely involve an attenuation of Ca2+ entry through L-type voltage-gated Ca2+ channels. These results provide further evidence that glucocorticoids rapidly modulate hormone secretion via a membrane-associated mechanism similar to that observed with the fast effects of peptides and neurotransmitters.

Dopamine Modulation of Calcium Currents in Pyloric Neurons of the Lobster Stomatogastric Ganglion

2003 ◽  
Vol 90 (2) ◽  
pp. 631-643 ◽  
Author(s):  
Bruce R. Johnson ◽  
Peter Kloppenburg ◽  
Ronald M. Harris-Warrick
Keyword(s):  
Calcium Channel ◽  
Transmitter Release ◽  
Stomatogastric Ganglion ◽  
Calcium Currents ◽  
Voltage Gated ◽  
Pyloric Network ◽  
Pyloric Dilator ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Dopamine Modulation

We examined the dopamine (DA) modulation of calcium currents (ICa) that could contribute to the plasticity of the pyloric network in the lobster stomatogastric ganglion. Pyloric somata were voltage-clamped under conditions designed to block voltage-gated Na+, K+, and H currents. Depolarizing steps from –60 mV generated voltage-dependent, inward currents that appeared to originate in electrotonically distal, imperfectly clamped regions of the cell. These currents were blocked by Cd2+ and enhanced by Ba2+ but unaffected by Ni2+. Dopamine enhanced the peak ICa in the pyloric constrictor (PY), lateral pyloric (LP), and inferior cardiac (IC) neurons and reduced peak ICa in the ventricular dilator (VD), pyloric dilator (PD), and anterior burster (AB) neurons. All of these effects, except for the AB, are consistent with DA's excitation or inhibition of firing in the pyloric neurons. Enhancement of ICa in PY and LP neurons and reduction of ICa in VD and PD neurons are also consistent with DA-induced synaptic strength changes via modulation of presynaptic ICa. However, the reduction of ICa in AB suggests that DA's enhancement of AB transmitter release is not directly mediated through presynaptic ICa. ICa in PY and PD neurons was more sensitive to nifedipine block than in AB neurons. In addition, nifedipine blocked DA's effects on ICa in the PY and PD neurons but not in the AB neuron. Thus the contribution of specific calcium channel subtypes carrying the total ICa may vary between pyloric neuron classes, and DA may act on different calcium channel subtypes in the different pyloric neurons.

K+ modulation of microglial superoxide production: involvement of voltage-gated Ca2+ channels

1994 ◽  
Vol 266 (6) ◽  
pp. C1650-C1655 ◽  
Author(s):  
C. A. Colton ◽  
M. Jia ◽  
M. X. Li ◽  
D. L. Gilbert
Keyword(s):  
Calcium Channel ◽  
Superoxide Anion ◽  
Calcium Influx ◽  
Bay K 8644 ◽  
Neonatal Rat ◽  
Extracellular Potassium ◽  
Superoxide Anion Production ◽  
Voltage Gated ◽  
Anion Production ◽  
Voltage Gated Calcium Channel

A variety of cytoactive factors produced during injury and inflammation are known to activate the central nervous system (CNS) macrophage, the microglia. Since extracellular potassium levels are known to rise rapidly at sites of injury in the CNS, we examined the possibility that changes in extracellular potassium could mediate changes in microglial function. The effect of an increase in potassium concentration on microglial superoxide anion production was studied in cultured neonatal rat microglia. Rather than directly inducing superoxide anion production, exposure to media containing 25 and 55 mM potassium enhanced the production of superoxide induced by phorbol 12-myristate 13-acetate. This potentiation was blocked by nifedipine, a voltage-gated calcium channel blocker. Treatment of the microglia with BAY K 8644, an agonist for voltage-gated calcium channels, produced an enhancement of superoxide levels similar to that of potassium. Because these data indicated the presence of a voltage-gated calcium channel, we also examined whole cell current in cultured microglia. A small, voltage-dependent inward calcium current was seen that was increased by exposure of the microglia to BAY K 8644. The presence of a small but finite calcium influx via these channels may be an important factor in the regulation of intracellular microglial events such as activation of the NADPH oxidase and the consequent production of superoxide anion.

scholarly journals Subplasmalemmal hydrogen peroxide triggers calcium influx in gonadotropes

2018 ◽  
Vol 293 (41) ◽  
pp. 16028-16042 ◽  
Author(s):  
An K. Dang ◽  
Nathan L. Chaplin ◽  
Dilyara A. Murtazina ◽  
Ulrich Boehm ◽  
Colin M. Clay ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Calcium Channels ◽  
Nadph Oxidase ◽  
Calcium Channel ◽  
Anterior Pituitary ◽  
Calcium Influx ◽  
Ros Generation ◽  
Primary Mouse ◽  
The Impact ◽  
Stimulation Of

Gonadotropin-releasing hormone (GnRH) stimulation of its eponymous receptor on the surface of endocrine anterior pituitary gonadotrope cells (gonadotropes) initiates multiple signaling cascades that culminate in the secretion of luteinizing and follicle-stimulating hormones, which have critical roles in fertility and reproduction. Enhanced luteinizing hormone biosynthesis, a necessary event for ovulation, requires a signaling pathway characterized by calcium influx through L-type calcium channels and subsequent activation of the mitogen-activated protein kinase extracellular signal-regulated kinase (ERK). We previously reported that highly localized subplasmalemmal calcium microdomains produced by L-type calcium channels (calcium sparklets) play an essential part in GnRH-dependent ERK activation. Similar to calcium, reactive oxygen species (ROS) are ubiquitous intracellular signaling molecules whose subcellular localization determines their specificity. To investigate the potential influence of oxidant signaling in gonadotropes, here we examined the impact of ROS generation on L-type calcium channel function. Total internal reflection fluorescence (TIRF) microscopy revealed that GnRH induces spatially restricted sites of ROS generation in gonadotrope-derived αT3-1 cells. Furthermore, GnRH-dependent stimulation of L-type calcium channels required intracellular hydrogen peroxide signaling in these cells and in primary mouse gonadotropes. NADPH oxidase and mitochondrial ROS generation were each necessary for GnRH-mediated stimulation of L-type calcium channels. Congruently, GnRH increased oxidation within subplasmalemmal mitochondria, and L-type calcium channel activity correlated strongly with the presence of adjacent mitochondria. Collectively, our results provide compelling evidence that NADPH oxidase activity and mitochondria-derived hydrogen peroxide signaling play a fundamental role in GnRH-dependent stimulation of L-type calcium channels in anterior pituitary gonadotropes.

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