scholarly journals Activation of Ca(2+)-dependent currents in cultured rat dorsal root ganglion neurones by a sperm factor and cyclic ADP-ribose.

1992 ◽  
Vol 3 (12) ◽  
pp. 1415-1425 ◽  
Author(s):  
K P Currie ◽  
K Swann ◽  
A Galione ◽  
R H Scott
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Calcium Release ◽  
Ruthenium Red ◽  
Buffering Capacity ◽  
Mammalian Sperm ◽  
Cyclic Adp Ribose ◽  
Sperm Factor ◽  
Calcium Induced Calcium Release ◽  
Mammalian Eggs

The effects of intracellular application of two novel Ca2+ releasing agents have been studied in cultured rat dorsal root ganglion (DRG) neurones by monitoring Ca(2+)-dependent currents as a physiological index of raised free cytosolic Ca2+ ([Ca2+]i). A protein based sperm factor (SF) extracted from mammalian sperm, has been found to trigger Ca2+ oscillations and to sensitize unfertilized mammalian eggs to calcium induced calcium release (CICR). In this study intracellular application of SF activated Ca(2+)-dependent currents in approximately two-thirds of DRG neurones. The SF induced activity was abolished by heat treatment, attenuated by increasing the intracellular Ca2+ buffering capacity of the cells and persisted when extracellular Ca2+ was replaced by Ba2+. In addition, activity could be triggered or potentiated by loading the cells with Ca2+ by activating a series of voltage-gated Ca2+ currents. Ca(2+)-activated inward current activity was also generated by intracellular application of cyclic ADP-ribose (cADPR), a metabolite of NAD+, which causes Ca2+ release in sea urchin eggs. This activity could also be enhanced by loading the cells with Ca2+. The cADPR induced activity, but not the SF induced activity, was abolished by depleting the caffeine sensitive Ca2+ store. Ruthenium red markedly attenuated SF induced activity but had little action on cADPR induced activity or caffeine induced activity. Our results indicate that both SF and cADPR release intracellular Ca2+ pools in DRG neurones and that they appear to act on subtly distinct stores or distinct intracellular Ca2+ release mechanisms, possibly by modulating CICR.

Angiotensin II Ca2+ signaling in rat afferent arterioles: stimulation of cyclic ADP ribose and IP3 pathways

2005 ◽  
Vol 288 (4) ◽  
pp. F785-F791 ◽  
Author(s):  
Susan K. Fellner ◽  
William J. Arendshorst
Keyword(s):  
Calcium Release ◽  
Rat Kidney ◽  
Ang Ii ◽  
High Concentration ◽  
Inositol Trisphosphate Receptor ◽  
Cyclic Adp Ribose ◽  
Specific Antagonist ◽  
Afferent Arterioles ◽  
Trisphosphate Receptor ◽  
Calcium Induced Calcium Release

ANG II induces a rise in cytosolic Ca2+ ([Ca2+]i) in vascular smooth muscle (VSM) cells via inositol trisphosphate receptor (IP3R) activation and release of Ca2+ from the sarcoplasmic reticulum (SR). The Ca2+ signal is augmented by calcium-induced calcium release (CICR) and by cyclic adeninediphosphate ribose (cADPR), which sensitizes the ryanodine-sensitive receptor (RyR) to Ca2+ to further amplify CICR. cADPR is synthesized from β-nicotinamide adenine dinucleotide (NAD+) by a membrane-bound bifunctional enzyme, ADPR cyclase. To investigate the possibility that ANG II activates the ADPR cyclase of afferent arterioles, we used inhibitors of the IP3R, RyR, and ADPR cyclase. Afferent arterioles were isolated from rat kidney with the magnetized microsphere and sieving technique and loaded with fura-2 to measure [Ca2+]i. In Ca2+-containing buffer, ANG II increased [Ca2+]i by 125 ± 10 nM. In the presence of the IP3R antagonists TMB-8 and 2-APB, the peak responses to ANG II were reduced by 74 and 81%, respectively. The specific antagonist of cADPR 8-Br ADPR and a high concentration of ryanodine (100 μM) inhibited the ANG II-induced increases in [Ca2+]i by 75 and 69%, respectively. Nicotinamide and Zn2+ are known inhibitors of the VSM ADPR cyclase. Nicotinamide diminished the [Ca2+]i response to ANG II by 66%. In calcium-free buffer, Zn2+ reduced the ANG II response by 68%. Simultaneous blockade of the IP3 and cADPR pathways diminished the [Ca2+]i response to ANG II by 83%. We conclude that ANG II initiates Ca2+ mobilization from the SR in afferent arterioles via the classic IP3R pathway and that ANG II may lead to activation of the ADPR cyclase to form cADPR, which, via its action on the RyR, substantially augments the Ca2+ response.

