scholarly journals Neonatal Intermittent Hypoxia Leads to Long-Lasting Facilitation of Acute Hypoxia-Evoked Catecholamine Secretion From Rat Chromaffin Cells

2009 ◽  
Vol 101 (6) ◽  
pp. 2837-2846 ◽  
Author(s):  
Dangjai Souvannakitti ◽  
Ganesh K. Kumar ◽  
Aaron Fox ◽  
Nanduri R. Prabhakar
Keyword(s):  
Intermittent Hypoxia ◽  
Chromaffin Cells ◽  
Acute Hypoxia ◽  
Adult Life ◽  
Underlying Mechanism ◽  
Ion Concentration ◽  
Rat Pups ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration

The objective of the present study was to examine the effects of intermittent hypoxia (IH) and sustained hypoxia (SH) on hypoxia-evoked catecholamine (CA) secretion from chromaffin cells in neonatal rats and assess the underlying mechanism(s). Experiments were performed on rat pups exposed to either IH (15-s hypoxia/5-min normoxia; 8 h/day) or SH (hypobaric hypoxia, 0.4 atm) or normoxia (controls) from P0 to P5. IH treatment facilitated hypoxia-evoked CA secretion and elevations in the intracellular calcium ion concentration ([Ca2+]i) and these responses were attenuated, but not abolished, by treatments designed to eliminate Ca2+ flux into cells (Ca2+-free medium or Cd2+), indicating that intracellular Ca2+ stores were augmented by IH. Norepinephrine (NE) and epinephrine (E) levels of adrenal medullae were elevated in IH-treated pups. IH treatment increased reactive oxygen species (ROS) production in adrenal medullae and antioxidant treatment prevented IH-induced facilitation of CA secretion, elevations in [Ca2+]i by hypoxia, and the up-regulation of NE and E. The effects of neonatal IH treatment on hypoxia-induced CA secretion and elevation in [Ca2+]i, CA, and ROS levels persisted in rats reared under normoxia for >30 days. In striking contrast, chromaffin cells from SH-treated animals exhibited attenuated hypoxia-evoked CA secretion. In SH-treated cells hypoxia-evoked elevations in [Ca2+]i, NE and E contents, and ROS levels were comparable with controls. These observations demonstrate that: 1) neonatal IH and SH evoke opposite effects on hypoxia-evoked CA secretion from chromaffin cells, 2) ROS signaling mediates the faciltatory effects of IH, and 3) the effects of neonatal IH on chromaffin cells persist into adult life.

scholarly journals Glutamate Regulates IP3-Type and CICR Stores in the Avian Cochlear Nucleus

1999 ◽  
Vol 81 (4) ◽  
pp. 1587-1596 ◽  
Author(s):  
B. Maya Kato ◽  
Edwin W Rubel
Keyword(s):  
Phorbol Ester ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptor ◽  
Ion Concentration ◽  
Metabotropic Glutamate ◽  
Highly Active ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration

Glutamate regulates IP3-type and CICR stores in the avian cochlear nucleus. Neurons of the avian cochlear nucleus, nucleus magnocellularis (NM), are activated by glutamate released from auditory nerve terminals. If this stimulation is removed, the intracellular calcium ion concentration ([Ca2+]i) of NM neurons rises and rapid atrophic changes ensue. We have been investigating mechanisms that regulate [Ca2+]i in these neurons based on the hypothesis that loss of Ca2+ homeostasis causes the cascade of cellular changes that results in neuronal atrophy and death. In the present study, video-enhanced fluorometry was used to monitor changes in [Ca2+]i stimulated by agents that mobilize Ca2+ from intracellular stores and to study the modulation of these responses by glutamate. Homobromoibotenic acid (HBI) was used to stimulate inositol trisphosphate (IP3)-sensitive stores, and caffeine was used to mobilize Ca2+ from Ca2+-induced Ca2+ release (CICR) stores. We provide data indicating that Ca2+responses attributable to IP3- and CICR-sensitive stores are inhibited by glutamate, acting via a metabotropic glutamate receptor (mGluR). We also show that activation of C-kinase by a phorbol ester will reduce HBI-stimulated calcium responses. Although the protein kinase A accumulator, Sp-cAMPs, did not have an effect on HBI-induced responses. CICR-stimulated responses were not consistently attenuated by either the phorbol ester or the Sp-cAMPs. We have previously shown that glutamate attenuates voltage-dependent changes in [Ca2+]i. Coupled with the present findings, this suggests that in these neurons mGluRs serve to limit fluctuations in intracellular Ca2+ rather than increase [Ca2+]i. This system may play a role in protecting highly active neurons from calcium toxicity resulting in apoptosis.

