Stimulus-secretion coupling in an insect salivary gland: cell activation by elevated potassium concentrations

1975 ◽  
Vol 62 (3) ◽  
pp. 629-636
Author(s):  
M. J. Berridge ◽  
B. D. Lindley ◽  
W. T. Prince

1. Fluid secretion by isolated salivary glands was stimulated by elevating the external potassium concentration. 2. The stimulatory effect of potassium was dependent on external calcium and was potentiated by a subthreshold dose of 5-hydroxytryptamine (5-HT). 3. During the action of 120 mM potassium there was a large calciumdependent decrease in transepithelial resistance similar to that produced with 5-HT at normal potassium concentrations. 4. These results on Calliphora salivary glands are compared with other cases where cells are activated by high potassium. In most cases, the effect of high potassium is dependent upon calcium, suggesting that the latter plays a primary role in cell activation.

1976 ◽  
Vol 64 (2) ◽  
pp. 311-322
Author(s):  
M. J. Berridge ◽  
B. D. Lindley ◽  
W. T. Prince

1. Potassium is the major cation in the secretion of the salivary glands of Calliphora and is necessary for full secretory rates. 2. Other ions (rubidium and sodium) can support secretion in the absence of potassium. 39. During stimulation with 5-HT a Nernst plot of the basal membrane potential has a slope of 53 mV for a tenfold change in external potassium concentration and the slope at rest deviates from this over the range I-20 mM external potassium. 4. Hyperpolarization of the basal membrane by 5-HT is abolished if the chloride in the bathing medium is replaced by isethionate. 5. The diuretic agent amiloride inhibits fluid secretion by a mechanism which may include a reduction in calcium entry in addition to its recognized effect on sodium permeability. 6. A model is proposed in which fluid secretion is driven by the active transport of potassium across the apical membrane with chloride following passively.


2007 ◽  
Vol 178 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Viravuth P. Yin ◽  
Carl S. Thummel ◽  
Arash Bashirullah

A pulse of the steroid hormone ecdysone triggers the destruction of larval salivary glands during Drosophila metamorphosis through a transcriptional cascade that converges on reaper (rpr) and head involution defective (hid) induction, resulting in caspase activation and cell death. We identify the CREB binding protein (CBP) transcriptional cofactor as essential for salivary gland cell death. We show that CBP acts 1 d before the onset of metamorphosis in apparent response to a mid-third instar ecdysone pulse, when CBP is necessary and sufficient for down-regulation of the Drosophila inhibitor of apoptosis 1 (DIAP1). It is only after DIAP1 levels are reduced that salivary glands become competent to die through rpr/hid-mediated cell death. Before this time, high levels of DIAP1 block salivary gland cell death, even in the presence of ectopic rpr expression. This study shows that naturally occurring changes in inhibitor of apoptosis levels can be critical for regulating cell death during development. It also provides a molecular mechanism for the acquisition of competence in steroid signaling pathways.


Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1443-1455 ◽  
Author(s):  
C.Y. Lee ◽  
E.H. Baehrecke

Apoptosis and autophagy are morphologically distinct forms of programmed cell death. While autophagy occurs during the development of diverse organisms and has been implicated in tumorigenesis, little is known about the molecular mechanisms that regulate this type of cell death. Here we show that steroid-activated programmed cell death of Drosophila salivary glands occurs by autophagy. Expression of p35 prevents DNA fragmentation and partially inhibits changes in the cytosol and plasma membranes of dying salivary glands, suggesting that caspases are involved in autophagy. The steroid-regulated BR-C, E74A and E93 genes are required for salivary gland cell death. BR-C and E74A mutant salivary glands exhibit vacuole and plasma membrane breakdown, but E93 mutant salivary glands fail to exhibit these changes, indicating that E93 regulates early autophagic events. Expression of E93 in embryos is sufficient to induce cell death with many characteristics of apoptosis, but requires the H99 genetic interval that contains the rpr, hid and grim proapoptotic genes to induce nuclear changes diagnostic of apoptosis. In contrast, E93 expression is sufficient to induce the removal of cells by phagocytes in the absence of the H99 genes. These studies indicate that apoptosis and autophagy utilize some common regulatory mechanisms.