A cytosolic sperm factor stimulates repetitive calcium increases and mimics fertilization in hamster eggs

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1295-1302 ◽  
Author(s):  
K. Swann
Keyword(s):  
G Protein ◽  
Calcium Release ◽  
Phorbol Esters ◽  
Free Calcium ◽  
Vitro Fertilization ◽  
Protein Factor ◽  
G Protein Signalling ◽  
Sperm Factor ◽  
Calcium Induced Calcium Release

Microinjection of cytosolic sperm extracts into unfertilized golden hamster eggs caused a series of increases in cytoplasmic free calcium, Ca2+i, and membrane hyperpolarizing responses, HRs. These HRs and Ca2+i transients are similar to those seen during in vitro fertilization of hamster eggs. The sperm factor that is responsible for causing these effects appears to be of high molecular weight and protein based. Injection of sperm factor activated eggs and mimicked fertilization in causing repetitive HRs in the presence of phorbol esters and in sensitizing the egg to calcium-induced calcium release. Since these effects cannot be mimicked by injecting G-protein agonists or calcium-containing solutions, it seems unlikely that a receptor-G-protein signalling system is involved at fertilization. These data instead suggest a novel signal transduction system operates during mammalian fertilization in which a protein factor is transferred from the sperm into the egg cytoplasm after gamete membrane fusion.

scholarly journals Effect of TRPV4-p38 MAPK Pathway on Neuropathic Pain in Rats with Chronic Compression of the Dorsal Root Ganglion

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Yu-Juan Qu ◽  
Xiao Zhang ◽  
Zhen-Zhen Fan ◽  
Juan Huai ◽  
Yong-Bo Teng ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Mechanical Allodynia ◽  
Mapk Pathway ◽  
Intrathecal Injection ◽  
Ruthenium Red ◽  
Protein Expressions ◽  
Intermediary Role ◽  
Ectopic Discharges

The aim of this study was to investigate the relationships among TRPV4, p38, and neuropathic pain in a rat model of chronic compression of the dorsal root ganglion. Mechanical allodynia appeared after CCD surgery, enhanced via the intrathecal injection of 4α-phorbol 12,13-didecanoate (4α-PDD, an agonist of TRPV4) and anisomycin (an agonist of p38), but was suppressed by Ruthenium Red (RR, an inhibitor of TRPV4) and SB203580 (an inhibitor of p38). The protein expressions of p38 and P-p38 were upregulated by 4α-PDD and anisomycin injection but reduced by RR and SB203580. Moreover, TRPV4 was upregulated by 4α-PDD and SB203580 and downregulated by RR and anisomycin. In DRG tissues, the numbers of TRPV4- or p38-positive small neurons were significantly changed in CCD rats, increased by the agonists, and decreased by the inhibitors. The amplitudes of ectopic discharges were increased by 4α-PDD and anisomycin but decreased by RR and SB203580. Collectively, these results support the link between TRPV4 and p38 and their intermediary role for neuropathic pain in rats with chronic compression of the dorsal root ganglion.

scholarly journals Calcium pools mobilized by calcium or inositol 1,4,5-trisphosphate are differentially localized in rat heart and brain.