Influence of the Membrane Potential on the Intracellular Light Induced Ca2+ -Concentration Change of the Limulus Ventral Photoreceptor Monitored by Arsenazo III under Voltage Clamp Conditions

1984 ◽  
Vol 39 (9-10) ◽  
pp. 986-992 ◽  
Author(s):  
I. Ivens ◽  
H. Stieve
Keyword(s):  
Voltage Clamp ◽  
Light Flash ◽  
Membrane Voltage ◽  
Ion Concentration ◽  
Arsenazo Iii ◽  
Substantial Part ◽  
Voltage Range ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Pass Through

Abstract The light induced transmission change (Arsenazo signal) of an Arsenazo III injected ventral photoreceptor cell of Limulus polyphemus was studied under voltage clamp. The transmission change which represents a change of free intracellular calcium ion concentration, [Ca2+]i, was investigated for its dependence upon membrane voltage. The peak amplitude of the Arsenazo signal decreases in a linear fashion with the clamp voltage in the examined voltage range (from -80 to + 40 mV). In low Ca2+ saline ([Ca2+]e = 250 μᴍ) this decrease in the amplitude of the Arsenazo signal was more pronounced, while in saline with increased Ca2+ ([Ca2+]e = 40, 50 and 100 mᴍ), there is almost no change of the Arsenazo signal with varied membrane voltage. The recovery of the Arsenazo signal (i.e. recovery of the transmission back to the value before the light flash) is faster during hyperpolarization, this recovery being slowed down when the cell is depolarized. From these experiments it is concluded that a substantial part of the Arsenazo signal is due to a light induced influx of Ca2+ from the extracellular space across the cell membrane into the cytoplasma. Conceivably the Ca2+ could pass through light activated Na+ channels. Subsequently the increased intracellular Ca2+ is lowered to the preillumination level, by a membrane voltage dependent mechanism possibly an Na+-Ca2+ exchange. The data do not exclude the possibility that a part of the Ca2+ responsible for the Arsenazo signal is released from intracellular stores.

Stimulus-Dependent Alterations in Quantal Neurotransmitter Release

2006 ◽  
Vol 96 (6) ◽  
pp. 3082-3087 ◽  
Author(s):  
Chad P. Grabner ◽  
Aaron P. Fox
Keyword(s):  
Neurotransmitter Release ◽  
Chromaffin Cells ◽  
Time Course ◽  
Ion Concentration ◽  
Fusion Pore ◽  
Release Process ◽  
Large Dense Core Vesicles ◽  
Intracellular Calcium Ion ◽  
Individual Vesicle ◽  
Digitonin Permeabilization

Neurotransmitter release is a steep function of the intracellular calcium ion concentration ([Ca2+]i) at the release sites. Both the Ca2+ amplitude and the time course appear to be important for specifying neurotransmitter release. Ca2+ influx regulates the number of vesicles exocytosed as well as the amount of neurotransmitter each individual vesicle releases. In our study we stimulated mouse chromaffin cells in two different ways to alter Ca2+ presentation at the release sites. One method, digitonin permeabilization followed by exposure to Ca2+, allows for a large uniform global elevation of [Ca2+]i, whereas the second method, application of nicotine, depolarizes chromaffin cells and activates voltage-dependent Ca2+ channels, thereby producing more phasic and localized changes in [Ca2+]i. Using amperometry to monitor catecholamine release, we show that both kinds of stimuli elicit the exocytosis of similar quantities of neurotransmitter per large dense core vesicles (LDCVs) released. Even so, the release process was quite different for each stimulus; nicotine-elicited events were small and slow, whereas digitonin events were, in comparison, large and fast. In addition, the transient opening of the fusion pore, called the “foot,” was essentially absent in digitonin-stimulated cells, but was quite common in nicotine-stimulated cells. Thus even though both strong stimuli used in this study elicited the release of many vesicles it appears that the differences in the Ca2+ levels at the release sites were key determinants for the fusion and release of individual vesicles.

scholarly journals Platelet activating factor raises intracellular calcium ion concentration in macrophages.