1973 ◽  
Vol 58 (1) ◽  
pp. 29-43
Author(s):  
C. R. HOUSE

1. Some aspects of neuroglandular transmission in isolated salivary glands of the cockroach have been studied. 2. The membrane potential of acinar cells is -32.3±0.8 mV (mean±S..E; N = 600 cells) when the gland is bathed in Ringer solution. 3. Upon delivering a single shock by ‘field stimulation’ to the salivary nerves the gland cell membrane undergoes after an initial latency of 1 second a transient hyperpolarization of about 1-30 mV which lasts for about 10 sec. 4. When the salivary nerves are stimulated by trains of current pulses the hyperpolarization that occurs is larger in amplitude and longer in duration than that after a single stimulus. 5. The amplitude of the responses to single shocks and stimulus trains depends on the external potassium concentration. Thus, the neurotransmitter may increase membrane permeability to potassium ions. 6. The electrical response of the gland cell to 5-hydroxytryptamine in concentrations from 2.5-250x10-7 M is similar in sign and magnitude to that of nervous stimulation. 7. Occasionally small fluctuations in the membrane potential are observed and these are similar in sign and duration to responses elicited by single shocks to the salivary nerves.


1960 ◽  
Vol 43 (3) ◽  
pp. 597-607 ◽  
Author(s):  
J. C. Dalton ◽  
W. J. Adelman

Experiments were performed to determine the quantitative relation existing between action potential and resting potential of the lobster giant axon. Resting potential changes were induced by either increasing the external potassium concentration or by reducing the external calcium concentration. For either treatment the action potential amplitude is proportional to the logarithm of the resting potential minus a constant. This constant is equivalent to the minimum resting potential at which a propagated spike is possible, and is larger for depolarization in low calcium than in high potassium. Thus the change in action potential per unit change in resting potential is greater in low external calcium than in high external potassium. Analog computer solutions to the Hodgkin-Huxley equations for squid axon membrane potentials show that, if the initial conditions are properly specified, the action potential is proportional to the logarithm of the potassium potential minus a constant. The experimental results and the analog computations suggest that reducing external calcium produces changes in the invertebrate axon that cannot be accounted for solely on the basis of alterations in the potassium potential.


2011 ◽  
Vol 43 (4) ◽  
pp. 622-631 ◽  
Author(s):  
Ola M. Maria ◽  
Osama Maria ◽  
Younan Liu ◽  
Svetlana V. Komarova ◽  
Simon D. Tran

2019 ◽  
Vol 97 ◽  
pp. 122-130 ◽  
Author(s):  
Jomy J. Varghese ◽  
M. Eva Hansen ◽  
Azmeer Sharipol ◽  
Matthew H. Ingalls ◽  
Martha A. Ormanoski ◽  
...  

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4673-4683 ◽  
Author(s):  
C. Jiang ◽  
E.H. Baehrecke ◽  
C.S. Thummel

During insect metamorphosis, pulses of the steroid hormone 20-hydroxyecdysone (ecdysone) direct the destruction of obsolete larval tissues and their replacement by tissues and structures that form the adult fly. We show here that larval midgut and salivary gland histolysis are stage-specific steroid-triggered programmed cell death responses. Dying larval midgut and salivary gland cell nuclei become permeable to the vital dye acridine orange and their DNA undergoes fragmentation, indicative of apoptosis. Furthermore, the histolysis of these tissues can be inhibited by ectopic expression of the baculovirus anti-apoptotic protein p35, implicating a role for caspases in the death response. Coordinate stage-specific induction of the Drosophila death genes reaper (rpr) and head involution defective (hid) immediately precedes the destruction of the larval midgut and salivary gland. In addition, the diap2 anti-cell death gene is repressed in larval salivary glands as rpr and hid are induced, suggesting that the death of this tissue is under both positive and negative regulation. Finally, diap2 is repressed by ecdysone in cultured salivary glands under the same conditions that induce rpr expression and trigger programmed cell death. These studies indicate that ecdysone directs the death of larval tissues via the precise stage- and tissue-specific regulation of key death effector genes.


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