Interaction between 3’,5’-cyclic monophosphate, volume-regulated anion channels and the Na+-HCO3- cotransporter NBCe1 in the regulation of nutrient- and hypotonicity-induced insulin release from rat pancreatic islets and tumoral insulin-producing BRIN-BD11 cells

info:eu-repo/semantics/published

Arsenate-induced phosphate release from soils and its effect on plant phosphorus

Adsorption of arsenic onto soil was investigated as a means of understanding arsenic-induced release of phosphate. In batch adsorption experiments As adsorption was accompanied by P desorption. At low As additions, the ratio As adsorbed: P desorbed remained constant. At higher As additions, P desorption reached a maximum while As adsorption continued to increase. The P desorption maximum coincided with an increase in pH. Barley plants were grown on soils spiked with arsenate (0-360 mg As kg(-1)) to investigate the effect on plant growth and P uptake. As arsenic concentration increased, above ground plant yield decreased and the plants showed symptoms typical of As toxicity and P deficiency. At low As additions to the soil, uptake of As and P by barley increased. At higher As additions P uptake decreased. It is argued that this was due to the change in As:P ratio in the soil solution. It is concluded that input of arsenic to the soil could mobilise phosphate. Crop yield is likely to be affected, either due to reduced phosphate availability at low arsenic additions or arsenic toxicity at higher additions.

Scallop size does not predict amount or rate of induced sperm release

Within populations of broadcast spawning marine invertebrates such as scallops, larger animals typically have larger gonads. Presumably, this means those larger males have more sperm to release than small males. However, there has never been a direct test of whether larger males actually release more sperm, at a higher rate, during spawning. To address this, we compared the allometry of induced sperm release with that of reproductive investment (gonad weight) in ripe males of 2 species of scallops, Chlamys bifrons and Chlamys asperrima. We did not find that larger scallops released more sperm or released it faster than small scallops, and were able to reject the hypothesis that instantaneous sperm release was related to body size in the same way as gonad weight. Consequently, we speculate that if larger broadcast spawning males do release more sperm, they may do so by spawning on more occasions within a reproductive season.

Cortisol delays the estradiol-induced LH surge : is this dependent on prior ovarian steroid exposure?

Glucocorticoids can inhibit pulsatile LH secretion and can delay or even block the preovulatory LH surge. Previous work in ovariectomized ewes has indicated that cortisol can delay the estradiol-induced LH surge in an artificial follicular phase model but the results suggest this effect may be influenced by prior exposure to ovarian steroids. Here we tested the hypothesis that this disruptive effect of cortisol on the positive feedback action of estradiol is dependent on prior exposure to the ovarian steroidal milieu of the estrous cycle. Using long-term ovariectomized ewes, sequential artificial estrous cycles were created in the anestrous season by treatment and subsequent withdrawal of progesterone (CIDRs inserted for 9 d) followed by estradiol implants simulating the pre-ovulatory estradiol rise that induces the LH surge. Following the first artificial estrous cycle, a second cycle was initiated. Progesterone was again administered for 9 d followed by a second artificial follicular phase two weeks later. Beginning 2 hr prior to estradiol administration and ending at 40 hr, animals received either a cortisol infusion (elevate plasma levels to ∼170 ng/ml) or vehicle. Jugular blood was sampled hourly to assess occurrence and timing of the LH surge. Four different treatment sequences were tested (Cycle 1-Cycle 2): cortisol-cortisol; vehicle-cortisol; cortisol-vehicle; and vehicle-vehicle (n=5-6/sequence). If prior exposure to the ovarian steroidal milieu of the estrous cycle was necessary for cortisol to interfere with the positive feedback action of estradiol, then we would predict that cortisol would only delay the LH surge when it was delivered in Cycle 2 but not Cycle 1. Our results failed to support this prediction. Cortisol delayed the surge in both cycles (p<0.01), and the extent of the delay was the same in both Cycles 1 and 2 (4 hrs). Cortisol did not significantly affect surge amplitude in either cycle. These findings reinforce our previous conclusion that cortisol can delay the estradiol-induced LH surge but they do not support the hypothesis that this action of cortisol is dependent upon exposure to the ovarian steroidal milieu of the previous estrous cycle. (NIH-HD-30773)

Exocyst subunits are involved in isoproterenol-induced amylase release from rat parotid acinar cells

Exocytosis of secretory granules in parotid acinar cells requires multiple events: tethering, docking, priming, and fusion with a luminal plasma membrane. The exocyst complex, which is composed of eight subunits (Sec3, Sec5, Sec6, Sec8, Sec10, Sec15, Exo70, and Exo84) that are conserved in yeast and mammalian cells, is thought to participate in the exocytotic pathway. However, to date, no exocyst subunit has been identified in salivary glands. In the present study, we investigated the expression and function of exocyst subunits in rat parotid acinar cells. The expression of mRNA for all eight exocyst subunits was detected in parotid acinar cells by RT-PCR, and Sec6 and Sec8 proteins were localized on the luminal plasma membrane. Sec6 interacted with Sec8 after 5 min of stimulation with isoproterenol. In addition, antibodies to-Sec6 and Sec8 inhibited isoproterenol-induced amylase release from streptolysin O-permeabilized parotid acinar cells. These results suggest that an exocyst complex of eight subunits is required for amylase release from parotid acinar cells.

Mitochondrial Ca2+-induced Ca2+ Release Mediated by the Ca2+ Uniporter

We have reported that a population of chromaffin cell mitochondria takes up large amounts of Ca2+ during cell stimulation. The present study focuses on the pathways for mitochondrial Ca2+ efflux. Treatment with protonophores before cell stimulation abolished mitochondrial Ca2+ uptake and increased the cytosolic [Ca2+] ([Ca2+]c) peak induced by the stimulus. Instead, when protonophores were added after cell stimulation, they did not modify [Ca2+]c kinetics and inhibited Ca2+ release from Ca2+-loaded mitochondria. This effect was due to inhibition of mitochondrial Na+/Ca2+ exchange, because blocking this system with CGP37157 produced no further effect. Increasing extramitochondrial [Ca2+]c triggered fast Ca2+ release from these depolarized Ca2+-loaded mitochondria, both in intact or permeabilized cells. These effects of protonophores were mimicked by valinomycin, but not by nigericin. The observed mitochondrial Ca2+-induced Ca2+ release response was insensitive to cyclosporin A and CGP37157 but fully blocked by ruthenium red, suggesting that it may be mediated by reversal of the Ca2+ uniporter. This novel kind of mitochondrial Ca2+-induced Ca2+ release might contribute to Ca2+ clearance from mitochondria that become depolarized during Ca2+ overload.

Nicotinic cholinergic signaling in hippocampal astrocytes involves calcium-induced calcium release from intracellular stores

In this report we provide evidence that neuronal nicotinic acetylcholine receptors (nAChRs) are present on hippocampal astrocytes and their activation produces rapid currents and calcium transients. Our data indicate that these responses obtained from astrocytes are primarily mediated by an AChR subtype that is functionally blocked by α-bungarotoxin (αBgt) and contains the α7 subunit (αBgt-AChRs). Furthermore, their action is unusual in that they effectively increase intracellular free calcium concentrations by activating calcium-induced calcium release from intracellular stores, triggered by influx through the receptor channels. These results reveal a mechanism by which αBgt-AChRs on astrocytes can efficiently modulate calcium signaling in the central nervous system in a manner distinct from that observed with these receptors on neurons.