1986 ◽  
Vol 103 (2) ◽  
pp. 439-450 ◽  
Author(s):  
G W Conrad ◽  
T J Rink
Keyword(s):  
Heavy Metals ◽  
Intracellular Calcium ◽  
Calcium Ion ◽  
Platelet Activating Factor ◽  
Ion Concentration ◽  
Early Event ◽  
Acetoxymethyl Ester ◽  
Intracellular Calcium Ion ◽  
The Times ◽  
Calcium Ion Concentration

Peritoneal cells from thioglycollate-stimulated mice were allowed to adhere to coverglasses for 2 h to give a dense monolayer of adherent cells greater than 95% of which were macrophages. After incubation with the tetra-acetoxymethyl ester of quin2, coverglasses were rinsed with Ca2+-free saline, oriented at a 45 degree angle in square cuvettes containing a magnetically driven stir bar, and analyzed for changes in quin2 fluorescence in a spectrofluorimeter. Such fluorescence, taken as an indication of intracellular calcium ion concentration ([Ca2+]i), increased as exogenous calcium ion concentration ([Ca2+]o) was raised to 1 mM. At [Ca2+]o approximately equal to 10 microM, [Ca2+]i = 72 +/- 14 nM (n = 26); at [Ca2+]o = 1 mM, [Ca2+]i = 140-220 nM, levels not increased by N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine, a membrane-permeant chelator of heavy metals than can quench quin2. Addition of mouse alpha + beta fibroblast interferon, lipopolysaccharide, thrombin, collagen, vasopressin, ADP, compound 48/80, or U46619 did not change [Ca2+]i. However, addition of platelet activating factor (PAF) (2-20 ng/ml) raised [Ca2+]i by 480 nM within 1 min if [Ca2+]o = 1 mM. In the presence of 5 mM EGTA, PAF raised [Ca2+]i by 25 nM. This suggests that PAF causes influx of exogenous Ca2+, as well as releasing some Ca2+ from intracellular stores. Consistent with these results, when PAF was added to 1 mM Ca2+ in the presence of 100 microM Cd2+ or Mn2+ to block Ca2+ influx, [Ca2+]i increased by only intermediate amounts; at the times of such dampened peak response, [Ca2+]i could be raised within 1 min to normal PAF-stimulated levels by chelation of the exogenous heavy metals with diethylenetriaminepentaacetic acid. Normal PAF responses were observed in the presence of indomethacin. The lowest dose of PAF observed to raise [Ca2+]i was 0.1 ng/ml. Response of [Ca2+]i to 2-20 ng/ml PAF was transient, and second applications had no effect. The PAF response also was seen in cell suspensions. These results suggest that an increase in [Ca2+]i may be an early event in PAF activation of macrophages.

scholarly journals Induction of Filopodia by Direct Local Elevation of Intracellular Calcium Ion Concentration

1999 ◽  
Vol 145 (6) ◽  
pp. 1265-1276 ◽  
Author(s):  
Pak-ming Lau ◽  
Robert S. Zucker ◽  
David Bentley
Keyword(s):  
Intracellular Calcium ◽  
Calcium Ion ◽  
Intracellular Signaling ◽  
Growth Cones ◽  
Ion Concentration ◽  
Rhodamine Phalloidin ◽  
Small Areas ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration ◽  
Neuronal Growth Cones

In neuronal growth cones, cycles of filopodial protrusion and retraction are important in growth cone translocation and steering. Alteration in intracellular calcium ion concentration has been shown by several indirect methods to be critically involved in the regulation of filopodial activity. Here, we investigate whether direct elevation of [Ca2+]i, which is restricted in time and space and is isolated from earlier steps in intracellular signaling pathways, can initiate filopodial protrusion. We raised [Ca2+]i level transiently in small areas of nascent axons near growth cones in situ by localized photolysis of caged Ca2+ compounds. After photolysis, [Ca2+]i increased from ∼60 nM to ∼1 μM within the illuminated zone, and then returned to resting level in ∼10–15 s. New filopodia arose in this area within 1–5 min, and persisted for ∼15 min. Elevation of calcium concentration within a single filopodium induced new branch filopodia. In neurons coinjected with rhodamine-phalloidin, F-actin was observed in dynamic cortical patches along nascent axons; after photolysis, new filopodia often emerged from these patches. These results indicate that local transient [Ca2+]i elevation is sufficient to induce new filopodia from nascent axons or from existing filopodia.

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