1992 ◽  
Vol 3 (6) ◽  
pp. 621-631 ◽  
Author(s):  
A Verma ◽  
D J Hirsch ◽  
S H Snyder
Keyword(s):  
Binding Sites ◽  
Calcium Release ◽  
Cardiac Tissue ◽  
Coronary Vessels ◽  
Medial Septum ◽  
Ruthenium Red ◽  
Cardiac Conduction ◽  
Inositol 1,4,5 Trisphosphate ◽  
Calcium Induced Calcium Release ◽  
The Brain

Calcium-induced calcium release (CICR) pools have been demonstrated in brain and heart microsomes biochemically and autoradiographically by the sensitivity of 45Ca2+ accumulation to Mg2+, ATP, ruthenium red, caffeine, and tetracaine. The CICR pool colocalizes with [3H]ryanodine binding sites, supporting the notion that [3H]ryanodine labels CICR pools. Sites of CICR pools in the brain contrast with those of inositol 1,4,5-trisphosphate (IP3)-sensitive Ca2+ pools with reciprocal localizations between the two Ca2+ pools in several structures. Thus, in the hippocampus CA-1 is enriched in IP3-sensitive Ca2+ pools, whereas CICR pools are highest in CA-3 and the dentate gyrus. The corpus striatum and cerebellum are enriched in IP3 pools, whereas the medial septum and olfactory bulb have high CICR densities. In cardiac tissue, CICR is localized to atrial and ventricular muscle, whereas IP3 pools are concentrated in coronary vessels and cardiac conduction fibers. The reciprocal enrichment of IP3 and CICR Ca2+ pools implies differential regulation of Ca2+ hemostasis in these tissues.

ATP-induced calcium release from the intracellular stores in murine dorsal root ganglion neurons

1997 ◽  
Vol 29 (4-5) ◽  
pp. 302-302
Author(s):  
N. V. Svichar ◽  
A. N. Verkhratsky ◽  
P. G. Kostyuk
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Calcium Release ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons

Cyclic ADP-ribose and the regulation of calcium-induced calcium release in eggs and cardiac myocytes

1998 ◽  
Vol 28 (1) ◽  
pp. 19-30 ◽  
Author(s):  
Antony Galione ◽  
Yi Cui ◽  
Ruth Empson ◽  
Shigao Iino ◽  
Heather Wilson ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Calcium Release ◽  
Cyclic Adp Ribose ◽  
Calcium Induced Calcium Release

Venom From the Platypus,Ornithorhynchus anatinus,Induces a Calcium-Dependent Current in Cultured Dorsal Root Ganglion Cells

2001 ◽  
Vol 85 (3) ◽  
pp. 1340-1345 ◽  
Author(s):  
G. M. de Plater ◽  
P. J. Milburn ◽  
R. L. Martin
Keyword(s):  
Dorsal Root Ganglion ◽  
Natriuretic Peptide ◽  
Dorsal Root ◽  
Calcium Release ◽  
Ganglion Cells ◽  
Reversal Potential ◽  
Serine Kinase ◽  
Cationic Current ◽  
Ornithorhynchus Anatinus ◽  
Dorsal Root Ganglion Cells

The platypus ( Ornithorhynchus anatinus), a uniquely Australian species, is one of the few living venomous mammals. Although envenomation of humans by many vertebrate and invertebrate species results in pain, this is often not the principal symptom of envenomation. However, platypus envenomation results in an immediate excruciating pain that develops into a very long-lasting hyperalgesia. We have previously shown that the venom contains a C-type natriuretic peptide that causes mast cell degranulation, and this probably contributes to the development of the painful response. Now we demonstrate that platypus venom has a potent action on putative nociceptors. Application of the venom to small to medium diameter dorsal root ganglion cells for 10 s resulted in an inward current lasting several minutes when the venom was diluted in buffer at pH 6.1 but not at pH 7.4. The venom itself has a pH of 6.3. The venom activated a current with a linear current-voltage relationship between −100 and −25 mV and with a reversal potential of −11 mV. Ion substitution experiments indicate that the current is a nonspecific cationic current. The response to the venom was blocked by the membrane-permeant Ca2+-ATPase inhibitor, thapsigargin, and by the tyrosine- and serine-kinase inhibitor, k252a. Thus the response appears to be dependent on calcium release from intracellular stores. The identity of the venom component(s) that is responsible for the responses we have described is yet to be determined but is probably not the C-type natriuretic peptide or the defensin-like peptides that are present in the venom.

Sign in / Sign up

Export Citation Format

Share Document